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Indonesia bans traditional Ramadan exodus to rein in COVID-19 spread

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Indonesia bans traditional Ramadan exodus to rein in COVID-19 spread

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21 Apr 2020

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JAKARTA: Indonesia will ban its traditional annual exodus of people streaming out of cities at the end of the Muslim fasting month in May, as the Southeast Asian nation looks to curb the spread of COVID-19, President Joko Widodo said on Tuesday (Apr 21).

Indonesia's tally of 590 coronavirus deaths is the highest in East Asia after China, but Widodo had previously resisted a ban, seeking instead to persuade people to stay put.

But health experts had warned that allowing millions in the world's biggest Muslim-majority country to travel to their home villages after Ramadan could hasten the spread of the disease.

"I have taken the decision that we will ban 'mudik'," Widodo told a Cabinet meeting, using the Indonesian term for the journey. "That is why the relevant preparation needs to be done."

He cited a survey by the transport ministry that showed 24 per cent of the archipelago's population of more than 260 million were insisting on joining the exodus after Ramadan.

Luhut Pandjaitan, the coordinating minister for maritime affairs and investment said that the ban will come into effect on Friday.

Last year, about 19.5 million people in the archipelago made the journey, the government says, and Widodo added that 7 per cent of Indonesians had already set out this year.

In a study last week, researchers at the University of Indonesia's public health faculty warned that if the exodus was permitted, it could lead to a million infections by July on Java, the most populous island, home to the capital Jakarta.
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Without the exodus, that figure could be cut to 750,000 cases, the researchers said.

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Indonesia bans traditional Ramadan exodus to rein in COVID-19 spread

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(Updated: ) Share this content JAKARTA: Indonesia will ban its traditional annual exodus of people streaming out of cities at the end of the Muslim fasting month in May, as the Southeast Asian nation looks to curb the spread of COVID-19, President Joko Widodo said on Tuesday (Apr 21).

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COVID-19: PM Lee announces 4-week extension of Singapore circuit breaker to Jun 1

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COVID-19: PM Lee announces 4-week extension of Singapore circuit breaker to Jun 1

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21 Apr 2020

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[LIVE HD] COVID-19: PM Lee announces 4-week extension of Singapore circuit breaker to Jun 1

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COVID-19 circuit breaker extended until Jun 1 as Singapore aims to bring down community cases ‘decisively’: PM Lee

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COVID-19 circuit breaker extended until Jun 1 as Singapore aims to bring down community cases ‘decisively’: PM Lee

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21 Apr 2020

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Explaining the need to extend the circuit breaker period, Mr Lee said Singapore will not be able to completely lift the restrictions after May 4 and go back to business as usual.

"We will therefore extend the circuit breaker for four more weeks beyond May 4, in other words until Jun 1. Then, provided we have brought the community numbers down, we can make further adjustments and consider easing some measures," he said.

"This way, we can be more assured that we have made definite progress and consolidated our position.

"Many will be disappointed by the extension of the circuit breaker, especially our business and workers, who are hurting greatly," said Mr Lee. "But I hope you understand that this short-term pain is to stamp out the virus, protect the health and safety of our loved ones, and allow us to revive our economy."

UNLINKED CASES A CONCERN
Singapore on Tuesday reported 1,111 new cases of COVID-19, just a day after it confirmed a record daily high of 1,426 new coronavirus infections. Eleven people have died so far from complications due to COVID-19.

The Prime Minister acknowledged that the circuit breaker is starting to have an effect, as the number of community cases has fallen in recent days.

"This is the result of all of us coming together, making sacrifices and adhering to the circuit breaker rules. But, we cannot afford to be complacent. We must press on to bring down daily infections more sharply, to single digit, or even zero," he said.

However, Mr Lee also raised concerns about the number of unlinked cases.

"Unfortunately that number has not come down, and this suggests there is a larger, hidden reservoir of COVID-19 cases in the community, and this reservoir is the source of these unlinked cases, which we have not detected," he said.

On how Singapore can exit from the circuit breaker, Mr Lee stressed that the country needs to take things one step at a time - first by opening up incrementally, in small steps, to make sure that people are safe.

"Second, we need to scale up testing for COVID-19 substantially, so that we can quickly detect any new cases that pop up," Mr Lee said. "This we are progressively doing, not only by procuring test kits and equipment from other countries, but also by developing and manufacturing our own test kits."

Singapore will also need to make full use of IT, so that when it discovers COVID-19 cases, it can trace more efficiently where people have been, and whom they have been in contact with, Mr Lee added.

"I know this has not been an easy time for everyone. We are making progress, but we have not yet succeeded, by a long way," the Prime Minister said.

"The results show that the circuit breaker is working. Now we all need to do a little bit more, make best use of the next two weeks of the tightened circuit breaker, and the four weeks of the extension beyond that," he added.

"I ask for your support and cooperation. I ask for your trust and your confidence. Let us go all out to beat the virus, and break the chain of transmission. We will overcome this together."

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COVID-19 circuit breaker extended until Jun 1 as Singapore aims to bring down community cases 'decisively': PM Lee

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SINGAPORE: Singapore will extend its COVID-19 "circuit breaker" period by four weeks until Jun 1, as well as implement tighter measures such as closing more workplaces, said Prime Minister Lee Hsien Loong on Tuesday (Apr 21). In a televised address to the nation, Mr Lee said that

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Investigation on Practical Usefulness of Body-worn Devices that Claim to Release Chlorine Dioxide

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Investigation on Practical Usefulness of Body-worn Devices that Claim to Release Chlorine Dioxide

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July 2017

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How does coronavirus kill? Clinicians trace a ferocious rampage through the body, from brain to toes

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How does coronavirus kill? Clinicians trace a ferocious rampage through the body, from brain to toes

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17 Apr 2020

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On rounds in a 20-bed intensive care unit one recent day, physician Joshua Denson assessed two patients with seizures, many with respiratory failure and others whose kidneys were on a dangerous downhill slide. Days earlier, his rounds had been interrupted as his team tried, and failed, to resuscitate a young woman whose heart had stopped. All shared one thing, says Denson, a pulmonary and critical care physician at the Tulane University School of Medicine. "They are all COVID positive."

As the number of confirmed cases of COVID-19 surges past 2.2 million globally and deaths surpass 150,000, clinicians and pathologists are struggling to understand the damage wrought by the coronavirus as it tears through the body. They are realizing that although the lungs are ground zero, its reach can extend to many organs including the heart and blood vessels, kidneys, gut, and brain.

"[The disease] can attack almost anything in the body with devastating consequences," says cardiologist Harlan Krumholz of Yale University and Yale-New Haven Hospital, who is leading multiple efforts to gather clinical data on COVID-19. "Its ferocity is breathtaking and humbling."

Understanding the rampage could help the doctors on the front lines treat the fraction of infected people who become desperately and sometimes mysteriously ill. Does a dangerous, newly observed tendency to blood clotting transform some mild cases into life-threatening emergencies? Is an overzealous immune response behind the worst cases, suggesting treatment with immune-suppressing drugs could help? What explains the startlingly low blood oxygen that some physicians are reporting in patients who nonetheless are not gasping for breath? "Taking a systems approach may be beneficial as we start thinking about therapies," says Nilam Mangalmurti, a pulmonary intensivist at the Hospital of the University of Pennsylvania (HUP).

What follows is a snapshot of the fast-evolving understanding of how the virus attacks cells around the body, especially in the roughly 5% of patients who become critically ill. Despite the more than 1000 papers now spilling into journals and onto preprint servers every week, a clear picture is elusive, as the virus acts like no pathogen humanity has ever seen. Without larger, prospective controlled studies that are only now being launched, scientists must pull information from small studies and case reports, often published at warp speed and not yet peer reviewed. "We need to keep a very open mind as this phenomenon goes forward," says Nancy Reau, a liver transplant physician who has been treating COVID-19 patients at Rush University Medical Center. "We are still learning."

The infection begins

When an infected person expels virus-laden droplets and someone else inhales them, the novel coronavirus, called SARS-CoV-2, enters the nose and throat. It finds a welcome home in the lining of the nose, according to a preprint from scientists at the Wellcome Sanger Institute and elsewhere. They found that cells there are rich in a cell-surface receptor called angiotensin-converting enzyme 2 (ACE2). Throughout the body, the presence of ACE2, which normally helps regulate blood pressure, marks tissues vulnerable to infection, because the virus requires that receptor to enter a cell. Once inside, the virus hijacks the cell's machinery, making myriad copies of itself and invading new cells.

As the virus multiplies, an infected person may shed copious amounts of it, especially during the first week or so. Symptoms may be absent at this point. Or the virus' new victim may develop a fever, dry cough, sore throat, loss of smell and taste, or head and body aches.

If the immune system doesn't beat back SARS-CoV-2 during this initial phase, the virus then marches down the windpipe to attack the lungs, where it can turn deadly. The thinner, distant branches of the lung's respiratory tree end in tiny air sacs called alveoli, each lined by a single layer of cells that are also rich in ACE2 receptors.

Normally, oxygen crosses the alveoli into the capillaries, tiny blood vessels that lie beside the air sacs; the oxygen is then carried to the rest of the body. But as the immune system wars with the invader, the battle itself disrupts this healthy oxygen transfer. Front-line white blood cells release inflammatory molecules called chemokines, which in turn summon more immune cells that target and kill virus-infected cells, leaving a stew of fluid and dead cells-pus-behind. This is the underlying pathology of pneumonia, with its corresponding symptoms: coughing; fever; and rapid, shallow respiration (see graphic). Some COVID-19 patients recover, sometimes with no more support than oxygen breathed in through nasal prongs.

But others deteriorate, often quite suddenly, developing a condition called acute respiratory distress syndrome (ARDS). Oxygen levels in their blood plummet and they struggle ever harder to breathe. On x-rays and computed tomography scans, their lungs are riddled with white opacities where black space-air-should be. Commonly, these patients end up on ventilators. Many die. Autopsies show their alveoli became stuffed with fluid, white blood cells, mucus, and the detritus of destroyed lung cells.

Some clinicians suspect the driving force in many gravely ill patients' downhill trajectories is a disastrous overreaction of the immune system known as a "cytokine storm," which other viral infections are known to trigger. Cytokines are chemical signaling molecules that guide a healthy immune response; but in a cytokine storm, levels of certain cytokines soar far beyond what's needed, and immune cells start to attack healthy tissues. Blood vessels leak, blood pressure drops, clots form, and catastrophic organ failure can ensue.

Some studies have shown elevated levels of these inflammation-inducing cytokines in the blood of hospitalized COVID-19 patients. "The real morbidity and mortality of this disease is probably driven by this out of proportion inflammatory response to the virus," says Jamie Garfield, a pulmonologist who cares for COVID-19 patients at Temple University Hospital.

But others aren't convinced. "There seems to have been a quick move to associate COVID-19 with these hyperinflammatory states. I haven't really seen convincing data that that is the case," says Joseph Levitt, a pulmonary critical care physician at the Stanford University School of Medicine.

He's also worried that efforts to dampen a cytokine response could backfire. Several drugs targeting specific cytokines are in clinical trials in COVID-19 patients. But Levitt fears those drugs may suppress the immune response that the body needs to fight off the virus. "There's a real risk that we allow more viral replication," Levitt says.

Meanwhile, other scientists are zeroing in on an entirely different organ system that they say is driving some patients' rapid deterioration: the heart and blood vessels.

Striking the heart

In Brescia, Italy, a 53-year-old woman walked into the emergency room of her local hospital with all the classic symptoms of a heart attack, including telltale signs in her electrocardiogram and high levels of a blood marker suggesting damaged cardiac muscles. Further tests showed cardiac swelling and scarring, and a left ventricle-normally the powerhouse chamber of the heart-so weak that it could only pump one-third its normal amount of blood. But when doctors injected dye in the coronary arteries, looking for the blockage that signifies a heart attack, they found none. Another test revealed why: The woman had COVID-19.

How the virus attacks the heart and blood vessels is a mystery, but dozens of preprints and papers attest that such damage is common. A 25 March paper in JAMA Cardiology documented heart damage in nearly 20% of patients out of 416 hospitalized for COVID-19 in Wuhan, China. In another Wuhan study, 44% of 36 patients admitted to the ICU had arrhythmias.

The disruption seems to extend to the blood itself. Among 184 COVID-19 patients in a Dutch ICU, 38% had blood that clotted abnormally, and almost one-third already had clots, according to a 10 April paper in Thrombosis Research. Blood clots can break apart and land in the lungs, blocking vital arteries-a condition known as pulmonary embolism, which has reportedly killed COVID-19 patients. Clots from arteries can also lodge in the brain, causing stroke. Many patients have "dramatically" high levels of D-dimer, a byproduct of blood clots, says Behnood Bikdeli, a cardiovascular medicine fellow at Columbia University Medical Center.

"The more we look, the more likely it becomes that blood clots are a major player in the disease severity and mortality from COVID-19," Bikdeli says.

Infection may also lead to blood vessel constriction. Reports are emerging of ischemia in the fingers and toes-a reduction in blood flow that can lead to swollen, painful digits and tissue death.

Behnood Bikdeli, Columbia University Irving Medical Center

In the lungs, blood vessel constriction might help explain anecdotal reports of a perplexing phenomenon seen in pneumonia caused by COVID-19: Some patients have extremely low blood-oxygen levels and yet are not gasping for breath. It's possible that at some stages of disease, the virus alters the delicate balance of hormones that help regulate blood pressure and constricts blood vessels going to the lungs. So oxygen uptake is impeded by constricted blood vessels, rather than by clogged alveoli. "One theory is that the virus affects the vascular biology and that's why we see these really low oxygen levels," Levitt says.

If COVID-19 targets blood vessels, that could also help explain why patients with pre-existing damage to those vessels, for example from diabetes and high blood pressure, face higher risk of serious disease. Recent Centers for Disease Control and Prevention (CDC) data on hospitalized patients in 14 U.S. states found that about one-third had chronic lung disease-but nearly as many had diabetes, and fully half had pre-existing high blood pressure.

Mangalmurti says she has been "shocked by the fact that we don't have a huge number of asthmatics" or patients with other respiratory diseases in HUP's ICU. "It's very striking to us that risk factors seem to be vascular: diabetes, obesity, age, hypertension."

Scientists are struggling to understand exactly what causes the cardiovascular damage. The virus may directly attack the lining of the heart and blood vessels, which, like the nose and alveoli, are rich in ACE2 receptors. Or perhaps lack of oxygen, due to the chaos in the lungs, damages blood vessels. Or a cytokine storm could ravage the heart as it does other organs.

"We're still at the beginning," Krumholz says. "We really don't understand who is vulnerable, why some people are affected so severely, why it comes on so rapidly ... and why it is so hard [for some] to recover."

Multiple battlefields

The worldwide fears of ventilator shortages for failing lungs have received plenty of attention. Not so a scramble for another type of equipment: dialysis machines. "If these folks are not dying of lung failure, they're dying of renal failure," says neurologist Jennifer Frontera of New York University's Langone Medical Center, which has treated thousands of COVID-19 patients. Her hospital is developing a dialysis protocol with different machines to support additional patients. The need for dialysis may be because the kidneys, abundantly endowed with ACE2 receptors, present another viral target.

According to one preprint, 27% of 85 hospitalized patients in Wuhan had kidney failure. Another reported that 59% of nearly 200 hospitalized COVID-19 patients in China's Hubei and Sichuan provinces had protein in their urine, and 44% had blood; both suggest kidney damage. Those with acute kidney injury (AKI), were more than five times as likely to die as COVID-19 patients without it, the same Chinese preprint reported.

"The lung is the primary battle zone. But a fraction of the virus possibly attacks the kidney. And as on the real battlefield, if two places are being attacked at the same time, each place gets worse," says Hongbo Jia, a neuroscientist at the Chinese Academy of Sciences's Suzhou Institute of Biomedical Engineering and Technology and a co-author of that study.

Viral particles were identified in electron micrographs of kidneys from autopsies in one study, suggesting a direct viral attack. But kidney injury may also be collateral damage. Ventilators boost the risk of kidney damage, as do antiviral compounds including remdesivir, which is being deployed experimentally in COVID-19 patients. Cytokine storms also can dramatically reduce blood flow to the kidney, causing often-fatal damage. And pre-existing diseases like diabetes can increase the chances of kidney injury. "There is a whole bucket of people who already have some chronic kidney disease who are at higher risk for acute kidney injury," says Suzanne Watnick, chief medical officer at Northwest Kidney Centers.

Buffeting the brain

Another striking set of symptoms in COVID-19 patients centers on the brain and central nervous system. Frontera says neurologists are needed to assess 5% to 10% of coronavirus patients at her hospital. But she says that "is probably a gross underestimate" of the number whose brains are struggling, especially because many are sedated and on ventilators.

Frontera has seen patients with the brain inflammation encephalitis, with seizures, and with a "sympathetic storm," a hyperreaction of the sympathetic nervous system that causes seizurelike symptoms and is most common after a traumatic brain injury. Some people with COVID-19 briefly lose consciousness. Others have strokes. Many report losing their sense of smell. And Frontera and others wonder whether in some cases, infection depresses the brain stem reflex that senses oxygen starvation. This is another explanation for anecdotal observations that some patients aren't gasping for air, despite dangerously low blood oxygen levels.

ACE2 receptors are present in the neural cortex and brain stem, says Robert Stevens, an intensive care physician at Johns Hopkins Medicine. But it's not known under what circumstances the virus penetrates the brain and interacts with these receptors. That said, the coronavirus behind the 2003 severe acute respiratory syndrome (SARS) epidemic-a close cousin of today's culprit-could infiltrate neurons and sometimes caused encephalitis. On 3 April, a case study in the International Journal of Infectious Diseases, from a team in Japan, reported traces of new coronavirus in the cerebrospinal fluid of a COVID-19 patient who developed meningitis and encephalitis, suggesting it, too, can penetrate the central nervous system.

But other factors could be damaging the brain. For example, a cytokine storm could cause brain swelling, and the blood's exaggerated tendency to clot could trigger strokes. The challenge now is to shift from conjecture to confidence, at a time when staff are focused on saving lives, and even neurologic assessments like inducing the gag reflex or transporting patients for brain scans risk spreading the virus.

Last month, Sherry Chou, a neurologist at the University of Pittsburgh Medical Center, began to organize a worldwide consortium that now includes 50 centers to draw neurological data from care patients already receive. The early goals are simple: Identify the prevalence of neurologic complications in hospitalized patients and document how they fare. Longer term, Chou and her colleagues hope to gather scans, lab tests, and other data to better understand the virus' impact on the nervous system, including the brain.

Chou speculates about a possible invasion route: through the nose, then upward and through the olfactory bulb-explaining reports of a loss of smell-which connects to the brain. "It's a nice sounding theory," she says. "We really have to go and prove that."

Most neurological symptoms "are reported from colleague to colleague by word of mouth," Chou adds. "I don't think anybody, and certainly not me, can say we're experts."

Reaching the gut

In early March, a 71-year-old Michigan woman returned from a Nile River cruise with bloody diarrhea, vomiting, and abdominal pain. Initially doctors suspected she had a common stomach bug, such as Salmonella. But after she developed a cough, doctors took a nasal swab and found her positive for the novel coronavirus. A stool sample positive for viral RNA, as well as signs of colon injury seen in an endoscopy, pointed to a gastrointestinal (GI) infection with the coronavirus, according to a paper posted online in The American Journal of Gastroenterology ( AJG).

Her case adds to a growing body of evidence suggesting the new coronavirus, like its cousin SARS, can infect the lining of the lower digestive tract, where the crucial ACE2 receptors are abundant. Viral RNA has been found in as many as 53% of sampled patients' stool samples. And in a paper in press at Gastroenterology, a Chinese team reported finding the virus' protein shell in gastric, duodenal, and rectal cells in biopsies from a COVID-19 patient. "I think it probably does replicate in the gastrointestinal tract," says Mary Estes, a virologist at Baylor College of Medicine.

Recent reports suggest up to half of patients, averaging about 20% across studies, experience diarrhea, says Brennan Spiegel of Cedars-Sinai Medical Center in Los Angeles, co-editor-in-chief of AJG. GI symptoms aren't on CDC's list of COVID-19 symptoms, which could cause some COVID-19 cases to go undetected, Spiegel and others say. "If you mainly have fever and diarrhea, you won't be tested for COVID," says Douglas Corley of Kaiser Permanente, Northern California, co-editor of Gastroenterology.

The presence of virus in the GI tract raises the unsettling possibility that it could be passed on through feces. But it's not yet clear whether stool contains intact, infectious virus, or only RNA and proteins. To date, "We have no evidence" that fecal transmission is important, says coronavirus expert Stanley Perlman of the University of Iowa. CDC says that based on experiences with SARS and with the virus that causes Middle East respiratory syndrome, another dangerous cousin of the new coronavirus, the risk from fecal transmission is probably low.

The intestines are not the end of the disease's march through the body. For example, up to one-third of hospitalized patients develop conjunctivitis-pink, watery eyes-although it's not clear that the virus directly invades the eye. Other reports suggest liver damage: More than half of COVID-19 patients hospitalized in two Chinese centers had elevated levels of enzymes indicating injury to the liver or bile ducts. But several experts told Science that direct viral invasion isn't likely the culprit. They say other events in a failing body, like drugs or an immune system in overdrive, are more likely driving the liver damage.

This map of the devastation that COVID-19 can inflict on the body is still just a sketch. It will take years of painstaking research to sharpen the picture of its reach, and the cascade of cardiovascular and immune effects it might set in motion. As science races ahead, from probing tissues under microscopes to testing drugs on patients, the hope is for treatments more wily than the virus that has stopped the world in its tracks.
*Correction, 20 April, 12:25 p.m.: This story has been updated to correct the description of a sympathetic storm. It has also been updated to more accurately describe the geographic locations of the patients found to have protein and blood in their urine.

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How does coronavirus kill? Clinicians trace a ferocious rampage through the body, from brain to toes

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On rounds in a 20-bed intensive care unit one recent day, physician Joshua Denson assessed two patients with seizures, many with respiratory failure and others whose kidneys were on a dangerous downhill slide. Days earlier, his rounds had been interrupted as his team tried, and failed, to resuscitate a young woman whose heart had stopped.

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16 Apr 2020, by George Yeo

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This week's note is from George Yeo, Brunswick Geopolitical Principal and former Singapore Cabinet member for Health (1994-97), Trade and Industry (1999-2004) and Foreign Affairs (2004-11). This article represents his own personal views.

At 10am on Saturday April 4, which was Qing Ming or China's All Souls Day, sirens rang across the country for three minutes. The entire country paused to mourn all those who succumbed to COVID-19. It was a moment of national solidarity after a terrifying experience which seared the collective memory. According to official figures, over 3,300 Chinese died out of a total of over 83,000 infected. A few western reports have cast doubt on these numbers much to the indignation of Chinese authorities. Even if there were significantly more infections and deaths, it does not change the overall picture.

China's leaders took the fateful decision of locking down Wuhan, a city of eleven million people on January 23, two days before Chinese New Year. All modes of public transportation suddenly ceased operating - airport, train station, metro, river ports. By the afternoon, highways leading out of Wuhan were sealed off. Within a few days, the sixteen cities of Hubei Province with a population of almost sixty million people came under quarantine. By confining the main epidemic to Hubei province, China was able to prevent other major outbreaks of the epidemic in the country. For two months, the people of Hubei endured varying degrees of hardship, Wuhan the worst. Help poured in from the rest of the country. Within ten days, two special hospitals were built with a total of 2500 beds. Tens of thousands of healthcare personnel were dispatched from other provinces and the People's Liberation Army to reinforce a public healthcare system that would otherwise have collapsed from the sudden increase of critically ill patients. The Central Government ensured that every city in Hubei had a major province to lean on for general support. In gratitude, Hubei residents came out to the streets in large numbers to send off these 'foreign' contingents when they finally left Wuhan and other cities a few weeks ago.

Imagine if China's Central Government had dithered. The internal debate must have been ferocious. Wuhan is a major hub in China for air, rail, road and riverine transport. During the war against Japan, Wuhan was Chiang Kai-shek's temporary HQ after Nanjing fell. Great battles were fought to defend Wuhan while Chiang evacuated his administration to Chongqing which was upstream of the Yangtze River gorges and therefore much less accessible. Perhaps no other city is as well-connected to all of China than Wuhan. It has the biggest student population of any city in China with large numbers from other provinces. During the week-long Chinese New Year holidays, Chinese people go back to their hometowns for family reunions. The annual Spring migration in China is the biggest movement of human beings on earth.

Looking back, if Beijing had not taken this decision to confine Wuhan, the COVID-19 epidemic would have spread to all corners of China within a week. The World Health Organisation described the action as 'unprecedented' in the history of public health. There could easily have been fifty Wuhan outbreaks and the Chinese Communist Party would have been shaken to its core. At that time in late January, the nature of COVID-19 was still poorly understood and even today is still not well understood. Chinese authorities made serious mistakes in December and January including the persecution of whistleblowers by local officials. (Key provincial leaders involved in the early coverup have since been removed including the Party Secretaries of Hubei Province and Wuhan City.) But, on the most critical decision, China's Central Government made the right call. That saved China and bought the world precious weeks which unfortunately were not put to good use despite repeated alarms by the World Health Organisation.

For a few weeks, many people thought in their hearts that COVID-19 was a virus that mostly affected Chinese people and other East Asians, like SARS. That fueled conspiracy theories about the origin of the virus. As the number of infections and deaths rose day by day in China, the reaction of the external world was mixed. Some showed sympathy and extended help. Others sneered. Anti-China and anti-Chinese sentiments infected large parts of the world affecting not only Mainland Chinese but East Asians generally. Beijing took careful note of these different reactions. When the Wall Street Journal described China as 'the real sick man of Asia', it caused considerable offense among ordinary Chinese. In contrast, the modest donation of masks by the Vatican was applauded.

China, which once had to appeal for supplies from the rest of the world to supplement its own inadequate production, is now the principal supplier of such lifesaving material to the world.

Since then, the tables have turned dramatically. China has succeeded in bringing down the number of new cases to less than a hundred a day, the majority of them imported. The country remains dead scared of an epidemic rebound and has put in place comprehensive safeguards. Instead of the world locking in China, China is now locking out the world. Particular care is taken to protect Beijing. International flights to Beijing must first land in one of twelve provincial cities so that every incoming passenger is carefully checked and quarantined if necessary. At the same time, the Central Government has progressively relaxed controls on normal economic activities. All indicators (highway traffic, consumption of luxury goods, housing sales, coal consumption, air pollution etc.) show the economy quickly reviving. China's GDP is likely to register positive growth this year. The export sector remains badly affected of course but China's dependence on it is not as large as before because of the size of its internal market. China is the most vertically integrated economy in the world. Last July, McKinsey published a report that while the world's economic exposure to China is growing, China's exposure to the rest of the world is reducing.

In the meantime, COVID-19 has spread with a vengeance to the rest of the world on a scale much bigger than that which affected China. The economies of US and the EU are almost in free fall as priority is rightly placed on measures to control what has become a pandemic. Unemployment rates have shot up and national governments are spending trillions of dollars to help struggling businesses and individuals stay afloat. Masks, protective clothing and respirators are in woefully short supply. In some cities in Lombardy and Spain, a system of heart-wrenching triage was in place to decide who were more deserving of lifesaving treatment. China, which once had to appeal for supplies from the rest of the world to supplement its own inadequate production, is now the principal supplier of such lifesaving material to the world. China's factories operating 24/7 now make 200 million masks a day, much of which for export.

We do not know how long it will take for Europe and the US to get out of the current situation. COVID-19 is such a contagious virus, no country is safe until all countries are safe. Even after Europe and the US have contained the virus, its spread to other parts of the world (Middle East, Africa, South Asia, Southeast Asia, Latin America) will make it a recurrent threat to everyone until good vaccines are found to inoculate entire populations. What China has done, no other country can do. China's uniquely centralized system has deep roots in Chinese history and is not peculiar to the People's Republic. For over two thousand years, the ideal in the minds of ordinary people is of a well-functioning centralized system with good and wise leaders at the top. Great walls are repeatedly built to protect the country from baleful external influence. This is China's great strength but also its great weakness.f

The immediate impact of COVID-19 is to public health. The longer-term impact of COVID-19 is on the global economy and geopolitics. More than ten years after the Global Financial Crisis, another downturn is perhaps due. Some fear that this time it will be much worse. Governmental attempts to inject liquidity and suspend contractual obligations can only provide temporary relief. Eventually, the problem of excessive debt, caused in no small part to unprecedented infusion of liquidity into the global system since the Global Financial Crisis, will have to be resolved one way or another. As companies collapse with cascading knock-on effects on other companies and creditors, sorting out the financial mess may take years. With so much human suffering, affecting disproportionately those who are poorer off, existing political systems and structures will inevitably be called into question. In some countries, there will be social upheaval. What is weak will collapse and become history. What is strong will become stronger and built upon. In global politics and economics, the league table of leading countries and companies will change again.

In the US, the mixed response to COVID-19 is becoming a key issue for the coming elections. New leaders are being thrown up. In the EU, COVID-19 is testing European solidarity to its elastic limit. If COVID-19 becomes much worse in India, its rambunctious democracy will come under severe stress. In China, what began as a threat to the Communist Party has become vindication of its leadership, at least for the time being. Chinese history goes through long cycles. Every schoolboy in China is familiar with the opening lines of the Romance of the Three Kingdoms: In the great affairs of men, long disunity leads to unity and long unity leads to disunity.

China is now in pole position to lead the world out of global recession.

Provided it can prevent a second round of the epidemic, China is now in pole position to lead the world out of global recession. It is now the only tunnel with bright light at the end of it. China's leaders will naturally want to turn this to political advantage. Already we see how China doles out masks and other material (either by outright donation or through export licenses) to foreign countries based on political considerations. As its economy recovers, we can expect China to offer preferential access to its domestic market to friendly countries along the Belt and Road. For the US and Europe, China will try to make use of its current advantage to blunt anti-China sentiments and build long-term relations.

Anti-China sentiments in the west have gone from bad to worse in recent years caused partly by fear of a rising China and party by a clash of civilizational values. Even among those who admire China's success in overcoming COVID-19 there is antipathy towards China's authoritarian ways. When the Central Government shut down Wuhan, the people of Wuhan had no say in the decision. When President Trump considered shutting down New York City, Government Cuomo objected furiously. In China, national interest comes before human rights. In the liberal west, there is continuous tension between the two which is the source of western creativity from the time of Greece and Rome. It is interesting to compare the national reaction to two whistleblowers - China's Dr Li Wenliang who first sounded the alarm in Wuhan and Captain Brett Crozier who publicized the deteriorating situation onboard USS Theodore Roosevelt. Both men came down with the virus. In Dr Li's case, he has been officially vindicated after his death and the dossier is closed by central edict. In Captain Crozier's case, the debate will never cease whatever the White House might say. China and the US are built on different foundations, each having the weakness of its strength. Global cooperation requires each to accept the other for what it is.

Provided China does not overplay its hand this round, it may emerge a big winner out of the COVID-19 pandemic. It must curb the tendency of its officials to be overly truculent in their defense of China's position or condescending in their treatment of lesser powers. It will do well to heed Winston Churchill's wise words: In defeat, defiance; in victory, magnanimity; in peace, goodwill. At the recent Extraordinary G-20 Leaders Summit conducted through videoconference, President Xi Jinping called for greater international cooperation to fight the pandemic and to revive the global economy through coordination of macro-economic policy and facilitation of trade.

China is likely to convene the twin meetings of the National People's Congress and the National People's Political Consultative Committee soon. They had been postponed because of COVID-19. How China adjusts its domestic and foreign policy - economic and political - will be of interest not only to China but also to the world. COVID-19 is a global tragedy but it is also a historic opportunity for China and the world to reset course, rebuild trust, work together more and bring about a safer world. The alternative is a tragedy much worse than the pandemic.

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This week's note is from George Yeo, Brunswick Geopolitical Principal and former Singapore Cabinet member for Health (1994-97), Trade and Industry (1999-2004) and Foreign Affairs (2004-11). This article represents his own personal views. At 10am on Saturday April 4, which was Qing Ming or China's All Souls Day, sirens rang across the country for three minutes.

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Body-worn devices do not ward off Covid-19 or kill the coronavirus

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Body-worn devices do not ward off Covid-19 or kill the coronavirus

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Don't take any chances, wear your face mask.

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Besides putting on face masks, many are finding other ways to protect themselves from Covid-19.

Some methods, unfortunately, do not provide real protection, but only a false sense of security.

Body-worn devices claim to be able to kill coronavirus

Body-worn devices such as "EA mask" badges and "health tag" lanyards have been marketed as being able to inactivate viruses and kill bacteria.

They are particularly popular among senior folks, who probably find these gadgets more comfortable than face masks in the hot and humid weather.

Here are some examples:

These devices are being sold online, and even at high-end shopping stores like Takashimaya.

On the website, EA masks sell for S$16.50.

They are misleadingly advertised to "work harder than a conventional mask", because of the chlorine dioxide that the gadgets release.

The advertising copy read, "EA Mash and EA Bear gives you a 1m radius protection around your body 24/7".

Japan study finds body-worn devices do not kill influenza viruses

A 2017 study in Japan looked into four brands of such devices and find that the viral load in the air is similar to that found close to all devices tested, suggesting that these devices are not effective at all.

"Viral loads were found to be similar between viral samplings in the air collected from the site close to the device for all devices and in the controlled air, indicating that no virucidal activity was found against the air-borne influenza viruses with selected devices in these conditions."

Malaysian agency warns of tags that claim to kill Covid-19

More recently, Malaysiakini also reported on March 30 that Malaysia's National Poison Centre has issued a Facebook post to debunk claims that such products can ward off Covid-19 for users.

Moreover, the "heath tags" lanyards that emit chlorine dioxide can act as irritants toward the respiratory system, the authorities warned.

What concerns the authorities is the fact that people who blindly believe in these body-worn devices tend to let their guard down against Covid-19.

Such products have created much online chatter as well:

When in doubt, some common sense will help:

Top photos via Takashimaya website

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Body-worn devices do not ward off Covid-19 or kill the coronavirus

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Besides putting on face masks, many are finding other ways to protect themselves from Covid-19. Some methods, unfortunately, do not provide real protection, but only a false sense of security. Body-worn devices such as "EA mask" badges and "health tag" lanyards have been marketed as being able to inactivate viruses and kill bacteria.

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Cytokine release syndrome in severe COVID-19

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Cytokine release syndrome in severe COVID-19

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17 Apr 2020

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Abstract

Lessons from arthritis and cell therapy in cancer patients point to therapy for severe disease

In December 2019, a new strain of coronavirus, severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), was recognized to have emerged in Wuhan, China. Along with SARS-CoV and Middle East respiratory syndrome-coronavirus (MERS-CoV), SARS-CoV-2 is the third coronavirus to cause severe respiratory illness in humans, called coronavirus disease 2019 (COVID-19). This was recognized as a pandemic by the World Health Organization (WHO) in March 2020 and has had considerable global economic and health impacts. Although the situation is rapidly evolving, severe disease manifested by fever and pneumonia, leading to acute respiratory distress syndrome (ARDS), has been described in up to 20% of COVID-19 cases. This is reminiscent of cytokine release syndrome (CRS)-induced ARDS and secondary hemophagocytic lymphohistiocytosis (sHLH) observed in patients with SARS-CoV and MERS-CoV as well as in leukemia patients receiving engineered T cell therapy. Given this experience, urgently needed therapeutics based on suppressing CRS, such as tocilizumab, have entered clinical trials to treat COVID-19.

SARS-CoV-2 is a betacoronavirus that is most closely related to SARS-CoV. Both viruses use the angiotensin-converting enzyme-related carboxypeptidase (ACE2) receptor to gain entry to cells. This receptor is widely expressed in cardiopulmonary tissues but also in some hematopoietic cells, including monocytes and macrophages. A key feature of COVID-19 infection is lymphopenia (low blood lymphocyte count), which correlates with clinical severity (). SARS-CoV efficiently infects primary human monocytes and dendritic cells, whereas MERS-CoV infects monocytes and T cells via dipeptidyl peptidase 4 (DPP4) (, ). It is possible that SARS-CoV-2 also infects dendritic cells. T cell apoptosis and exhaustion resulting from defective activation due to dendritic cell dysfunction might contribute to the immunopathology of COVID-19 (, ). However, lymphopenia as a biomarker of poor prognosis for COVID-19 is not specific because it was also a biomarker that correlated with fatality in the 2009 influenza A (H1N1) pandemic ().

CRS was found to be the major cause of morbidity in patients infected with SARS-CoV and MERS-CoV (). Elevated serum concentrations of the cytokine interleukin-6 (IL-6) and other inflammatory cytokines are hallmarks of severe MERS-CoV infections (). CRS is common in patients with COVID-19, and elevated serum IL-6 correlates with respiratory failure, ARDS, and adverse clinical outcomes (, ). Elevated serum C-reactive protein (CRP), a protein whose expression is driven by IL-6, is also a biomarker of severe betacoronavirus infection.

Betacoronavirus infection of monocytes, macrophages, and dendritic cells results in their activation and secretion of IL-6 and other inflammatory cytokines. IL-6 has prominent proinflammatory properties (see the figure). IL-6 can signal through two main pathways referred to as classic cis signaling or trans signaling (). In cis signaling, IL-6 binds to membrane-bound IL-6 receptor (mIL-6R) in a complex with gp130; downstream signal transduction is mediated by JAKs (Janus kinases) and STAT3 (signal transducer and activator of transcription 3). Membrane-bound gp130 is ubiquitously expressed, whereas mIL-6R expression is restricted largely to immune cells. Activation of cis signaling results in pleiotropic effects on the acquired immune system (B and T cells) as well as the innate immune system [neutrophils, macrophages, and natural killer (NK) cells], which can contribute to CRS ().

In trans signaling, high circulating concentrations of IL-6 bind to the soluble form of IL-6R (sIL-6R), forming a complex with a gp130 dimer on potentially all cell surfaces. The resultant IL-6-sIL-6R-JAK-STAT3 signaling is then activated in cells that do not express mIL-6R, such as endothelial cells. This results in a systemic "cytokine storm" involving secretion of vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 (MCP-1), IL-8, and additional IL-6, as well as reduced E-cadherin expression on endothelial cells (). VEGF and reduced E-cadherin expression contribute to vascular permeability and leakage, which participate in the pathophysiology of hypotension and pulmonary dysfunction in ARDS.

sHLH is a hyperinflammatory syndrome characterized by CRS, cytopenias (low blood cell counts), and multiorgan failure (including the liver) (). In adults, sHLH is most commonly triggered by severe viral infections but also occurs in leukemia patients receiving engineered T cell therapy. In addition to elevated serum cytokines, high concentrations of ferritin are characteristic of sHLH. CD163-expressing macrophages are implicated as the source of ferritin given their role in reticuloendothelial iron signaling, hence sHLH is alternatively known as macrophage activation syndrome. A retrospective study of COVID-19 patients found that elevated serum ferritin and IL-6 correlated with nonsurvivors ().

Patients receiving chimeric antigen receptor (CAR) T cell therapy can also develop CRS and sHLH. This therapy involves engineering patient T cells to express CAR molecules that recognize antigens on tumor cells. When transplanted back into the patient, these engineered T cells target tumor cells, thereby activating immune clearance. Emily Whitehead, the first patient to receive CD19-targeted CAR T cells to treat pediatric B cell acute lymphoblastic leukemia in 2012, developed severe CRS and sHLH, leading to ARDS with multiorgan failure and hypotension that was refractory to standard treatment with steroids (). Because of greatly elevated serum IL-6 in this patient, she was treated empirically with tocilizumab, an IL-6R antagonist approved at the time to treat rheumatic conditions such as juvenile idiopathic arthritis. She received a single dose of tocilizumab on day 7 after CAR T cell administration, with rapid resolution of fever within hours followed by weaning from vasopressors (which treat hypotension) and from ventilator support as ARDS resolved. Tocilizumab is now approved by the U.S. Food and Drug Administration (FDA) for the treatment of CAR T cell-induced CRS, with confirmed efficacy and minimal side effects in hundreds of patients.

The efficacy of IL-6-IL-6R antagonists for the treatment of CRS as well as sHLH underscores the central role of IL-6 signaling in the pathophysiology of cytokine-driven hyperinflammatory syndromes (). Severe COVID-19 cases may benefit from IL-6 pathway inhibition given the associated CRS- and sHLH-like serum cytokine elevations. Indeed, preliminary results from an open-label study in 21 patients with COVID-19 treated with tocilizumab in China are encouraging (). Fever subsided in all patients within the first day of receiving tocilizumab. Oxygen requirements were reduced in 75% of the patients ().

Controlled clinical trials are under way worldwide to test IL-6 and IL-6R antagonists for the management of COVID-19 patients with severe respiratory complications. One issue to resolve is whether there will be differential effectiveness between IL-6 antagonists and IL-6R antagonists. Relevant to this is that IL‐6R inhibitors can suppress both cis and trans signaling as well as trans presentation, a recently described third mode of signaling. Trans presentation involves IL-6 binding to mIL-6R expressed on an immune cell, which forms a complex with gp130 on T helper 17 (T H 17) cells, leading to downstream T cell signaling that may be involved in ARDS (, , ). However, IL‐6 inhibitors can suppress only cis and trans signaling. The immediate goal of IL-6 antagonism is to ameliorate severe COVID-19 cases so that requirements for advanced care are minimized. The long-term goal should include a focus on the development of antivirals and vaccines that prevent or ameliorate the infection.

There are a number of caveats to consider, given the global urgency of mitigating the COVID-19 pandemic. In sepsis-associated ARDS, corticosteroids are often administered. However, corticosteroid use in SARS and MERS patients did not improve mortality and resulted in delayed viral clearance (). As a result, the expert consensus from infectious disease authorities and the WHO is to avoid systemic corticosteroids in COVID-19 patients at present. A theoretical possibility is that the suppression of inflammation by IL-6 antagonism might delay viral clearance. However, IL-6 blockade also results in rapid reduction of serum IL-10, an immunosuppressive cytokine secreted by macrophages, which may mitigate concerns about prolonging viral clearance (). Moreover, one or two doses of an IL-6 antagonist are unlikely to result in complications, such as fungal infections or osteonecrosis of the jaw, which occur in patients dosed monthly on these drugs for chronic conditions such as rheumatoid arthritis. It is notable that tocilizumab was first approved for rheumatic conditions, then for CRS in patients receiving CAR T cell therapy, and is now being further repurposed for the COVID-19 pandemic. It is possible that IL-6 directed therapies will be used in future pandemics involving other viruses such as influenza and Ebola (, ).

Acknowledgments: This work was funded by NIH grant 2R01CA120409 (C.H.J.) and a sponsored research grant from the Parker Institute for Cancer Immunotherapy. J.B.M. is an employee of the U.S. Government. This work was prepared as part of his official duties. The views expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Department of the Navy, the Department of Defense, or the U.S. Government. The therapeutics discussed in this Perspective are undergoing clinical testing and are not currently approved for the treatment of COVID-19.

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Cytokine release syndrome in severe COVID-19

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Lessons from arthritis and cell therapy in cancer patients point to therapy for severe disease In December 2019, a new strain of coronavirus, severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), was recognized to have emerged in Wuhan, China. Along with SARS-CoV and Middle East respiratory syndrome-coronavirus (MERS-CoV), SARS-CoV-2 is the third coronavirus to cause severe respiratory illness in humans, called coronavirus disease 2019 (COVID-19).

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Comparative pathogenesis of COVID-19, MERS, and SARS in a nonhuman primate model

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Comparative pathogenesis of COVID-19, MERS, and SARS in a nonhuman primate model

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17 Apr 2020

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Abstract

The current pandemic coronavirus, SARS-CoV-2, was recently identified in patients with an acute respiratory syndrome, COVID-19. To compare its pathogenesis with that of previously emerging coronaviruses, we inoculated cynomolgus macaques with SARS-CoV-2 or MERS-CoV and compared the pathology and virology with historical reports of SARS-CoV infections. In SARS-CoV-2-infected macaques, virus was excreted from nose and throat in the absence of clinical signs, and detected in type I and II pneumocytes in foci of diffuse alveolar damage and in ciliated epithelial cells of nasal, bronchial, and bronchiolar mucosae. In SARS-CoV-infection, lung lesions were typically more severe, while they were milder in MERS-CoV infection, where virus was detected mainly in type II pneumocytes. These data show that SARS-CoV-2 causes COVID-19-like disease in macaques, and provides a new model to test preventive and therapeutic strategies.

Following the first reports of an outbreak of an acute respiratory syndrome in China in December 2019, a novel coronavirus, SARS-CoV-2, was identified (, ). As of March 14, 2020, over 140,000 cases were reported worldwide with over 5,400 deaths, surpassing the combined number of cases and deaths of two previously emerging coronaviruses, SARS-CoV and MERS-CoV (). The disease caused by this virus, COVID-19, is characterized by a range of symptoms, including fever, cough, dyspnoea and myalgia in most cases (). In severe cases, bilateral lung involvement with ground-glass opacity is the most common chest computed tomography (CT) finding (). Similarly to the 2002/2003 outbreak of SARS, the severity of COVID-19 disease is associated with increased age and/or a comorbidity, although severe disease is not limited to these risk groups (). However, despite the large number of cases and deaths, limited information is available on the pathogenesis of this virus infection. Two reports on the histological examination of the lungs of three patients showed bilateral diffuse alveolar damage (DAD), pulmonary edema and hyaline membrane formation, indicative of acute respiratory distress syndrome (ARDS), as well as characteristic syncytial cells in the alveolar lumen (, ), similar to findings during the 2002/2003 outbreak of SARS-CoV (). The pathogenesis of SARS-CoV infection was previously studied in a non-human primate model (cynomolgus macaques) where aged animals were more likely to develop disease (-). In the current study, SARS-CoV-2 infection was characterized in the same animal model and compared with infection with MERS-CoV and historical data on SARS-CoV (, , ).

First, two groups of four cynomolgus macaques (both young adult (young), 4-5 years of age; and old adult (aged), 15-20 years of age) were inoculated by a combined intratracheal (IT) and intranasal (IN) route with a SARS-CoV-2 strain from a German traveler returning from China. No overt clinical signs were observed in any of the infected animals, except for a serous nasal discharge in one aged animal on day 14 post inoculation (p.i.). No significant weight loss was observed in any of the animals during the study. By day 14 p.i. all remaining animals seroconverted as revealed by the presence of SARS-CoV-2 specific antibodies against the virus S1 domain and nucleocapsid proteins in their sera (Fig. S1).

As a measure of virus shedding, nasal, throat and rectal swabs were assayed for virus by RT-qPCR and virus culture. In nasal swabs, detection of SARS-CoV-2 RNA peaked by day 2 p.i. in young animals, by day 4 p.i. in aged animals, was detected up to at least day 8 p.i. in two out of four animals and up to day 21 p.i. in one out of four animals ( Fig. 1A). Overall, higher levels of SARS-CoV-2 RNA were detected in nasal swabs of aged animals compared with young animals. SARS-CoV-2 RNA detection in throat swabs peaked at day 1 p.i. in young and day 4 p.i. in aged animals and decreased more rapidly over time by comparison with the nasal swabs, but could still be detected intermittently up to day 10 p.i. ( Fig. 1B). Low levels of infectious virus were cultured from throat and nasal swabs up to day 2 and 4, respectively (Table S1). In support of virus shedding by these animals, environmental sampling was performed to determine potential contamination of surfaces. Environmental sampling indicated the presence of low levels of SARS-CoV-2 RNA on surfaces through both direct contact (hands) and indirect contamination within the isolator (Table S2). SARS-CoV-2 RNA was only detected in a rectal swab from one animal on day 14 p.i. and no viral RNA was detected in whole blood at any time point throughout the study.

On autopsy of four macaques on day 4 p.i., two had foci of pulmonary consolidation in the lungs ( Fig. 2A). One animal (aged: 17 years) showed consolidation in the right middle lobe, representing less than 5% of the lung tissue. A second animal (young: 5 years) had two foci in the left lower lobe, representing about 10% of the lung tissue ( Fig. 2A). The consolidated lung tissue was well-circumscribed, red-purple, level, and less buoyant than normal. The other organs in these two macaques, as well as the respiratory tract and other organs of the other two animals were normal.

Virus replication was assessed by RT-qPCR on day 4 p.i. in tissues from the respiratory, digestive, urinary, and cardiovascular tracts, from endocrine and central nervous systems, as well as from various lymphoid tissues. Virus replication was primarily restricted to the respiratory tract (nasal cavity, trachea, bronchi and lung lobes) with highest levels of SARS-CoV-2 RNA in lungs ( Fig. 1C). Interestingly, in three out of four animals, SARS-CoV-2 RNA was also detected in ileum and tracheo-bronchial lymph nodes ( Fig. 1C).

The main histological lesion in the consolidated pulmonary tissues of both the young and aged animals involved the alveoli and bronchioles and consisted of areas with acute or more advanced DAD ( Fig. 2B). In these areas, the lumina of alveoli and bronchioles were variably filled with protein-rich edema fluid, fibrin, and cellular debris, alveolar macrophages, and fewer neutrophils and lymphocytes ( Fig. 2C-E). There was epithelial necrosis with extensive loss of epithelium from alveolar and bronchiolar walls. Hyaline membranes were present in a few damaged alveoli. In areas with more advanced lesions, the alveolar walls were moderately thickened and lined by cuboidal epithelial cells (type II pneumocyte hyperplasia), and the alveolar lumina were empty. Alveolar and bronchiolar walls were thickened by edema fluid, mononuclear cells, and neutrophils. There were aggregates of lymphocytes around small pulmonary vessels. Moderate numbers of lymphocytes and macrophages were present in the lamina propria and submucosa of the bronchial walls, and a few neutrophils in the bronchial epithelium. Regeneration of epithelium was seen in some bronchioles, visible as an irregular layer of squamous to high cuboidal epithelial cells with hyperchromatic nuclei. There were occasional multinucleated giant cells (syncytia) free in the lumina of bronchioles and alveoli ( Fig. 2F), and, based on positive pan-keratin staining and negative CD68 staining, these appeared to originate from epithelial cells ( Fig. 2F, inset).

SARS-CoV-2 antigen expression was detected in moderate numbers of type I pneumocytes and a few type II pneumocytes within foci of DAD ( Fig. 2G, Fig. 2H, fig. S2). The pattern of staining was similar to that in lung tissue from SARS-CoV-infected macaques (positive control). SARS-CoV-2 antigen expression was not observed in any of the syncytia. In addition, SARS-CoV-2 antigen expression was detected in non-lesional tissues of all lung lobes in three out of four macaques (both young and one aged) in a few type I and II pneumocytes, bronchial ciliated epithelial cells, and bronchiolar ciliated epithelial cells. The other aged macaque, without virological or pathological evidence of SARS-CoV-2 infection in the lungs, did have SARS-CoV-2 antigen expression in ciliated epithelial cells of nasal septum ( Fig. 2I), nasal concha, and palatum molle, in absence of associated histopathological changes. No SARS-CoV-antigen expression was detected in other sampled tissues, including brain and intestine .

To assess the severity of infection with SARS-CoV-2 compared with MERS-CoV, young cynomolgus macaques (3-5 years of age) were inoculated with MERS-CoV via the IN and IT route. All animals remained free of clinical signs. At day 21 p.i., all remaining animals (n=2) seroconverted as revealed by the presence of MERS-CoV specific antibodies in their sera by ELISA (Fig. S3).

MERS-CoV RNA was detected in nasal ( Fig. 3A) and throat swabs ( Fig. 3B) on days 1-11 p.i., with peaks on days 1 and 2 p.i., respectively. Low levels (between 1-85 TCID50 equivalent/mL) of MERS-CoV RNA were detected in rectal swabs on days 2 and 3 p.i.

At autopsy of four macaques at day 4 p.i., three animals had foci of pulmonary consolidation, characterized by slightly depressed areas in the lungs, representing less than 5% of the lung tissue ( Table 1). Similar to SARS-CoV-2 infection in both young and aged animals, on day 4 p.i., MERS-CoV RNA was primarily detected in the respiratory tract of inoculated animals ( Fig. 3C). Infectious virus titers were comparable to SARS-CoV-2, but lower compared to SARS-CoV infection of young macaques ( Table 1). In addition, MERS-CoV RNA was detected in the spleen ( Table 1).

Consistent with the presence of virus in the lower respiratory tract at day 4 p.i., histopathological changes characteristic for DAD were observed in the lungs of inoculated animals ( Fig. 3D). The alveolar septa were thickened owing to infiltration of neutrophils and macrophages, and moderate type II pneumocyte hyperplasia and hypertrophy. In the alveolar lumina, there were elevated alveolar macrophages and some edema fluid containing fibrin and some neutrophils ( Fig. 3D). Few syncytial cells were seen in the alveolar lumina. Interestingly, MERS-CoV antigen was not detected in tissues on day 4 p.i. in any part of the respiratory tract. We therefore sampled four young macaques at day 1 p.i. At this time we observed. multifocal expression of viral antigen, predominantly in type II pneumocytes and occasionally in type I pneumocytes, bronchiolar and bronchial epithelial cells and some macrophages ( Fig. 3D).

In summary, we inoculated young and aged cynomolgus macaques with a low passage clinical isolate of SARS-CoV-2, which resulted in productive infection in the absence of overt clinical signs. Recent studies in human cases have shown that presymptomatic and asymptomatic cases can also shed virus (, ). Increased age did not affect disease outcome, but there was prolonged viral shedding in the upper respiratory tract of aged animals. Prolonged shedding has been observed in both SARS-CoV-2 and SARS-CoV patients (, ). Interestingly, SARS-CoV-2 shedding in our asymptomatic model, peaked early in the course of infection, similar to what is seen in symptomatic patients (). Also, SARS-CoV-2 antigen was detected in ciliated epithelial cells of nasal mucosae at day 4 p.i., which was not seen for SARS-CoV () or MERS-CoV infections (this manuscript) in this animal model. Viral tropism for the nasal mucosa fits with efficient respiratory transmission, as has been seen for influenza A virus (). This early peak in virus shedding for SARS-CoV-2 is similar to influenza virus shedding () and may explain why case detection and isolation may not be as effective for SARS-CoV-2 as it was for the control of SARS-CoV (). SARS-CoV-2 was primarily detected in tissues of the respiratory tract, however SARS-CoV-2 RNA was also detectable in other tissues such as intestines, in line with a recent report (). Similar results regarding viral shedding and tissue and cell tropism were recently also reported following SARS-CoV-2 inoculation in rhesus macaques. However, unlike in our model, SARS-CoV-2 infection in rhesus macaques does result in transient respiratory disease and weight loss (, ).

Two out of four animals had foci of DAD on day 4 p.i. The colocalisation of SARS-CoV-2-antigen expression and DAD provides strong evidence that SARS-CoV-2 infection caused this lesion. The histological character of the DAD, including alveolar and bronchiolar epithelial necrosis, alveolar edema, hyaline membrane formation, and accumulation of neutrophils, macrophages and lymphocytes, corresponds with the limited pathological analyses of human COVID-19 cases (, ). In particular, the presence of syncytia in the lung lesions is characteristic of respiratory coronavirus infections. Whereas MERS-CoV primarily infects type II pneumocytes in cynomolgus macaques, both SARS-CoV and SARS-CoV-2 also infect type I pneumocytes. Injury to type I pneumocytes can result in pulmonary edema, and formation of hyaline membranes (), which may explain why hyaline membrane formation is a hallmark for SARS and COVID-19 (, ), but not frequently reported for MERS (, ).

These data show that cynomolgus macaques are permissive to SARS-CoV-2 infection, shed virus for a prolonged period of time and display COVID-19-like disease. In this non-human primate model, SARS-CoV-2 replicates efficiently in respiratory epithelial cells throughout the respiratory tract, including nasal cavity, bronchi, bronchioles, and alveoli. Replication in the upper respiratory tract fits with efficient transmission between hosts, while replication in the lower respiratory tract fits with the development of lung disease. An in-depth comparison of infection with SARS-CoV, MERS-CoV and SARS-CoV-2 in this model may identify key pathways in the pathogenesis of these emerging viruses. This study provides a novel infection model which will be critical in the evaluation and licensure of preventive and therapeutic strategies against SARS-CoV-2 infection for use in humans, as well as evaluating the efficacy of repurposing species specific existing treatments, such as pegylated interferon ().

This is an open-access article distributed under the terms of the Creative Commons Attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Acknowledgments: We thank L. de Meulder, A. van der Linden, I. Chestakova and F. van der Panne for technical assistance. Y.Kap, D. Akkermans, V. Vaes, M. Sommers, F. Meijers for assistance with the animal studies. Funding: This research is (partly) financed by the NWO Stevin Prize awarded to M.K. by the Netherlands Organisation for Scientific Research (NWO), H2020 grant agreement 874735 - VEO to M.K., NIH/NIAID contract HHSN272201400008C to R.F., and H2020 grant agreement 101003651 - MANCO to B.H. Author contributions: Conceptualization, B.R., T.K., R.F., M.K., RdS, M.F. B.H.; investigation, B.R., T.K., S.H., T.B., M.L., D.d.M., G.v.A., J.v.d.B., N.O., D.S., P.v.R., L.L.; resources, B.H., C.D. E.V., B.V., J.L. supervision, B.R. and B.H.; writing, original draft, B.R., T.K. and B.H.; writing-review and editing, all authors; funding acquisition: S.H., B.H., R.F. and M.K. Animal welfare: Research was conducted in compliance with the Dutch legislation for the protection of animals used for scientific purposes (2014, implementing EU Directive 2010/63) and other relevant regulations. The licensed establishment where this research was conducted (Erasmus MC) has an approved OLAW Assurance # A5051-01. Research was conducted under a project license from the Dutch competent authority and the study protocol (#17-4312) was approved by the institutional Animal Welfare Body. Competing interests: TB, RF and BH are listed as an inventor on a patent application related to MERS-coronavirus diagnostics, therapy and vaccines. Other authors declare no competing interests. Data and materials availability: All data are available in the main text or the supplementary materials. This work is licensed under a Creative Commons Attribution 4.0 International (CC BY 4.0) license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. This license does not apply to figures/photos/artwork or other content included in the article that is credited to a third party; obtain authorization from the rights holder before using such material.

# data[].attributes.attachment_link.title
Comparative pathogenesis of COVID-19, MERS, and SARS in a nonhuman primate model

# data[].attributes.attachment_link.description
The current pandemic coronavirus, SARS-CoV-2, was recently identified in patients with an acute respiratory syndrome, COVID-19. To compare its pathogenesis with that of previously emerging coronaviruses, we inoculated cynomolgus macaques with SARS-CoV-2 or MERS-CoV and compared the pathology and virology with historical reports of SARS-CoV infections.

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Chloroquine or hydroxychloroquine for prophylaxis of COVID-19

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Chloroquine or hydroxychloroquine for prophylaxis of COVID-19

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17 Apr 2020

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Covid-19 and Immunity in Aging Populations

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Covid-19 and Immunity in Aging Populations

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17 Apr 2020

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Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1

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Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1

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16 Apr 2020

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Droplets and Aerosols in the Transmission of SARS-CoV-2

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Droplets and Aerosols in the Transmission of SARS-CoV-2

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15 Apr 2020

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Structure of the RNA-dependent RNA polymerase from COVID-19 virus

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Structure of the RNA-dependent RNA polymerase from COVID-19 virus

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10 Apr 2020

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Abstract

A novel coronavirus (COVID-19 virus) outbreak has caused a global pandemic resulting in tens of thousands of infections and thousands of deaths worldwide. The RNA-dependent RNA polymerase (RdRp, also named nsp12) is the central component of coronaviral replication/transcription machinery and appears to be a primary target for the antiviral drug, remdesivir. We report the cryo-EM structure of COVID-19 virus full-length nsp12 in complex with cofactors nsp7 and nsp8 at 2.9-Å resolution. In addition to the conserved architecture of the polymerase core of the viral polymerase family, nsp12 possesses a newly identified β-hairpin domain at its N terminus. A comparative analysis model shows how remdesivir binds to this polymerase. The structure provides a basis for the design of new antiviral therapeutics targeting viral RdRp.

Corona Virus Disease 2019 (COVID-19) caused by a novel coronavirus emerged in December 2019 (-) and has since become a global pandemic. COVID-19 virus is reported to be a new member of the betacoronavirus genus and is closely related to severe acute respiratory syndrome coronavirus (SARS-CoV) and to several bat coronaviruses (). Compared to SARS-CoV and MERS-CoV, COVID-19 virus exhibits faster human-to-human transmission, thus leading to the WHO declaration of a world-wide public health emergency (, ).

CoVs employ a multi-subunit replication/transcription machinery. A set of non-structural proteins (nsp) produced as cleavage products of the ORF1a and ORF1ab viral polyproteins () assemble to facilitate viral replication and transcription. A key component, the RNA-dependent RNA polymerase (RdRp, also known as nsp12), catalyzes the synthesis of viral RNA and thus plays a central role in the replication and transcription cycle of COVID-19 virus, possibly with the assistance of nsp7 and nsp8 as co-factors (). Nsp12 is therefore considered a primary target for nucleotide analog antiviral inhibitors such as remdesivir, which shows potential for the treatment of COVID-19 viral infections (, ). To inform drug design we have determined the structure of nsp12, in complex with its cofactors nsp7 and nsp8 by cryo-Electron Microscopy (Cryo-EM) using two different protocols, one in the absence of DTT (Dataset-1) and the other in the presence of DTT (Dataset-2).

The bacterially expressed full-length COVID-19 virus nsp12 (residues S1-Q932) was incubated with nsp7 (residues S1-Q83) and nsp8 (residues A1-Q198), and the complex was then purified (fig. S1). Cryo-EM grids were prepared using this complex and preliminary screening revealed excellent particle density with good dispersion. After the collection and processing of 7,994 micrograph movies, we obtained a 2.9-Å resolution 3D reconstruction of an nsp12 monomer in complex with one nsp7-nsp8 pair and an nsp8 monomer, as was previously observed for SARS-CoV (). In addition to the nsp12-nsp7-nsp8 complex, we also observed single particle classes corresponding to the nsp12-nsp8 dimer, as well as individual nsp12 monomers, but these do not give atomic resolution reconstructions (fig. S2). However, the nsp12-nsp7-nsp8 complex reconstruction provides the structural information for complete structural analysis.

The structure of the COVID-19 virus nsp12 contains a "right hand" RdRp domain (residues S367-F920), and a nidovirus-unique N-terminal extension domain (residues D60-R249) that adopts a nidovirus RdRp-associated nucleotidyltransferase (NiRAN) () architecture. The polymerase domain and NiRAN domain are connected by an interface domain (residues A250-R365) ( Fig. 1, A and B). An additional N-terminal β-hairpin (D29-K50), built with the guidance of an unambiguous cryo-EM map (fig. S3A), inserts into the groove clamped by the NiRAN domain and the palm subdomain in the RdRp domain ( Fig. 2). The nsp7-nsp8 pair shows a conserved structure similar to the SARS-CoV nsp7-nsp8 pair (, ). The orientation of the N-terminal helix of the separate nsp8 monomer bound to nsp12 is shifted compared with that in the nsp7-nsp8 pair (fig. S4A). The 13 additional amino acid residues resolved at the N-terminal of nsp8 show that the long "shaft" of its well-known "golf club" shape is bent (fig. S4B).

The overall architecture of the COVID-19 virus nsp12-nsp7-nsp8 complex is similar to that of SARS-CoV with an rmsd value of 0.82 for 1,078 Cɑ atoms (fig. S4C). However, there are key features that distinguish the two. The cryo-EM map allowed us to build the complete structure of COVID-19 virus nsp12 including all residues except S1-D3 and G897-D901. In contrast the first 116 residues were not resolved in SARS-CoV nsp12 (). The portion of the NiRAN domain resolved in SARS-CoV-12 (residues 4 to 28 and 51 to 249) comprises eight helices with a five-stranded β-sheet at the N terminus. () ( Fig. 2A). In the COVID-19 virus structure we additionally resolved residues A4-R118. These constitute a structural block with five anti-parallel β-strands and two helices. Residues N215-D218 form a β-strand in COVID-19 virus nsp12 whereas these residues are less ordered in SARS-CoV nsp12. This region make contact with the strand that includes residues V96-A100, thus contributing to the stabilization of its conformation. As a result, these four strands form a compact semi β-barrel architecture. Therefore, we identify residues A4-T28 and Y69-R249 as the complete coronaviral NiRAN domain. With the resolution of N-terminal residues, we are also able to identify an N-terminal β-hairpin (D29 to K50, Figs. 1A and 2A). This β-hairpin inserts in the groove clamped by the NiRAN domain and the palm subdomain in the RdRp domain and forms a set of close contacts to stabilize the overall structure ( Fig. 2B and fig. S5). Another point to note is that, we have observed C301-C306 and C487-C645 form disulfide bonds in the absence of DTT (Dataset-1). However, in the presence of DTT (Dataset-2), chelated zinc ions are present and in the same location as that observe in SARS-CoV (fig. S3B).

The polymerase domain adopts the conserved architecture of the viral polymerase family () and is composed of three subdomains; a fingers subdomain (residues L366-A581 and K621-G679), a palm subdomain (residues T582-P620 and T680-Q815), and a thumb subdomain (residues H816-E920) ( Fig. 1). The catalytic metal ions, which are observed in several structures of viral polymerases that synthesize RNA (, ) are not observed here in the absence of primer-template RNA and NTPs.

The active site of the COVID-19 virus RdRp domain is formed by the conserved polymerase motifs A-G in the palm domain and configured like other RNA polymerases ( Figs. 1A and 3A and fig. S6). Motif A comprising residues 611-TPHLMGW DYPKCDRAM-626 contains the classic divalent-cation-binding residue D618, which is conserved in most viral polymerases including HCV ns5b (residue D220) and poliovirus (PV) 3D pol (residue D233) (, ) ( Fig. 3, B and C) and Motif C (residues 753-FSMMIL SDDAVVCFN-767) contains the catalytic residues (759- SDD-761) in the turn between two β-strands. These catalytic residues are also conserved in most viral RdRps, e.g., 317- GDD-319 in HCV ns5b and 327- GDD-329 PV 3D pol with the first residue being either serine or glycine.

In this structure, as in other RNA polymerases, the template/primer entry, nucleoside triphosphate (NTP) entry, and nascent strand exit paths are positively charged and solvent-accessible and converge in a central cavity where the RdRp motifs mediate template-directed RNA synthesis ( Fig. 3D). The configurations of the template/primer entry paths, the nucleoside triphosphate (NTP) entry channel, and the nascent strand exit path are similar to those described for SARS-CoV and for other RNA polymerases such as HCV and PV polymerase () ( Fig. 3, B and C). The NTP entry channel is formed by a set of hydrophilic residues, including K545, R553 and R555 in motif F. The RNA template is expected to enter the active site composed of motifs A and C through a groove clamped by motif F and G. Motif E and the thumb subdomain support the primer strand. The product-template hybrid exits the active site through the RNA exit tunnel at the front side of the polymerase.

Remdesivir, the single Sp isomer of the 2-ethylbutyl L-alaninate phosphoramidate prodrug () (fig. S7), has been reported to inhibit COVID-19 virus proliferation and therefore have clinical potential (, ). We will briefly discuss its possible binding and inhibition mechanism based on the results of this study. The efficacy of chain-terminating nucleotide analogs requires viral RdRps to recognize and successfully incorporate the active form of the inhibitors into the growing RNA strand. Sofosbuvir (2'-F-2'-C-methyluridine monophosphate) is a prodrug which targets HCV ns5b and has been approved for the treatment of chronic HCV infection (). It acts by binding to the catalytic site of HCV ns5b polymerase (12,16). Given that remdesivir and sofosbuvir are both nucleotide analogs and the structural conservation of the catalytic site between COVID-19 virus nsp12 and HCV ns5b polymerase (, ) (fig. S7), we modeled remdesivir diphosphate binding to COVID-19 virus nsp12 based on superposition with sofosbuvir bound to HCV ns5b ( Fig. 4A and fig. S4D). Overall, we found that the nsp12 of covid-19 virus has the highest similarity with the Apo state of ns5b. Given the conformational changes of ns5b in apo/elongation/inhibited states, it appears catalytic residues D760, D761 and the classic D618 will undergo a conformational change to coordinate the divalent cations ( Fig. 4B). The latter will anchor the phosphate group of the incoming nucleotide or inhibitors together with the allosteric R555 in motif F ( Fig. 4C). In the structures of HCV ns5b elongation complex or its complex with pp-sofosbuvir, a key feature is that the incorporated pp-sofosbuvir interacts with N291 (equivalent to N691 in COVID-19 virus) but, due to a fluorine substitution on its sugar moiety, is not capable to joint into the hydrogen bonding network with S282 and D225 ( Fig. 4D), which is necessary to stabilize the incoming natural nucleotide (). However, remdesivir keeps an intact ribose group, so it may be able to utilize this hydrogen bonds network like a native substrate. In addition, T680 in COVID-19 virus nsp12 is also likely to form hydrogen bonds with the 2' hydroxyl of Remdesivir and of course with incoming natural NTP ( Fig. 4D). Moreover, the hydrophobic side chain of V557 in motif F is likely to stack with and stabilize the +1 template RNA uridine base to base pair with the incoming triphosphate remdesivir (ppp-remdesivir) ( Fig. 4E).

The rapid global spread of COVID-19 virus has emphasized the need for the development of new coronavirus vaccines and therapeutics. The viral polymerase nsp12 looks an excellent target for new therapeutics, especially given that lead inhibitors already exist in the form of compounds such as Remdesivir. Considering the structural similarity of nucleoside analogs, the binding mode and inhibition mechanism discussed here may also be applicable to other such kind drugs or drug candidates include Favipiravir, which proves effective in clinical trials (). This target, in addition to other promising drug targets such as the main protease, could support the development of a cocktail of anti-coronavirus treatments that potentially can be used for the discovery of broad-spectrum antivirals.

This is an open-access article distributed under the terms of the Creative Commons Attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Acknowledgments: We would like to pay an exceptional tribute to ShanghaiTech University and their administrative team, as well as the Bio-Electron Microscopy Facility for their great care and support to our research team to enable us to carry out this research in a safe and healthy environment. It would have been impossible for us to attain this achievement without their tremendous efforts in the last two months during the COVID-19 pandemic. We also would like to convey our special thanks to Tsinghua University for their exceptional permission to allow five of Z. R.'s students to go back to the laboratory to prepare the protein samples for this study. We also must express our gratitude to the campus service team of ShanghaiTech University scientific research platform of Shanghai Institute for Advanced Immunochemical Studies (SIAIS), and National Center for Protein Science Shanghai (NCPSS), as well as all the manager and technician individuals those who provided onsite or remote technical support. Their kind help and fearless support are pivotal to this work during the epidemic. We would like to thank the University of Queensland and Diamond Light Source for their collaboration. Funding: This work was supported by the National Program on Key Research Project of China (grant no. 2017YFC0840300), the Strategic Priority Research Program of the Chinese Academy of Sciences (grant XDB08020200), the National Natural Science Foundation of China (grant nos. 81520108019, 813300237) and Science and Technology Commission of Shanghai Municipality (20431900200). Author contributions: Z.R. conceived, initiated, and coordinated the project. Y.H, L.Y., Yao.Z., H.W., Yan.Z., C.Z., Z.M., L.Z., J.G., L.Z., Yi.Z. and Tianyu.H. purified the protein; L.Y. supervised sample purification; Y.G., F.L., L.C., Q.S. and Tian.H. collected the cryo-EM data; Y.G., F.L. and T.W. processed cryo-EM data; Q.W., L.Y., Y.G. built and refined the structure model; and the manuscript was written by Z.L., Q.W., L.Y., Y.G., F.L., L.G. and Z.R.. All authors discussed the experiments and results, read and approved the manuscript. Competing interests: The authors declare no competing interests. Data and materials availability: The cryo-EM maps and the structures were deposited into the Electron Microscopy Data Bank (EMDB) and Protein Data Bank (PDB) with the accession numbers EMD-30127 and PDB 6M71 for Dataset-1, EMD-30178 and PDB 7BTF for Dataset-2 (under the reducing condition). This work is licensed under a Creative Commons Attribution 4.0 International (CC BY 4.0) license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. This license does not apply to figures/photos/artwork or other content included in the article that is credited to a third party; obtain authorization from the rights holder before using such material.

# data[].attributes.attachment_link.title
Structure of the RNA-dependent RNA polymerase from COVID-19 virus

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A novel coronavirus (COVID-19 virus) outbreak has caused a global pandemic resulting in tens of thousands of infections and thousands of deaths worldwide. The RNA-dependent RNA polymerase (RdRp, also named nsp12) is the central component of coronaviral replication/transcription machinery and appears to be a primary target for the antiviral drug, remdesivir.

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Structure of Mpro from COVID-19 virus and discovery of its inhibitors

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Structure of Mpro from COVID-19 virus and discovery of its inhibitors

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9 Apr 2020

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Structure of Mpro from COVID-19 virus and discovery of its inhibitors

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A new coronavirus (CoV) identified as COVID-19 virus is the etiological agent responsible for the 2019-2020 viral pneumonia outbreak that commenced in Wuhan1-4. Currently there are no targeted therapeutics and effective treatment options remain very limited.

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7 Apr 2020

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21 Mar 2020

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The recent outbreak of COVID-19 in Wuhan turned into a public health emergency of international concern. With no antiviral drugs nor vaccines, and the...

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Molecular immune pathogenesis and diagnosis of COVID-19

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Molecular immune pathogenesis and diagnosis of COVID-19

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5 Mar 2020

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Highlights

*.

The highly pathogenic SARS-CoV-2 appearing in December 2019 can cause COVID-19 and even death in infected persons.

*.

Coronavirus infections led to the damage of lung, while imbalanced and excessive immune responses may cause pneumonia.

*.

RT-PCR and CT scans are significant for the diagnosis of SARS-CoV-2 infection, and drugs and vaccines against SARS-CoV-2 are being developed.

Abstract

Coronavirus disease 2019 (COVID-19) is a kind of viral pneumonia with an unusual outbreak in Wuhan, China, in December 2019, which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The emergence of SARS-CoV-2 has been marked as the third introduction of a highly pathogenic coronavirus into the human population after the severe acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East respiratory syndrome coronavirus (MERS-CoV) in the twenty-first century. In this minireview, we provide a brief introduction of the general features of SARS-CoV-2 and discuss current knowledge of molecular immune pathogenesis, diagnosis and treatment of COVID-19 on the base of the present understanding of SARS-CoV and MERS-CoV infections, which may be helpful in offering novel insights and potential therapeutic targets for combating the SARS-CoV-2 infection.

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Molecular immune pathogenesis and diagnosis of COVID-19

# data[].attributes.attachment_link.description
The highly pathogenic SARS-CoV-2 appearing in December 2019 can cause COVID-19 and even death in infected persons. *. Coronavirus infections led to the damage of lung, while imbalanced and excessive immune responses may cause pneumonia. *. RT-PCR and CT scans are significant for the diagnosis of SARS-CoV-2 infection, and drugs and vaccines against SARS-CoV-2 are being developed.

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China virus epicentre Wuhan raises death toll by 50%

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China virus epicentre Wuhan raises death toll by 50%

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18 Apr 2020

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China's coronavirus ground-zero city of Wuhan on Friday admitted missteps in tallying its death toll as it abruptly raised the count by 50 percent -- and as world doubts mounted about how transparent China has been during the crisis.

The United States has led the charge in questioning Beijing's handling of the pandemic and how much information it has really shared with the international community since the virus emerged late last year.

Authorities in Wuhan initially tried to cover up the outbreak, punishing doctors who had raised the alarm online in December, and there have been questions about the government's recording of infections as it repeatedly changed its counting criteria at the peak of the outbreak.

Wuhan's epidemic control headquarters said in a social media posting on Friday that it had added 1,290 deaths to the tally in the city, which has suffered the vast majority of China's fatalities from COVID-19, the disease caused by the virus.

That brings the total number of deaths in the city to 3,869. But the city government only added 325 cases, raising the city's total number of infections to 50,333.

The change also pushes the nationwide death toll up by nearly 39 percent to 4,632, based on official national data released earlier on Friday.

The official toll in the country of 1.4 billion people, however, remains well below the number of fatalities in much smaller countries such as Italy and Spain.

- Pressure mounts -

China has come under increasing pressure from Western powers, with Washington and others raising doubts about transparency, and the US probing whether the virus actually originated in a Wuhan laboratory.

US President Donald Trump said China's death toll was "far higher" that it had admitted -- even after the new numbers were issued.

Chinese scientists have said the virus emerged from a Wuhan food market whose merchandise reportedly included exotic wild animals sold for human consumption.

"We'll have to ask the hard questions about how it came about and how it couldn't have been stopped earlier," British Foreign Secretary Dominic Raab said Thursday.

French President Emmanuel Macron told the Financial Times it would be "naive" to think China had handled the pandemic well, adding: "There are clearly things that have happened that we don't know about."

Chinese foreign ministry spokesman Zhao Lijian acknowledged that the virus's rapid spread had contributed to undercounting, but added: "There has never been any concealment, and we'll never allow any concealment."

There however has also been some domestic discontent over the authorities' handling of the outbreak, especially in Hubei province and its capital, Wuhan.

A civil servant in Yichang, which is in Hubei, said he had filed a lawsuit against provincial authorities for covering up the epidemic.

"Someone must be held accountable for this," Tan Jun, the civil servant, said on social media. He later said police ordered him not to talk about the matter.

- Data flip-flops -

State-run nationalistic tabloid Global Times defended the revision in an editorial, saying it was a "responsible correction" based on "facts" and that some in the West were "hyping" speculation.

"It is hoped the veracity of the data can put all controversy surrounding it to rest," it said.

Joseph Kam, professor of emerging infectious diseases at the Chinese University of Hong Kong, said local authorities may have been asked to hit a certain target in their reporting of deaths and confirmed cases.

"Given the naivety of these numbers, it seems very likely that this timing is to try to ameliorate foreign anger and distrust amidst the high infection and fatality rates we've seen," Kam told AFP.

Wuhan cited several reasons for the missed cases, including that medical staff were overwhelmed in the early days as infections climbed, leading to "late reporting, omissions or mis-reporting".

It also cited insufficient testing and treatment facilities, and said the deaths of some patients at home were not properly reported.

Hubei health authorities have previously flip-flopped on their figures.

Officials abruptly added nearly 15,000 cases to their count in mid-February, counting those who were diagnosed through lung imaging in addition to those who underwent lab tests.

Later, the National Health Commission removed 108 deaths from the toll after discovering that some fatalities were double-counted in Hubei.

Authorities changed their methodology again in late February, no longer adding cases identified through lung imaging.

More recently, China started counting asymptomatic cases.

Zhang Hai, a 52-year-old Wuhan man who has sought official answers after his elderly father died from the virus following unrelated surgery, said the revision was an "improvement".

"The number revision shows the local government can take into account the problems brought up by the relatives of the deceased, and this can bring some solace to grieving families," he said.

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China virus epicentre Wuhan raises death toll by 50%

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China's coronavirus ground-zero city of Wuhan on Friday admitted missteps in tallying its death toll as it abruptly raised the count by 50 percent -- and as world doubts mounted about how transparent China has been during the crisis. The United States has led the charge in questioning Beijing'

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Timeline: How the COVID-19 outbreak has evolved in Singapore so far

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Timeline: How the COVID-19 outbreak has evolved in Singapore so far

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18 Apr 2020

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(Updated: )
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SINGAPORE: It has been more than 12 weeks since Singapore reported its first COVID case on Jan 23 - a 66-year-old Chinese national who came to Singapore three days earlier.

Since then, there have been more than 5,000 cases and 11 deaths in Singapore from the disease, which was first detected in Wuhan, China.

This is how the outbreak has evolved in Singapore so far:

Dec 31, 2019: A cluster of severe pneumonia cases in Wuhan, China is reported to the World Health Organization. Doctors do not yet know its cause.
JANUARY
Jan 2, 2020: Singapore's Ministry of Health (MOH) says it is aware of the cases in Wuhan and will screen all inbound travellers from Wuhan from the evening of Jan 3.

There are no cases in Singapore.

Jan 4: The first suspect case in Singapore is a three-year-old Chinese national with pneumonia and travel history to Wuhan.

The next day, she tests negative for SARS and MERS-CoV and is diagnosed as having Respiratory Syncytial Virus, a common cause for childhood respiratory infection.

Jan 20: MOH announces it will expand temperature screening to all travellers coming in from China from Jan 22, in light of the Chinese New Year holidays and expected influx of Chinese travellers.

There have been several suspect cases in the days leading up to the announcement, but so far, everyone has tested negative.

Jan 22: Anyone with pneumonia and travel history to China within 14 days will be isolated, it is announced. Anyone with acute respiratory infection who had been to any hospital in China with 14 days will also be isolated in hospital in Singapore.

A multi-ministry task force, chaired by Health Minister Gan Kim Yong and National Development Minister Lawrence Wong, is formed.

Jan 23: FIRST CONFIRMED CASE IN SINGAPORE

A 66-year-old Chinese national from Wuhan arrived in Singapore on Jan 20. He is warded at the Singapore General Hospital and tests positive for the yet unnamed novel coronavirus. Contact tracing begins.

Temperature screening is implemented at all sea and land checkpoints, it is announced.

Wuhan is locked down by Chinese authorities as the number of cases spikes to the hundreds.

Jan 27: Children and pre-school employees in Singapore have to go on a 14-day leave of absence if they had travelled to mainland China.

Singaporeans are advised against making non-essential trips to the Hubei province, which was locked down by the Chinese government.

The POFMA Office issues the first correction direction regarding the coronavirus.

Jan 28: There are now seven cases of the coronavirus in Singapore, all Chinese nationals from Hubei.

New measures are put in by the task force. From noon on Jan 29, all visitors with recent travel history to Hubei or with passports issued in Hubei will not be allowed to enter or transit in Singapore.

Jan 30: Reports have emerged of shops hiking up the price of surgical masks. There are long queues at pharmacies and retail stores, and the Price Controller is called in to look at the issue.

"Profiteering is highly irresponsible and damaging in these uncertain times," the Ministry of Trade and Industry said.

There are now 13 cases in Singapore, all imported.

Jan 31: More correction directions are issued for posts on social media about the novel coronavirus. The first scams also emerge of people leveraging on the situation to cheat others.

92 Singaporeans are evacuated from Wuhan.

New visitors of any nationality with recent travel history to mainland China will not be allowed to enter or transit in Singapore from 11.59pm on Feb 1, the task force announces.
FEBRUARY
Feb 1: Four masks per household are handed out by the Government, with advice to wear the masks only when unwell and visiting a doctor.

There are 18 cases in Singapore and no evidence yet of community spread, says the health ministry.

Feb 4: FIRST CLUSTER AT YONG THAI HANG MEDICAL HALL

After two days without any new cases, Singapore reports six more novel coronavirus cases, with four involving human-to-human transmission.

The first cluster emerges - a Chinese medical hall that primarily serves tourists from China. Four cases are linked to the hall, including family members of employees.

There are now 24 cases in Singapore. More precautionary measures are put in place.

FEB 7: DORSCON ORANGE

The Disease Outbreak Response System Condition (DORSCON) level is raised from Yellow to Orange, with a few local cases emerging without links to previous cases or travel history to China.

Organisers are advised to cancel or defer non-essential large-scale events and people who are unwell, on leave of absence, or with recent travel history to China should not attend any events.

Workplaces should carry out temperature screening and schools will suspend inter-school and external activities till the end of the March school holidays, the task force says.

There are now 33 cases in Singapore.

There is panic buying in the supermarkets. Trade and Industry Minister Chan Chun Sing has reassured people that there is enough stock and asks people to stop panic buying.

Feb 8: Prime Minister Lee Hsien Loong addresses the nation, explaining that the novel coronavirus is more infectious than SARS, but much less dangerous, adding that the situation is evolving.

"Every day brings new developments, and we have to respond promptly and dynamically." He says Singapore is thinking ahead and "anticipating the next few steps".

There are seven more cases, bringing the total to 40.

A new cluster at The Life Church and Missions Singapore is announced, as is a cluster linked to a business meeting at Grand Hyatt Hotel.

There are now three active clusters. Two people have made a full recovery and have been discharged from hospital - the first time since the first case on Jan 23.

Feb 9: 174 Singaporeans and their family members are flown home from Wuhan.

Four more people are discharged from hospital. There are now 43 confirmed cases.

Feb 10: The Ministry of Manpower orders all dormitories to step up cleaning and precautionary measures.

All mass activities should be suspended and the use of common dormitory facilities should be staggered.

Feb 11: The coronavirus is named by the World Health Organization as SARS-CoV-2, and the virus causes the disease COVID-19.

Feb 12: TWO NEW CLUSTERS ANNOUNCED

Two new clusters - at the Grace Assembly of God church and Seletar Aerospace Heights construction site - emerge.

There are now 50 cases of COVID-19.

Six more cases are discharged, bringing the total number of recovered patients to 15.

Feb 17: A new stay-home notice is announced. More strict than a leave of absence, a person on a stay-home notice cannot leave their residence for 14 days.

All Singapore residents and pass holders returning from China must complete a 14-day stay-home notice.

There are two new confirmed cases, bringing the total to 77 cases. Twenty-four people have been discharged from hospital.

Feb 25: A breakthrough, as the contact tracing team finds a link between the Life Church and Missions and the Grace Assembly of God clusters.

It is also the first time serological testing has been used to uncover a COVID-19 patient, who recovered before he/she was tested for the disease.

More measures for employees returning from affected areas are introduced.

Feb 26: Two Chinese nationals will be charged under the Infectious Diseases Act for giving false information to MOH. A Singapore PR loses his permanent residence status and is barred from re-entering Singapore after breaching his stay-home notice.

Feb 27: A 12-year-old Raffles Institution student tests positive for COVID-19. RI is and MOE Learning Centre in Bishan close for disinfection.

There are now 96 cases in Singapore.

Feb 29: There are more than 100 COVID-19 cases in Singapore, including the announcement of another cluster at Wizlearn Technologies at Science Park.
MARCH
Mar 3: There are more than 90,000 cases around the world. Singapore authorities announce that travellers from Iran, Northern Italy and South Korea will not be allowed to transit or enter Singapore, with outbreaks starting in those countries.

The stay-home notice criteria is expanded.

Mar 5: A new cluster is reported, linked to an event at SAFRA Jurong.

Mar 6: There is a spike in cases, with the daily number of cases in Singapore going into double figures.

Thirteen new cases are announced, bringing the total to 130 cases.

Mar 10: Senior centric activities will be suspended for 14 days from Mar 11 as the SAFRA Jurong cluster, which includes several elderly people, starts to grow.

MOH found that many of the cases were transmitted during social activities and gatherings among seniors. The SAFRA Jurong cluster now has 39 cases.

Mar 12: Mr Lee addresses the nation a second time, warning that COVID-19 will be here "for a long time" and that Singapore needs to plan for a possible spike.

Mosques in Singapore are closed temporarily, after 90 Singaporeans attended a mass religious event in Kuala Lumpur that has been linked to dozens of cases in other countries.

Mar 13: Safe distancing measures are announced. All ticketed cultural, sports and entertainment events with 250 participants or more are to be deferred or cancelled.

Mar 15: The number of local cases accelerates. There are now 226 COVID-19 cases in Singapore, and contact tracing reveals new clusters. The number of imported cases rises slightly, as Singapore residents return from abroad.

Mar 17: Students overseas are advised to come home to Singapore, as countries around the world go on lock down.

Two days later, flights from the UK are offered to students first, then Singaporeans living overseas who might want to come home.

There are 23 new cases, bringing the total to 266 cases.

Mar 18: A movement control order starts in Malaysia, leading to some people to panic buy in Singaporeon concerns that produce from across the Causeway will be cut off. Mr Chan assures people that the supply chain remains intact.

All new and present work pass holders must gain MOM approval before coming back to Singapore. Upon arrival they must undergo a stay-home notice.

MOH announces 47 new cases, a record. Of the new cases, 33 are imported, as more Singaporeans rush home.

Singaporeans are advised to defer all travel abroad.

Mar 20: RISE IN IMPORTED CASES

There are 40 new cases, with 30 imported. Local transmission has come down slightly, but with more Singaporeans rushing home, the number of imported cases remain in the 30s.

COVID-19 is becoming a global challenge with infections across Europe and in the US increasing at a rapid rate.

Stricter safe-distancing measures are rolled out in Singapore, including new measures for F&B outlets.

Mar 21: SINGAPORE ANNOUNCES FIRST 2 DEATHS

A 75-year-old Singaporean woman and a 64-year-old Indonesian have died from COVID-19. Both had underlying health conditions and were in ICU.

89 work passes are cancelled for breach of stay-home notices and entry requirements.

Mar 22: All short-term pass holders are barred from entering or transiting in Singapore.

Mar 24: Safe-distancing measures are ramped up, the task force announces. All entertainment venues are closed, and restrictions are put in place at malls, museums and attractions.

F&B outlets must ensure sufficient separation of dine-in areas.

All religious gatherings must be cancelled. Tuition centres are to close.

Those coming back from US and the UK have to undergo their stay-home notice in dedicated facilities.

MOH reports 32 new imported and 17 new local COVID-19 cases. Local cases start to climb.

Mar 27: Mr Lee gives a wide-ranging interview to reporters about COVID-19, touching on the Resilience Budget and how Singapore plans to tackle COVID-19.

There are 49 new cases, of which 22 are imported, 18 are linked to previous clusters and nine cases are unlinked.

There are several new clusters by this time, and 732 cases in total.

Mar 29: THIRD DEATH

A 70-year-old Singaporean man becomes the third person to die from complications due to the disease in Singapore. He had a history of hypertension and hyperlipidaemia.

Mar 30: Several new clusters are announced, including one at the S11 dormitory in Punggol.

Mar 31: Imported cases start to drop, but local transmission cases rise.

Singapore announces 47 new COVID-19 cases, of which only 16 are imported. Of the rest, 13 are linked, and 18 are unlinked.

Lawrence Wong says: "Our focus now has to be on our locally transmitted cases, especially the cases that are still popping up; particularly worrying are the unlinked cases."

People are urged to stay at home as much as possible.

There are now 926 COVID-19 cases in Singapore, and another cluster in a dormitory is discovered.
APRIL
Apr 2: Fourth person dies from COVID-19, a 68-year-old Indonesian national who was a Singapore work pass holder. He had a history of diabetes and hypertension and had spent seven days in ICU.

Safe distancing measures are introduced at markets.

Apr 3: Fifth person dies from COVID-19, an 86-year-old Singaporean woman from Lee Ah Mooi nursing home, where a cluster has formed.

There are 65 new cases, of which nine are imported. Forty cases are linked to previous cases, while 16 are unlinked.

Prime Minister Lee Hsien Loong announces a "circuit breaker" will run from Apr 7 to May 4. Only essential services can continue to keep their premises open, and all schools will close and students shift to home-based learning.

Masks should be used when people leave the house for essential needs, but Singaporeans are urged to stay at home as much as possible.

Apr 4: Another person dies from COVID-19, an 88-year-old Singapore PR.

There are now clusters in several dormitories, including S11 @ Punggol, Westlite Toh Guan, and Toh Guan Dormitory. The next day, additional measures are announced to contain clusters in dormitories.

There are 75 new cases, of which six are imported. Local transmission numbers continue to rise, as do unlinked cases.

Apr 5: 120 new cases are announced - the biggest spike yet. Only four of these cases are imported as countries around the world lock down air travel. Fifty of the cases are linked to previous cases, but the unlinked cases spike, from 29 the day before to 66.

Apr 7: CIRCUIT BREAKER COMMENCES

Of the 106 new cases announced, only three are imported. More clusters are found in dormitories across Singapore.

There are now 1,481 cases in the country.

Apr 8: 142 new cases are reported. Local cases continue to rise as imported cases fall again - this time to just two. A total of 72 cases are pending contact tracing, as unlinked number of cases continue to rise.

Warnings are handed out to people flouting the "circuit breaker" rules.

Apr 9: The biggest spike yet, with 287 cases.

Of these, 217 are linked to known clusters, with those linked to the dormitories continuing to grow. There are only three imported cases.

More warnings and advisories are handed out.

Apr 10: A seventh person has died, a 86-year-old woman linked to the Lee Ah Mooi Old Age Home cluster. She died on Apr 9 night, after she was admitted to NCID on Apr 1.

Apr 11: An eighth person dies from COVID-19, a 90-year-old Singaporean man.

Apr 12: Stiffer penalties are introduced for those who continue to flout the rules - there will be no more written arnings and a S$300 fine for the first offence.

A total of 233 new cases are reported, with 167 pending contact tracing - 141 are work permit holders living in dormitories, work sites, or living quarters.

There are no imported cases for the third day in a row.

Apr 13: Singapore reports 386 infections, with the vast majority linked to dormitories. Eight foreign worker dormitories are declared isolation areas under the Infectious Diseases Act.

A 65-year-old male Singapore citizen dies from complications due to COVID-19 infection, MOH announced. He is the ninth person in Singapore to die from the disease.

Apr 14: A 70-year-old Singaporean man, who is linked to the SAFRA Jurong cluster, dies from COVID-19. He is the country's 10th fatality.

Singapore reports another 334 cases.

Apr 15: Singapore reports 447 new cases, with 404 linked to foreign worker dormitories.

An 80-year-old Malaysian who tested positive for COVID-19 posthumously died on Apr 13 from causes not related to COVID-19, said the ministry.

Apr 16: The record numbers continue to grow, with 728 new cases reported.

A total of 654 new cases are from foreign worker dormitories, while 26 are work permit holders residing outside dormitories. There are no new imported cases.

Apr 17: Singapore reports 623 new COVID-19 cases, taking the total number of cases past 5,000.

Of the new cases, 558 are linked to foreign workers dormitories, while 37 are work permit holders living outside dormitories.

MOH reported 27 cases in the community. It is day 11 of the circuit breaker, and the average number of cases has dropped - from an average of 40 cases per day in the week before to an average of 32 cases per day in the last week.

There is one new imported case.

A 95-year-old Singaporean man died on Apr 17 from complications due to COVID-19. He had tested positive for the infection four days before. The man is the 11th fatality in Singapore.
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Timeline: How the COVID-19 outbreak has evolved in Singapore so far

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(Updated: ) Share this content SINGAPORE: It has been more than 12 weeks since Singapore reported its first COVID case on Jan 23 - a 66-year-old Chinese national who came to Singapore three days earlier. Since then, there have been more than 5,000 cases and 11 deaths in Singapore from the disease, which was first detected in Wuhan, China.

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The Wuhan lab at the core of a coronavirus controversy

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The Wuhan lab at the core of a coronavirus controversy

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17 Apr 2020

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WUHAN, China: Nestled in the hilly outskirts of the city at the heart of the coronavirus crisis, a Chinese high-security bio-safety laboratory is now the subject of US claims it may be the cradle of the pandemic.

Chinese scientists have said the virus likely jumped from an animal to humans in a market that sold wildlife in Wuhan, but the existence of the lab has fuelled conspiracy theories that the germ spread from the facility.

The United States has now brought the allegations into the mainstream, with US Secretary of State Mike Pompeo saying officials were doing a "full investigation" into how the virus "got out into the world".
WHAT IS IT?
Here are some key questions about the Wuhan Institute of Virology:

The institute is home to the China Centre for Virus Culture Collection, the largest virus bank in Asia which preserves more than 1,500 strains, according to its website.

The complex contains Asia's first maximum security lab equipped to handle Class 4 pathogens (P4) - dangerous viruses that pose a high risk of person-to-person transmission, such as Ebola.

The 300 million yuan (US$42 million) lab was completed in 2015, and finally opened in 2018, with the founder of a French bio-industrial firm, Alain Merieux, acting as a consultant in its construction.

The institute also has a P3 laboratory that has been in operation since 2012.

The 3,000-square-metre P4 lab, located in a square building with a cylindrical annex, lies near a pond at the foot of a forested hill in Wuhan's remote outskirts.

On a recent visit AFP saw no sign of activity inside.

A poster outside the complex read, "Strong Prevention and Control, Don't Panic, Listen to Official Announcements, Believe in Science, Don't Spread Rumours".
IS IT THE SOURCE OF THE CORONAVIRUS?

The Washington Post and Fox News both quoted anonymous sources who voiced concern that the virus may have come - accidentally - from the facility.

US diplomatic cables seen by The Washington Post revealed that officials were especially concerned about inadequate safety standards over researchers' handling of SARS-like bat coronaviruses in the high-security lab.

Fox News said the pandemic's "patient zero" may have been infected by a strain of bat virus being studied at the facility and gone into the population in Wuhan.

President Donald Trump, asked about the lab theory, said that "more and more, we're hearing the story" and that the United States was "doing a very thorough investigation".

Various conspiracy theories about the alleged origin of the coronavirus in the lab have flourished online.

The institute declined to comment on Friday but it released a statement in February dismissing the rumours.

It said it received samples of the then-unknown virus on Dec 30, determined the viral genome sequence on Jan 2 and submitted information on the pathogen to the World Health Organization on Jan 11.

Chinese foreign ministry spokesman Zhao Lijian on Friday rejected allegations that the lab was responsible for the outbreak.
WHAT DO SCIENTISTS KNOW ABOUT THE VIRUS?
"A discerning person will understand at a glance that the purpose is to create confusion, divert public attention, and shirk their responsibility," said Zhao, who himself promoted conspiracy theories the US army may have brought the virus to China.

Scientists believe the virus originated in bats before being passed to humans through an intermediary species - possibly the endangered pangolin, whose scales are illegally trafficked in China for traditional medicine.

But a study by a group of Chinese scientists published in The Lancet in January revealed that the first COVID-19 patient had no connection to Wuhan's infamous animal market, and neither did 13 of the first 41 confirmed cases.

Institute researcher Shi Zhengli, one of China's leading experts on bat coronaviruses and the deputy director of the P4 lab, was part of the team that published the first study to suggest that SARS-CoV-2 came from bats.

In an interview with the Scientific American, Shi said the SARS-CoV-2 genome sequence did not match any of the bat coronaviruses her laboratory had previously collected and studied.

Filippa Lentzos, bio-security researcher at King's College London, said while there is currently no proof for the lab accident theory, there is also "no real evidence" that the virus came from the wet market.

"For me, the pandemic origin is still an open question," Lentzos told AFP.

There are some indications "that could point to a potential lab accident from basic scientific research", she said.

"But all of this needs considerable investigation for anyone to say anything with any certainty on the pandemic origins."

David Heymann, professor of infectious disease epidemiology at the London School of Hygiene and Tropical Medicine, also said there was no evidence about its origin but it is "closely related to a bat virus".
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"There are many theories of how humans could've been infected, and I don't think any of them are able to be substantiated at present."

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The Wuhan lab at the core of a coronavirus controversy

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(Updated: ) Share this content WUHAN, China: Nestled in the hilly outskirts of the city at the heart of the coronavirus crisis, a Chinese high-security bio-safety laboratory is now the subject of US claims it may be the cradle of the pandemic.

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China's Wuhan city revises up total COVID-19 death toll by 1,290

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China's Wuhan city revises up total COVID-19 death toll by 1,290

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17 Apr 2020

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WUHAN: The Chinese city where the coronavirus first emerged raised its death toll by 50 per cent on Friday (Apr 17), revealing the ground zero of the global pandemic had been much worse hit than Beijing had previously reported.

The revision came as a growing chorus of world leaders suggested China had not been entirely open about the full domestic impact of a virus that has killed more than 140,000 people globally and confined half of humanity to their homes.

It also followed US President Donald Trump ordering a cautious easing of lockdown restrictions in an effort to kickstart his stalling economy, and as GDP data revealed China's economy had slipped into reverse for the first time in decades.

In Wuhan - where the virus was first detected late last year - an official announcement raised the city's death toll by half, to a total of 3,869.

The additional deaths were cases that were "mistakenly reported" or missed entirely, the posting said.

But the revision will play into a growing narrative of Chinese untrustworthiness led by Trump's nationalist administration.

That has now garnered support from Britain and France, fuelled by two US media outlets reporting suspicions the virus accidentally slipped out of a sensitive Wuhan laboratory that studied bats.

British Foreign Secretary Dominic Raab, standing in for Prime Minister Boris Johnson who is still recovering from the virus, said there would be "hard questions" for Beijing.

French President Emmanuel Macron told the Financial Times it would be "naive" to think China had handled the pandemic well, adding: "There are clearly things that have happened that we don't know about."
LIFE-AND-DEATH BALANCE
Beijing and Moscow slapped down the attacks, with Russian President Vladimir Putin denouncing "attempts by some people to smear China."

World leaders are grappling with the question of when to re-open society, seeking a life-and-death balance between unfreezing stalled economies and preventing a deadly second coronavirus wave.

While Trump declared Thursday the time had come for the "next front in our war" with a phased re-opening of the US, others took the opposite path - Japan, Britain and Mexico all expanding current restrictions.

Despite the United States suffering a staggering 4,500 deaths in the last 24 hours - taking the national toll to almost 33,000 - Trump proclaimed: "We're opening up our country."

The president's approach was more cautious than previous hopes for a sudden re-opening however, with state governors given the lead.

Lightly affected states can open "literally tomorrow," said Trump, while others would receive White House "freedom and guidance" to achieve that at their own pace.

Top US government scientist Anthony Fauci said: "Light switch on and off is the exact opposite of what you see here."

In New York state for example - where more than 11,500 have died - Governor Andrew Cuomo extended a shutdown order until May 15.

New Yorker Jamie O'Reilly, owner of a dog-walking business, summed up the agonising predicament world leaders face.

"Why does the economy matter if we're not around to spend any money because we're all sick?" the 31-year-old told AFP.
Download our app or subscribe to our Telegram channel for the latest updates on the coronavirus outbreak: https://cna.asia/telegram
The shutdown was "stressful" but "you just have to roll with the punches ... That's what New Yorkers do".

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China's Wuhan city revises up total COVID-19 death toll by 1,290

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Share this content WUHAN: The Chinese city where the coronavirus first emerged raised its death toll by 50 per cent on Friday (Apr 17), revealing the ground zero of the global pandemic had been much worse hit than Beijing had previously reported.

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Sources believe coronavirus outbreak originated in Wuhan lab as part of China's efforts to compete with US

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Sources believe coronavirus outbreak originated in Wuhan lab as part of China's efforts to compete with US

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16 Apr 2020

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EXCLUSIVE: There is increasing confidence that the COVID-19 outbreak likely originated in a Wuhan laboratory, though not as a bioweapon but as part of China's attempt to demonstrate that its efforts to identify and combat viruses are equal to or greater than the capabilities of the United States, multiple sources who have been briefed on the details of early actions by China's government and seen relevant materials tell Fox News.

This may be the "costliest government cover-up of all time," one of the sources said.

The sources believe the initial transmission of the virus - a naturally occurring strain that was being studied there - was bat-to-human and that "patient zero" worked at the laboratory, then went into the population in Wuhan.

The "increasing confidence" comes from classified and open-source documents and evidence, the sources said. Fox News has requested to see the evidence directly. Sources emphasized -- as is often the case with intelligence -- that it's not definitive and should not be characterized as such. Some inside the administration and the intelligence and epidemiological communities are more skeptical, and the investigation is continuing.

What all of the sources agree about is the extensive cover-up of data and information about COVID-19 orchestrated by the Chinese government.
CLICK HERE FOR COMPLETE CORONAVIRUS COVERAGE
Asked by Fox News' John Roberts about the reporting, President Trump remarked at Wednesday's coronavirus press briefing, "More and more we're hearing the story...we are doing a very thorough examination of this horrible situation."

Documents detail early efforts by doctors at the lab and early efforts at containment. The Wuhan wet market initially identified as a possible point of origin never sold bats, and the sources tell Fox News that blaming the wet market was an effort by China to deflect blame from the laboratory, along with the country's propaganda efforts targeting the U.S. and Italy.

U.S. Embassy officials warned in January 2018 about inadequate safety at the Wuhan Institute of Virology lab and passed on information about scientists conducting risky research on coronavirus from bats, The Washington Post reported Tuesday.

Responding to the report, Gen. Mark Milley, the chairman of the Joint Chiefs of Staff, said on Tuesday afternoon: "It should be no surprise to you that we have taken a keen interest in that and we've had a lot of intelligence take a hard look at that. I would just say at this point, it's inconclusive, although the weight of evidence seems to indicate natural, but we don't know for certain."

"Even today, I see them withholding information and I think we need to do more to continue to press them to share," Secretary of Defense Mark Esper told " America's Newsroom" on Wednesday, referring to China. Esper added that he wouldn't speak to "intelligence reporting," but that "most people believe it began naturally - it was organic, if you will. I think in due course, once we get through the pandemic we're in right now, there'll be time to look back and really ascertain what happened and make sure we have a better understanding so we can prevent this in the future."

Sources point to the structure of the virus, in saying the genome mapping specifically shows it was not genetically altered.

Speaking to " The Story" Wednesday evening, Secretary of State Mike Pompeo remarked: "What we do know is we know that this virus originated in Wuhan, China. We know there is the Wuhan Institute of Virology just a handful of miles away from where the wet market was. There is still lots to learn. You should know that the United States government is working diligently to figure it out."

Concerning the State Department cables warning about the Wuhan laboratory, Pompeo said the installation "contained highly contagious materials - we knew that, we knew that they were working on this program, many countries have programs like this. In countries that are open and transparent, they have the ability to control them and keep them safe, and they allow outside observers in to make sure all the processes and procedures are right. I only wish that that had happened in this place."

On Thursday, China's foreign ministry pushed back on the suspicion that the virus escaped from the facility, by citing statements from the World Health Organization that there is no evidence the coronavirus came from a laboratory.

Americans were originally helping train the Chinese in a program called PREVENT well before the Chinese started working on this virus. The French government helped the Chinese set up the Wuhan lab.

China "100 percent" suppressed data and changed data, the sources tell Fox News. Samples were destroyed, contaminated areas scrubbed, some early reports erased, and academic articles stifled.
STATE DEPT LEAKED CABLES RENEW THEORIES ON ORIGINS OF CORONAVIRUS
There were doctors and journalists who were "disappeared" warning of the spread of the virus and its contagious nature and human to human transmission. China moved quickly to shut down travel domestically from Wuhan to the rest of China, but did not stop international flights from Wuhan.

Additionally, the sources tell Fox News the World Health Organization (WHO) was complicit from the beginning in helping China cover its tracks.

Trump announced at the White House coronavirus news briefing in the Rose Garden on Tuesday that the United States will immediately halt all funding for the WHO, saying it had put "political correctness over lifesaving measures." The United States is the WHO's largest single donor, and the State Department had previously planned to provide the agency $893 million in the current two-year funding period.

Senior administrations separately tell Fox News the rollout of the president's "blueprint for reopening the U.S. economy" will happen Thursday afternoon, first for governors and then briefed to the press.

Meanwhile, Trump's own handling of the crisis has come into focus. On January 24, for example, Trump tweeted in praise of China's " transparency" on coronavirus.

Though they were not speaking for the president, the sources ventured an explanation, saying it was diplomatic talk to make the Chinese "feel good" while the investigation was ongoing, with trade and other talks happening simultaneously.

In the six days after top Chinese officials secretly determined they likely were facing a pandemic from a new coronavirus, the city of Wuhan at the epicenter of the disease hosted a mass banquet for tens of thousands of people; millions began traveling through for Lunar New Year celebrations.
TRUMP CUTS ALL WORLD HEALTH ORGANIZATION FUNDING
President Xi Jinping warned the public on the seventh day, Jan. 20. But by that time, more than 3,000 people had been infected during almost a week of public silence, according to internal documents obtained by The Associated Press and expert estimates based on retrospective infection data.

"This is tremendous," said Zuo-Feng Zhang, an epidemiologist at the University of California, Los Angeles. "If they took action six days earlier, there would have been much fewer patients and medical facilities would have been sufficient. We might have avoided the collapse of Wuhan's medical system."
Fox News' Barnini Chakraborty and The Associated Press contributed to this report.

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Sources believe coronavirus outbreak originated in Wuhan lab as part of China's efforts to compete with US

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There is increasing confidence that COVID-19 likely originated in a Wuhan laboratory not as a bioweapon, but as part of China's effort to demonstrate that its efforts to identify and combat viruses are equal to or greater than the capabilities of the United States, multiple sources who have been briefed on the details of early actions by China's government and seen relevant materials tell Fox News.

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China knew the coronavirus could become a pandemic in mid-January but for 6 days claimed publicly that there was no evidence it could spread among humans

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China knew the coronavirus could become a pandemic in mid-January but for 6 days claimed publicly that there was no evidence it could spread among humans

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15 Apr 2020

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China knew the novel coronavirus could spread among humans and become a pandemic but didn't tell the world for six days, The Associated Press found.

A damning memo of a January 14 call obtained by the AP warned top officials about human-to-human transmission and said to prepare for a pandemic.

But in the six intervening days, China publicly said there was no evidence of human-to-human transmission. The World Health Organization relied on that to direct policy and advise other countries.

President Xi Jinping finally warned of the severity of the virus on January 20, the same day a top Chinese epidemiologist announced evidence of human-to-human transmission.

The report appears to substantiate President Donald Trump's accusations that WHO failed to vet China's data.

Visit Business Insider's homepage for more stories.

For six days in mid-January, China knew the novel coronavirus could become a deadly pandemic while it told the world there was nothing to fear, according to an Associated Press report published Wednesday.

A memo of a confidential phone call with Ma Xiaowei, the head of the National Health Commission, and provincial health officials on January 14, obtained by the AP, said that "human-to-human transmission is possible" and that "all localities must prepare for and respond to a pandemic."

The call was supposed to convey direct orders about the coronavirus from President Xi Jinping and other top Chinese government officials, according to the AP.

But in the six days that followed, Chinese health authorities publicly maintained that the virus posed a low risk to people.

The Wuhan Health Commission said on January 14, the same day as Ma's call, that it had "not found proof for human-to-human transmission."

The next day, Li Qun, the head of the Center for Disease Control and Prevention's emergency center, told state TV that "the risk of sustained human-to-human transmission is low," the AP reported.

At the time, the World Health Organization, which relies on countries to provide their own data, took China at its word and offered the same advice to other countries around the world.

"Preliminary investigations conducted by the Chinese authorities have found no clear evidence of human-to-human transmission," WHO tweeted on January 14.

Preliminary investigations conducted by the Chinese authorities have found no clear evidence of human-to-human transmission of the novel #coronavirus (2019-nCoV) identified in #Wuhan, #China????????. pic.twitter.com/Fnl5P877VG

- World Health Organization (WHO) (@WHO) January 14, 2020

WHO did not immediately respond to Business Insider's request for comment.

At the time, South Asian countries were looking for - and heeding - WHO's guidance on how to prepare for the coronavirus, which had already spread to Thailand.

Governments around the world were also considering which preventive measures to put in place and had their eyes glued to China's response. And for six days, the Chinese government suggested there was nothing to do, the AP found.

It was on January 20 that Xi finally told people to practice social distancing and avoid travel and that a Chinese epidemiologist, Zhong Nanshan, told state TV that the virus was, in fact, being transmitted among humans.

In the preceding six days, more than 3,000 people caught the coronavirus in China, the AP estimated. This period also marked the run-up to Lunar New Year, the biggest holiday in China, when millions of people around the country travel home to see their families.

If on January 14 Chinese authorities had told people to stay home, wear masks, and refrain from traveling, the number of cases might have been reduced by about 66%, a March 13 paper by scientists at the University of Southampton in the UK found. The paper has not been peer-reviewed.

"If they took action six days earlier, there would have been much fewer patients and medical facilities would have been sufficient," Zuo-Feng Zhang, an epidemiologist at the University of California at Los Angeles, told the AP. "We might have avoided the collapse of Wuhan's medical system."

On January 20, China had reported 224 coronavirus cases, but experts have said the true number was likely substantially higher.

On January 17, Wuhan had officially reported about 50 cases, but there were likely 35 times as many, retrospective modeling from Imperial College London found.

The first coronavirus case reported outside China - in Thailand on January 13 - was what prompted the Chinese government to take internal steps to stop the outbreak, the AP reported.

That case spooked Chinese officials, but it apparently was still not enough to alert WHO.

As early as December 6, doctors in Wuhan were raising concerns that people could catch the virus from other people.

Perhaps the most famous was Li Wenliang, who began sharing ominous data with fellow doctors but was silenced by the police in Wuhan and made to sign a confession saying he had lied. He later died of the coronavirus, prompting a flurry of online protests against state censorship.

As the authorities in Wuhan squashed Li's warnings, China's health authority was quietly mobilizing.

On January 15, on Ma's instructions, China's CDC initiated a "level one" internal response, the most extreme response level.

In the following week, CDC officials were dispatched across the country to train health workers, accrue funds, collect data on the virus, and supervise lab testing, according to the AP. Airports and bus and train stations in Hubei province, where Wuhan is, were told to check people's temperatures.

But outside this bubble, China's more than 1 billion residents and the rest of the world went about their lives as usual, unaware of a looming disaster.

President Donald Trump has repeatedly accused WHO of dropping the ball on the coronavirus crisis and insufficiently scrutinizing China's response.

Trump on Tuesday said he would pull the US's annual funding for WHO, saying it "willingly took China's assurances to face value" and "defended the actions of the Chinese government, even praising China for its so-called transparency."

WHO officials have consistently praised China's actions in tackling the crisis. On January 29, its director-general, Tedros Adhanom Ghebreyesus, said China "actually helped prevent the spread of coronavirus to other countries."

That day, Michael Ryan, the executive director of WHO's Health Emergencies Program, said that China "is doing the right things" and that WHO had "seen no obvious lack of transparency."

Throughout the coronavirus crisis, authorities in China sought to censor information, silencing journalists, doctors, and content on the internet critical of the state.

WHO declared the coronavirus outbreak a pandemic on March 11.

As of Wednesday, more than 127,000 people had died of the coronavirus and more than 2 million people had been infected.

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Bill Bostock, Business Insider US

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China knew the coronavirus could become a pandemic in mid-January but for 6 days claimed publicly that there was no evidence it could spread among humans

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China knew the novel coronavirus could spread among humans and become a pandemic but didn't tell the world for six days, The Associated Press found. A damning memo of a January 14 call obtained by the AP warned top officials about human-to-human transmission and said to prepare for a pandemic.

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China Concealed Extent of Virus Outbreak, U.S. Intelligence Says

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China Concealed Extent of Virus Outbreak, U.S. Intelligence Says

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1 Apr 2020

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Is China hiding COVID-19 death toll? 21 million cell phones disappeared, why?

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Is China hiding COVID-19 death toll? 21 million cell phones disappeared, why?

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29 Mar 2020

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International Business Times, Singapore Edition

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Since the outbreak of Novel Coronavirus which emerged in China's Wuhan, the pandemic has killed 15,374 people globally and infected 351,731 individuals. Recently the death toll in Italy surpassed the initial epicentre of the outbreak in China, where officially 3,153 people have died due to the COVID-19.

But recently Beijing authorities announced on March 19 that more than 21 million cell phone accounts were cancelled while in past three months 840,000 landlines were closed in China, which gives an idea that probably these closed numbers belonged to the people who died due to the disease.

Tang Jingyuan, a US-based China Affairs commentator told The Epoch Times on March 21:

"The digitization level is very high in China. People can't survive without a cell phone. Dealing with the government for pensions and social security, buying train tickets, shopping... no matter what people want to do, they are required to use cell phones.

"The Chinese regime requires all Chinese use their cell phones to generate a health code. Only with a green health code are Chinese allowed to move in China now.

"It's impossible for a person to cancel his cell phone."

China telecom stats
The Chinese authority introduced mandatory facial scans on December 1, 2019, to confirm the identity of the person who registered the phone. The people in China also have to sync their bank accounts and social security account with their cell phone as all the apps can detect the SIM card and then check with the database to make sure the number belongs to the person.

In China, it is mandatory to install a cell phone app and register their personal health information. The app can generate a QR code which is possible in three colours to classify a person's health condition. In this case, red means the person has an infectious disease, while yellow and green represent the possibility of infectious disease and no sign of such illness respectively.

Beijing claimed that the health code has helped China to prevent the spread of Coronavirus in the country where 81,496 people got infected by the COVID-19.

What about 21 million cell phone accounts?
On March 19, China's Ministry of Industry and Information Technology (MIIT) announced the numbers of cell phone users in every province in February. When these numbers are compared to the December 2019 data, it revealed that both cell phone users and landline users dropped dramatically.

The comparison showed that the number of cell phone users decreased from 1.600957 billion to 1.579927 billion, while landline users dropped from 190.83 million to 189.99 million.

It is possible that the nationwide lockdown in February was the reason behind the drop in the numbers of landline users as many companies were shut down, the quarantine scenario can't be a reason behind the drop in the cell phone users.

It should be noted that as per the reports China Telecom is the second-largest carrier which has lost 5.6 million users in February 2020 and lost 0.43 million users in January 2020. China Unicom also lost 1.186 million users in January 2020.

While the drop in these numbers showed a dramatic scenario in China, Tang said, "It's possible that some migrant workers had two cell phone numbers before. One is from their hometown, and the other is from the city they work in. In February, they might close the number in the city they work in because they couldn't go there."

It is possible that these workers may have gone to their home city for the Chinese New Year and after the travel ban, they did not get a chance to come back to China. It should be noted that in China there is a basic monthly fee to hold a cell phone account and the majority of migrant workers, who belong to the lowest income group, likely only have one cell phone account.

The economic downturn caused by the outbreak could have forced the Chinese people, who have two cell phones to cancel one of them.

While explaining the scenario in China, Tang said,"At present, we don't know the details of the data. If only 10 percent of the cell phone accounts were closed because the users died because of the CCP virus [Novel Coronavirus], the death toll would be two million."

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Is China hiding COVID-19 death toll? 21 million cell phones disappeared, why?

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Since the outbreak of Novel Coronavirus which emerged in China's Wuhan, the pandemic has killed 15,374 people globally and infected 351,731 individuals. Recently the death toll in Italy surpassed the initial epicentre of the outbreak in China, where officially 3,153 people have died due to the COVID-19.

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MOH flags concern over unlinked COVID-19 cases, says tests on patients at primary care facilities indicate 'undetected cases in community'

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MOH flags concern over unlinked COVID-19 cases, says tests on patients at primary care facilities indicate 'undetected cases in community'

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18 Apr 2020

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(Updated: )

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SINGAPORE: The health ministry on Friday (Apr 17) flagged concern over unlinked cases of COVID-19 in Singapore, saying that tests on a sample of individuals at primary care facilities have picked up several positive diagnoses, which indicate "undetected cases in the community".

Primary care facilities in Singapore include polyclinics and general practitioner clinics.

Singapore on Friday reported 623 new cases of COVID-19 and one more death, taking its total to 5,050 infections and 11 fatalities, the Ministry of Health (MOH) said in a daily update.

Most of the new COVID-19 cases were from foreign worker dormitories, although MOH also raised concern over a rising number of unlinked cases.

"We are particularly concerned that it is increasingly difficult to link the new cases and identify the source of infection," said MOH in its press release on Friday.

"In fact, the number of unlinked cases in the community has increased slightly, from an average of 19 cases per day in the week before, to an average of 22 per day in the past week," it added.

MOH also said that an ongoing surveillance programme on a small sample of patients at primary care facilities has revealed several positive cases.

"We have picked up some cases through these tests, which is an indication of undetected cases in the community," it said. No further information was provided by MOH.

On Friday, MOH reported that a 34-year-old nurse at Bright Vision Hospital had contracted COVID-19.

The Malaysian woman had been in Malaysia between Jan 29 and Apr 8. Following her return to Singapore, she had been on a stay-home notice and had not gone to work.

On Wednesday, MOH reported that a 41-year-old administrative staff at KK Women's and Children's Hospital had tested positive for the coronavirus. The Singaporean woman, who had no recent travel history to affected places, felt ill on Apr 10 and tested positive four days later.

On Tuesday, MOH reported that a 22-year-old nurse at Singapore General Hospital and a 41-year-old doctor at Tan Tock Seng Hospital had contracted COVID-19.

The nurse is a family member of a previous case, while the doctor is an unlinked case.

Singapore has imposed a range of "circuit breaker" measures to curb the spread of the pandemic, including closing non-essential workplaces and schools.
Download our app or subscribe to our Telegram channel for the latest updates on the coronavirus outbreak: https://cna.asia/telegram
The one-month circuit breaker period will be in place until May 4.

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MOH flags concern over unlinked cases, says tests on patients at primary care facilities indicate 'undetected cases in community'

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(Updated: ) Share this content SINGAPORE: The health ministry on Friday (Apr 17) flagged concern over unlinked cases of COVID-19 in Singapore, saying that tests on a sample of individuals at primary care facilities have picked up several positive diagnoses, which indicate "undetected cases in the community".

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COVID-19 map: Tracking the coronavirus outbreak worldwide

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COVID-19 map: Tracking the coronavirus outbreak worldwide

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LIVE UPDATES

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COVID-19 map: Tracking the coronavirus outbreak worldwide

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How many COVID-19 cases are there in the United States, Brazil, India, Europe, the Middle East or China? This map tracks the novel coronavirus outbreak in each country worldwide.

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Hand sanitizer is selling out, but soap is a much better defense against the coronavirus

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Hand sanitizer is selling out, but soap is a much better defense against the coronavirus

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13 Mar 2020

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People are stocking up on hand sanitizer but soap and water is the gold standard for preventing disease.

The new coronavirus comes encased in a layer of fat, or lipid envelope, which soap can break apart, making you less likely to get infected.

While bar soap and liquid soap are equally effective, bar soap should not be used outside of your home.

Visit Insider's homepage for more stories.

Amid the panic over the coronavirus outbreak, it seems, people have forgotten that soap and water are our best defense against disease.

Pharmacies are full of people looking to stock up on hand sanitizer. Demand reached such a fever pitch this week that New York Governor Andrew Cuomo announced the state would be producing a free sanitizer. On Ebay and Amazon, hand sanitizers have been sold at a 200% markup.

Intriguingly, some Twitter users have reported witnessing people frantically stock up on hand sanitizer, but ignoring the soap available.

And yet, soap is the best defense we have, experts say.

"The humble act of washing with soap and water, followed by drying with a clean towel is the gold standard," Elizabeth Scott, an expert in home and community hygiene and professor at Simmons University, told Insider. "Hand washing with soap employs mechanical action that loosens bacteria and viruses from the skin, rinsing them into the drain."

The drying that follows makes the skin less hospitable to the bacteria and viruses that can make us sick.

simplehuman/Amazon

Soap breaks down pathogens, and you're better off using liquid soap over barsoap in public

Evidence suggests the novel coronavirus is transmitted via droplets from sneezing or coughing that can land on anything, from tables to laptops to credit cards. It can live on surfaces for hours a day. If people touch something a droplet has landed on and then touch their faces, they can get infected.

The pathogen itself is encased in a lipid envelope, or layer of fat. Soap helps destroy that layer of fat, making the virus less capable of infecting you. Hand-washing can also remove pathogens from dirty hands.

Soap contains fat-like substances known as amphiphiles, which are similar to the lipids in the virus' envelope, Scott told Insider. These amphiphiles compete with the lipids in the virus envelope and deactivate the virus.

While bar and liquid soap are both equally effective, bar soap should not be used in public places, says Scott. Bar soaps are for home only, and shouldn't be used by people with skin infections.

Hand sanitizer should only be an option when you don't have access to a sink

Hand sanitizers with an alcohol content that is greater than 62% can also destroy these lipid membranes, according to Scott. But they are ineffective against non-enveloped viruses, like norovirus and rhinovirus, which are variations of the common cold. Plus they provide none of the virus-destroying friction that rubbing your hands together and rinsing provides.

According to Christopher Friese, a professor of nursing, health management and policy at the University of Michigan, hand sanitizer poses three challenges. There must be a high enough alcohol concentration to be effective, the entire surface of the hands and fingers must be covered, and skin irritation may occur. That's natural when rubbing something that is over 60% alcohol into your skin.

Friese tells all his patients to carry hand sanitizer when they can't make it to the sink.

Hand sanitizer is universally used in hospitals, nursing homes, and schools. "Maybe it seems more like a 'medical application,'" said Scott.

Epidemiologist Sandra Albrecht, of Columbia University, theorized that it was the convenience of hand sanitizer that made it more popular than soap. "With sanitizers, you just need one thing - the sanitizer. With soap, you also need access to a clean water source and that's often not an option when you're out and about," she told Insider. "Soap also feels messier than sanitizer, and it also takes longer to use it. Sanitizers are quick and convenient."

Perhaps that's why people are fighting over it in chain stores.

Here's how to wash your hands

According to the CDC, it doesn't matter whether you use hot or cold water, and there is no added benefit to using antibacterial soap. In fact, there is so little benefit that in September 2016, the FDA had to issue a ruling stating that 19 ingredients commonly marketed in anti-bacterial soaps had zero added benefit and were no longer going to be marketed to people.

"Using soap to wash hands is more effective than using water alone because the surfactants in soap lift soil and microbes from skin, and people tend to scrub hands more thoroughly when using soap, which further removes germs," says the CDC.

To wash your hands, lather them with soap and scrub for at least 20 seconds. Make sure to focus on places people tend to forget; the back of your hands, between your fingers, and under your nails, where microbes tend to build up. Rinse under clean running water and dry with a clean towel, as germs can easily be transferred to and from wet hands.

This should be simple enough, but a number of studies show that people tend to not wash their hands, or not wash them for the requisite 20 seconds. One 2009 study, cited by the CDC, showed that 69% of men don't wash their hands after using the bathroom, compared to 35% of women. Another 2013 Michigan State University study found that 95% of people do not wash their hands long enough to kill harmful bacteria. Most recently, in 2019, a YouGov survey of 24,000 Americans found that 40% of them do not always wash their hands with soap after using the bathroom.

So instead of scouring the shelves for hand sanitizer, next time stock up on soap, and wash for 20 seconds.
A Survivor contestant and scarcity expert explains why you're panic-buying Coronavirus live updates: Nearly 125,000 people have been infected and over 4,500 have died. The US has reported 31 deaths. Here's everything we know. Coins carry viruses better than paper money, experts say as China begins sterilizing cash

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Hand sanitizer is selling out, but soap is a much better defense against the coronavirus

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People are stocking up on hand sanitizer but soap and water is the gold standard for preventing disease. The new coronavirus comes encased in a layer of fat, or lipid envelope, which soap can break apart, making you less likely to get infected.

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Photos show why hand sanitizer doesn’t work as well as soap and water to remove germs

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Photos show why hand sanitizer doesn’t work as well as soap and water to remove germs

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6 Mar 2020

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Actress Kristen Bell posted a photo on Instagram of her mom's hands, lit up with UV-light to show the germs.

The photos showed how much of a difference it makes to rinse your hands for six seconds, or to scrub them with soap and water for 30 seconds.

Business Insider conducted a similar experiment, comparing hand sanitizer and hand-washing, which showed a marked difference.

Health officials say it's important everyone has access to hand sanitizer for times they do not have access to a sink, but not to use it as a substitute if you do have the option of soap and water.

Visit Business Insider's homepage for more stories.

It can be hard to change the way you've been doing something for your whole life.

But with widespread concern about the spread of the coronavirus, it's a challenge many people face.

All of us (hopefully) wash our hands daily, and yet it's rare to see somebody standing at the sink next to you do a full 20- to 30-second lather and scrub, as we're now all being advised to do by health officials.

If you're finding it challenging to get into the habit of washing for longer, the actress Kristen Bell has some inspiration for you.

On Wednesday, Bell posted a series of photos on Instagram that her mom had sent her, showing her hands at different stages of cleanliness.

Using a UV light and a cream called Glo-Germ - a mineral oil that clings to germs, and is only visible under a UV light when it does cling to germs - she was able to capture how much dirt was on her hands, even though they seemed clean to the naked eye.

It showed a dramatic difference between the potency of a six-second wash with soap and a 15-second wash with soap.

Though more similar, there was also a marked difference between a 15-second wash with soap and a 30-second one: After 15 seconds, Bell's mom still had some stubborn traces of bacteria stuck in the wrinkles of her fingers and her knuckles, which faded after a 30-second scrub.

We did the same experiment comparing a soapy hand-wash with hand sanitizer

Last week, Business Insider conducted a similar experiment, comparing hand sanitizer and a thorough hand-wash.

Health officials agree that it's a good idea for everyone to use hand sanitizer, particularly those with underlying conditions like asthma or emphysema, but urge people not to view it as a replacement for soap and water.

As we found with our own experiment, hand sanitizer is effective, but nowhere near as effective as hand-washing.

I put on Glo-Germ and got a UV-lit photo taken of my dirty hand after I'd gone to the pharmacy to buy some household items, using cash and also touching a keypad to type in my rewards card number. As you can see, they were quite dirty.

Then, I put on a liberal dose of Purell hand sanitizer. (In order to make sure hand sanitizer does its temporary job, you need almost a teaspoon of it, according to the American Council on Science and Health.)

With that, the germs cleared up quite a bit. However, hand sanitizer does not remove bacteria (as hand soap does). It simply neutralizes the bacteria, but leaves it on your hand, allowing it to resurge later.

The most striking photo was the final one, after I lathered my hands for 20 seconds and rinsed for five to 10 seconds. It's the photo that glows the least, because there are so few germs for the Glo-Germ to cling to.

There is a hand-washing gender gap

Research has long-shown that hand-washing isn't a given for everyone.

An international study in 2014, led by UK researchers, found 19% of people wash their hands with soap after coming into contact with feces.

Health officials insist it's imperative we turn those numbers around - according to recent research by MIT increasing hand-washing at just 10 airports in the US would reduce the spread of the coronavirus by 60 percent.

And yet, Insider Data conducted a poll last month which found that while many people are washing their hands more, there is a significant gender gap: of the 1,000 people surveyed, 65% of women said they were taking more care to wash their hands, compared to 52% of men.

Wash and scrub your hands for 20 seconds - and if you don't like singing "Happy Birthday," try "Jolene"

A useful way to keep your hand-washing on track is to sing a song in your head (or out loud), and only stopping when you've finished.

The classic is to sing "Happy Birthday" twice. But on Monday, Insider compiled a list of other songs you can scrub to, including "Jolene" and "Raspberry Beret."

And remember, even after the song is over, take the time to dry your hands thoroughly - new germs flourish in moisture.

About our polling: SurveyMonkey Audience polls from a national sample balanced by census data of age and gender. Respondents are incentivized to complete surveys through charitable contributions. Generally speaking, digital polling tends to skew toward people with access to the internet. SurveyMonkey Audience doesn't try to weigh its sample based on race or income. A total of 1,051 respondents were collected February 27, 2020, a margin of error plus or minus 3.09 percentage points with a 95% confidence level.

Read more:

13 tips for protecting your child against the coronavirus, according to a pediatrician

Between 40% and 70% of adults worldwide could get the coronavirus, one Harvard expert says. That's at least 3 billion cases.

Only a handful of children have been diagnosed with the coronavirus - and experts have a few guesses as to why

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Mia de Graaf, Business Insider US

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Photos show why hand sanitizer doesn't work as well as soap and water to remove germs

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Actress Kristen Bell posted a photo on Instagram of her mom's hands, lit up with UV-light to show the germs. The photos showed how much of a difference it makes to rinse your hands for six seconds, or to scrub them with soap and water for 30 seconds.

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8 Apr 2020

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WHO is continuously monitoring and responding to this pandemic. This questions and answers page will be updated as more is known about COVID-19, how it spreads and how it is affecting people worldwide. For more information, regularly check the WHO coronavirus pages. https://www.who.int/covid-19

COVID-19 is the disease caused by a coronavirus called SARS-CoV-2. WHO first learned of this new virus on 31 December 2019, following a report of a cluster of cases of so-called viral pneumonia in Wuhan, People's Republic of China.

The most common symptoms of COVID-19 are

Other symptoms that are less common and may affect some patients include:

muscle aches

severe fatigue or tiredness

runny or blocked nose, or sneezing

headache

sore eyes

dizziness

new and persistent cough

tight chest or chest pain

shortness of breath

hoarse voice

heavy arms/legs

numbness/tingling

nausea, vomiting, abdominal pain/ belly ache, or diarrhoea

appetite loss

loss or change of sense of taste or smell

difficulty sleeping.

Symptoms of severe COVID‐19 disease which need immediate medical attention include:

difficulty in breathing, especially at rest, or unable to speak in sentences

confusion

drowsiness or loss of consciousness

persistent pain or pressure in the chest

skin being cold or clammy, or turning pale or a bluish colour

loss of speech or movement.

If possible, call your health care provider, hotline or health facility first, so you can be directed to the right clinic.

People who have pre-existing health problems are at higher risk when they have COVID-19; they should seek medical help early if worried about their condition. These include, but are not limited to: those taking immunosuppressive medication; those with chronic heart, lung, liver or rheumatological problems; those with HIV, diabetes, cancer or dementia.

As testing rates fall, it is more difficult to know how many people have COVID-19 and do not seek any treatment. At the start of the pandemic, 15% of people were thought to become seriously unwell and require hospital treatment and oxygen. More recent estimates suggest that hospitalization is required in around 3% of people with COVID-19. This is partly due to immunization, partly due to changes in the virus (especially the Omicron variants), and partly due to the availability of targeted medical treatments.

Most people make a full recovery without needing hospital treatment. For those with COVID-19 who are at high risk of severe illness (see question below), WHO has made recommendations on which drug treatments are effective in improving outcomes and preventing hospital admissions.

It is also important to be vigilant in recognizing people with severe disease and those needing hospital treatment so that they are treated early. The consequences of severe COVID-19 include death, respiratory failure, sepsis, thromboembolism (blood clots), and multiorgan failure, including injury of the heart, liver or kidneys.

In rare situations, children can develop a severe inflammatory syndrome a few weeks after infection.

People aged 60 years and over, and those with underlying medical problems like high blood pressure, diabetes, other chronic health problems (for example those affecting the heart, lungs, kidneys, and brain), low immune function / immunosuppression (including HIV), obesity, cancer, and unvaccinated people are most at risk of severe illness.

However, anyone at any age can get sick with COVID-19 and become seriously ill or die.

Some people who have had COVID-19, whether they have needed hospitalization or not, continue to experience symptoms, including fatigue, respiratory and neurological symptoms. These long-term effects are called post COVID-19 condition (also called long COVID). For further information on long COVID, see post COVID-19 condition and questions and answers.

You can protect yourself and others from COVID-19 by following preventive measures, such as keeping a distance, wearing a mask in crowded and poorly ventilated spaces, practicing hand hygiene, respiratory etiquette (covering your mouth and nose with a bent elbow or a tissue when you cough or sneeze), getting vaccinated and staying up to date with booster doses.

Check local advice where you live and work.

Read our public advice page for more information.

Anyone with symptoms such as acute onset of fever and cough should be tested, wherever possible, to ensure that they receive appropriate clinical care. People who do not have symptoms but have had close contact with someone who is, or may be, infected may also consider testing. Contact your local health guidelines and follow their guidance.

While a person is waiting for test results, they should preferably wear a mask when interacting with others in or outside of their household or sharing space with others. Where testing capacity is limited, tests should first be done for those at higher risk of infection, such as health workers, and those at higher risk of severe illness such as older people, especially those living in seniors' residences or long-term care facilities.

Individuals with signs and symptoms suggestive of COVID-19 or those who test positive for the virus should wear a mask when interacting with others in or outside of one's household or sharing space with others.

There are two main types of tests that can confirm whether you are infected with SARS-CoV-2, the virus that causes COVID-19. Molecular tests, such as polymerase chain reaction (PCR), are the most accurate tests for diagnosing SARS-CoV-2 infection. Molecular tests detect virus in the sample by amplifying viral genetic material to detectable levels. Rapid antigen tests (sometimes known as rapid diagnostic tests or RDTs) detect viral proteins (known as antigens). RDTs are a simpler and faster option than molecular tests and are available for testing by trained operators or by the individual themselves (sometimes called self-tests). They perform best when there is more virus circulating in the community and when sampled from an individual during the time they are most infectious, generally within the first 5-7 days following symptom onset. Samples for both types of tests are collected from the nose and/or throat with a swab.

Learn more about what kind of COVID-19 tests are available
Why testing for SARS-CoV-2 is important Use of Ag-RDTs What you need to know about self-testing

Antibody tests can tell us whether someone has had an infection in the past, even if they have not had symptoms. Also known as serological tests, these tests detect antibodies produced in response to an infection or vaccination. In most people, antibodies start to develop after days to weeks and can indicate if a person has had past infection or has been vaccinated. Antibody tests cannot be used to diagnose SARS-CoV-2 infection in the early stages of infection or disease but can indicate whether or not someone has had the disease in the past. If you have been vaccinated, many antibody tests are not able to distinguish between whether you were previously infected or have been vaccinated (or both), so in such situations you will test positive in either case.

Both isolation and quarantine are methods of preventing the spread of COVID-19.

Quarantine is used for certain persons who are a contact of someone infected with SARS-CoV-2, the virus that causes COVID-19, whether the infected person has symptoms or not. Quarantine means that you remain separated from others because you have been exposed to the virus and you may be infected and can take place in a designated facility or at home. For COVID-19, this means staying in the facility or at home for several days.

Isolation is used for people with COVID-19 symptoms or who have tested positive for the virus. Being in isolation means being separated from other people, ideally in a medical facility where you can receive clinical care. If isolation in a medical facility is not possible and you are not in a high-risk group for developing severe disease, isolation can take place at home. If you have symptoms, you should remain in isolation for at least 10 days. If you are infected and do not develop symptoms, you should remain in isolation for 5 days from the time you test positive. You can be discharged from isolation early if you test negative on a rapid antigen test.

If you have been exposed to someone with COVID-19, you may become infected, even if you feel well.

After exposure to someone who has COVID-19, do the following:

Call your healthcare provider to get tested or test yourself.

Stay home if you feel unwell.

Wear a mask when interacting with others in or outside of your household or sharing space with others.

Clean your hands regularly.

Practice respiratory etiquette: cover your mouth and nose with your bent elbow or a tissue when you cough or sneeze.

Avoid crowded, enclosed or poorly ventilated spaces.

Get vaccinated and stay up to date with booster doses.

The time from exposure to COVID-19 to the moment when symptoms begin is, on average, 5-6 days and can range from 1-14 days. This is why people who have been exposed to the virus are advised to remain at home and stay away from others in order to prevent the spread of the virus.

Yes. There are several COVID-19 vaccines validated for use by WHO (given Emergency Use Listing) and from other stringent national regulatory agencies (SRAs). The first mass vaccination programme started in early December 2020 and the number of vaccination doses administered is updated on a regular basis here. For more information on vaccine for COVID-19, see the vaccine questions and answers: Coronavirus disease (COVID-19): Vaccines (who.int)

If you are unwell, stay at home.

If you have any symptoms suggestive of COVID-19, wear a mask when interacting with others in or outside of your household or sharing space with others. If you have shortness of breath or pain or pressure in the chest, seek medical attention at a health facility immediately. Call your health care provider or hotline in advance for direction to the right health facility.

Get tested for COVID-19, regardless of your vaccination status, and especially if you are at high-risk for severe illness and could therefore be eligible for drug treatments.

Practice protective and preventive measures. Wear a mask, avoid crowded and poorly ventilated areas, improve ventilation in indoor spaces, keep a distance, practice hand hygiene, and respiratory etiquette (covering your mouth and nose with a bent elbow or a tissue when you cough or sneeze), get vaccinated and stay up to date with booster doses.

There has been huge progress in developing treatments for patients with COVID-19. Treatments for COVID-19 should be decided on an individual basis between the person and the healthcare professional looking after them. The choice will depend on the severity of disease and the risk of disease worsening (including the person's age and whether they have any health problems). WHO maintains a list of recommended treatments, together with the evidence for each, available at https://app.magicapp.org/#/guideline/nBkO1E.

These currently include:

for non-severe COVID-19: nirmatrelvir-ritonavir; molnupiravir; remdesivir

for severe COVID-19: corticosteroids (including dexamethasone); IL-6 receptor blockers (tocilizumab or sarilumab); baricitinib; remdesivir.

Apart from these medications, amongst the most commonly and globally used, and important treatments is oxygen for severely ill patients. WHO leads work which aims to improve global capacity and access to oxygen production, distribution and supply to patients.

For corticosteroids, further specific information can be found in the Corticosteroids, including dexamethasone questions and answers.

Antibiotics do not work against viruses; they only work on bacterial infections. COVID-19 is caused by a virus, so antibiotics do not work. Antibiotics should not be used as a means of prevention or treatment of COVID-19.

In hospitals, physicians will sometimes use antibiotics to treat secondary bacterial infections, which can be a complication of COVID-19 in severely ill patients. They should only be used as directed by a physician to treat a bacterial infection.

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WHO is continuously monitoring and responding to this pandemic. This questions and answers page will be updated as more is known about COVID-19, how it spreads and how it is affecting people worldwide. For more information, regularly check the WHO coronavirus pages. https://www.who.int/covid-19

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Trump passionately vows to investigate why initial COVID-19 info was hidden

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Trump passionately vows to investigate why initial COVID-19 info was hidden

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17 Apr 2020

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Trump passionately vows to investigate why initial COVID-19 info was hidden

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LIVE UPDATES

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COVID - Coronavirus Statistics - Worldometer

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Daily and weekly updated statistics tracking the number of COVID-19 cases, recovered, and deaths. Historical data with cumulative charts, graphs, and updates.

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Coronavirus: Experts say big jump in infections is stretching the healthcare system

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Coronavirus: Experts say big jump in infections is stretching the healthcare system

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17 Apr 2020

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SINGAPORE - Singapore will have to change the way it handles Covid-19 patients as the recent surge in infections is stretching the capacity of the healthcare system, said interviewed experts on Thursday (April 16).

Associate Professor Hsu Liyang of the NUS Saw Swee Hock School of Public Health said more foreign workers will continue testing positive in the coming days, as those who had contracted it before being rehoused according to safe distancing measures start falling sick.

Prof Hsu, who is both an infectious diseases expert and an epidemiologist, said the spread of Covid-19 in dormitories "must be slowed or else there is a high chance that our hospitals will be overwhelmed whatever we do".

His colleague and vice-dean of research at the school, Associate Professor Alex Cook, said: "We could easily see 10,000 to 20,000 cases by the end of the month if we do not put in place fast and effective measures ensuring actual safe distancing among the workers currently in the dorms."

Professor Dale Fisher, a senior infectious diseases expert at the National University Hospital (NUH), said both healthcare facilities and manpower are still managing, "but it's stretched".

All three agreed that what is needed is a good system for isolating and monitoring patients with mild symptoms outside of hospitals.

Fortunately, these foreign workers are generally younger and in better health, so the number who may become seriously ill will likely be lower, they said.

Nevertheless, as the number of infections rises, more will need to be hospitalised.

Prof Fisher estimates that between 5 and 10 per cent would need to be hospitalised, and perhaps 1 to 2 per cent would become critically ill.

This is lower than the general population norm of 15-20 per cent falling seriously ill and about 5 per cent needing intensive care.

But Prof Cook warned that should many of the workers smoke or have high blood pressure, they risk becoming critically ill if infected.

Singapore had a total of 11,321 acute hospital beds at the end of last year, of which 9,400 are in the public sector.

After postponing non-urgent treatments since January, bed occupancy rates at public hospitals have gone down from around 90 per cent at the start of the year to about 75 per cent by the end of March, freeing up more than 2,000 public hospital beds.

But with increasing numbers of people being infected over the past two months, these are being rapidly filled up.

On April 3, 473 Covid-19 patients were in hospital. By yesterday, the number had surged to 1,886, according to the Ministry of Health.

Private hospitals, which have slightly more than 1,600 beds, are also helping to care for coronavirus patients.

Prof Hsu suggested: "Covid-19 cases should be triaged and those with minimal risk of complications should be sent to community isolation facilities immediately rather than face a period of observation in an acute hospital.

"They will need to be monitored more carefully at the facility, so that they can be rapidly transferred to an acute hospital in the rare event that they deteriorate."

Prof Cook said the current procedure of simply moving out the less serious cases to other facilities, such as the Expo, may not be sustainable for long: "We'll have to accept that milder cases be managed outside of the formal healthcare environment."

Prof Hsu added that Singapore needs "to be agile and creative about how we deploy existing manpower and resources", such as building additional facilities and training people to care for the large influx of mild Covid-19 cases.

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Coronavirus: Experts say big jump in infections is stretching the healthcare system

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Singapore could easily see 10,000 to 20,000 cases by the end of the month if it does not put in place fast and effective measures ensuring actual safe distancing among the workers currently in the dorms, say experts.. Read more at straitstimes.com.

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28-day circuit breaker may not be enough if Singaporeans don't play their part

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28-day circuit breaker may not be enough if Singaporeans don't play their part

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16 Apr 2020

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SINGAPORE: A 28-day "circuit breaker" may not be enough if Singaporeans continue to flout measures put in place to stem the spread of COVID-19, said Environment and Water Resources Minister Masagos Zulkifli on Thursday (Apr 16).

He warned against complacency as the number of COVID-19 cases continues to grow, saying that 150 people will be issued fines for breaching safe distancing measures on Thursday - day 10 of the circuit breaker period. Another 50 people were caught in public spaces without face masks.

"We are still finding people eating at hawker centres despite dine-in being disallowed, crowds returning to some popular markets, and others loitering and hanging out in groups at parks and public spaces," said Mr Masagos in a Facebook post.

"We all know that if we do not play our part to observe the circuit breaker strictly, the 28 days may not be enough to break the chain of transmission, don't we?"

Mr Masagos said he was "glad to know the majority" of people have been wearing masks when outside their homes, and "only close to 50 people" were found without masks in public spaces on Thursday.

"Looking around, at photographs that enforcement officers have been sending me, I'm quite pleased, and of course, we can do better," the minister said on an interview on News 5.

On Tuesday, it was made mandatory for everyone in Singapore to wear masks while outdoors with certain exemptions.

Mr Masagos said that besides people who are doing strenuous exercise like running, or children below two years old, everyone should wear a mask when they leave their house, but exceptions can be made for people with special needs.

"It's important to remind ourselves that the safe distancing measures are to protect ourselves and those around us," he said in the TV interview.

He added that the most important thing to remember is to stay home as much as possible.

The minister acknowledged that the battle against COVID-19 has been "difficult for everyone" and that "tough but essential decisions" have had to be made.

"But we must do whatever it takes to keep Singaporeans and Singapore safe," said Mr Masagos. "Every lapse weakens our collective defence against the virus."

"When things look like they're getting better ... we must not let our guard down. Our resolve to complete the circuit breaker with seriousness, to the end, is critical."

He also paid tribute to safe distancing ambassadors and public officers, whom he commended for working hard on the front lines and behind the scenes.
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"Despite the many challenges, I am proud that they have remained dedicated and steadfast," said Mr Masagos.

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28-day circuit breaker may not be enough if Singaporeans don't play their part, says Masagos

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(Updated: ) Share this content SINGAPORE: A 28-day "circuit breaker" may not be enough if Singaporeans continue to flout measures put in place to stem the spread of COVID-19, said Environment and Water Resources Minister Masagos Zulkifli on Thursday (Apr 16).

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Respiratory Protection for Airborne Exposure to Biohazards

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Respiratory Protection for Airborne Exposure to Biohazards

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Respiratory Protection for Airborne Exposures to Biohazards_TDB174

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Viruses are microscopic parasites that lack the capacity to thrive and reproduce outside of a host body.

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If you have read How Cells Work, you know how both bacteria cells and the cells in your body work. A cell is a stand-alone living entity able to eat, grow and reproduce. Viruses are nothing like that. If you could look at a virus, you would see that a virus is a tiny particle. Virus particles are about one-millionth of an inch (17 to 1,000 nanometers) long [source: Milo and Phillips].

Most viruses are many times smaller than bacteria, though giant viruses - first discovered in 2003 - are about the same size [source: Pennisi]. Bacteria, in turn, are much smaller than most human cells. Viruses are so small that most cannot be seen with a light microscope, but must be observed with an electron microscope.

A virus particle, or virion, consists of the following:

Nucleic acid - set of genetic instructions, either DNA or RNA, either single-stranded or double-stranded (see How Cells Work for details on DNA and RNA)

Coat of protein - surrounds the DNA or RNA to protect it

Lipid membrane - surrounds the protein coat (found only in some viruses, including influenza; these types of viruses are called enveloped viruses as opposed to naked viruses)

Viruses vary widely in their shape and complexity. Some look like round popcorn balls, while others have a complicated shape that looks like a spider or the Apollo lunar lander.

Unlike human cells or bacteria, viruses don't contain the chemical machinery ( enzymes) needed to carry out the chemical reactions for life. Instead, viruses carry only one or two enzymes that decode their genetic instructions. So, a virus must have a host cell (bacteria, plant or animal) in which to live and make more viruses. Outside of a host cell, viruses cannot function. For this reason, viruses tread the fine line that separates living things from nonliving things. Most scientists agree that viruses are alive because of what happens when they infect a host cell.

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If you have read How Cells Work, you know how both bacteria cells and the cells in your body work. A cell is a stand-alone living entity able to eat, grow and reproduce. Viruses are nothing like that. If you could look at a virus, you would see that a virus is a tiny particle.

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Although viruses challenge our concept of what "living" means, they are vital members of the web of life

By Luis P. Villarreal

Editor's Note: This story was originally published in the December 2004 issue of Scientific American.

In an episode of the classic 1950s television comedy The Honeymooners, Brooklyn bus driver Ralph Kramden loudly explains to his wife, Alice, "You know that I know how easy you get the virus." Half a century ago even regular folks like the Kramdens had some knowledge of viruses-as microscopic bringers of disease. Yet it is almost certain that they did not know exactly what a virus was. They were, and are, not alone.

For about 100 years, the scientifi c community has repeatedly changed its collective mind over what viruses are. First seen as poisons, then as life-forms, then biological chemicals, viruses today are thought of as being in a gray area between living and nonliving: they cannot replicate on their own but can do so in truly living cells and can also affect the behavior of their hosts profoundly. The categorization of viruses as nonliving during much of the modern era of biological science has had an unintended consequence: it has led most researchers to ignore viruses in the study of evolution. Finally, however, scientists are beginning to appreciate viruses as fundamental players in the history of life.

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Coming to Terms
It is easy to see why viruses have been diffi cult to pigeonhole. They seem to vary with each lens applied to examine them. The initial interest in viruses stemmed from their association with diseases-the word "virus" has its roots in the Latin term for "poison." In the late 19th century researchers realized that certain diseases, including rabies and foot-and-mouth, were caused by particles that seemed to behave like bacteria but were much smaller. Because they were clearly biological themselves and could be spread from one victim to another with obvious biological effects, viruses were then thought to be the simplest of all living, gene-bearing life-forms.

Their demotion to inert chemicals came after 1935, when Wendell M. Stanley and his colleagues, at what is now the Rockefeller University in New York City, crystallized a virus- tobacco mosaic virus-for the fi rst time. They saw that it consisted of a package of complex biochemicals. But it lacked essential systems necessary for metabolic functions, the biochemical activity of life. Stanley shared the 1946 Nobel Prize- in chemistry, not in physiology or medicine-for this work.

Further research by Stanley and others established that a virus consists of nucleic acids (DNA or RNA) enclosed in a protein coat that may also shelter viral proteins involved in infection. By that description, a virus seems more like a chemistry set than an organism. But when a virus enters a cell (called a host after infection), it is far from inactive. It sheds its coat, bares its genes and induces the cell's own replication machinery to reproduce the intruder's DNA or RNA and manufacture more viral protein based on the instructions in the viral nucleic acid. The newly created viral bits assemble and, voilà, more virus arises, which also may infect other cells.

These behaviors are what led many to think of viruses as existing at the border between chemistry and life. More poetically, virologists Marc H. V. van Regenmortel of the University of Strasbourg in France and Brian W. J. Mahy of the Centers for Disease Control and Prevention have recently said that with their dependence on host cells, viruses lead "a kind of borrowed life." Interestingly, even though biologists long favored the view that viruses were mere boxes of chemicals, they took advantage of viral activity in host cells to determine how nucleic acids code for proteins: indeed, modern molecular biology rests on a foundation of information gained through viruses.

Molecular biologists went on to crystallize most of the essential components of cells and are today accustomed to thinking about cellular constituents-for example, ribosomes, mitochondria, membranes, DNA and proteins-as either chemical machinery or the stuff that the machinery uses or produces. This exposure to multiple complex chemical structures that carry out the processes of life is probably a reason that most molecular biologists do not spend a lot of time puzzling over whether viruses are alive. For them, that exercise might seem equivalent to pondering whether those individual subcellular constituents are alive on their own. This myopic view allows them to see only how viruses co-opt cells or cause disease. The more sweeping question of viral contributions to the history of life on earth, which I will address shortly, remains for the most part unanswered and even unasked.

To Be or Not to Be
The seemingly simple question of whether or not viruses are alive, which my students often ask, has probably defi ed a simple answer all these years because it raises a fundamental issue: What exactly defi nes "life?" A precise scientifi c defi nition of life is an elusive thing, but most observers would agree that life includes certain qualities in addition to an ability to replicate. For example, a living entity is in a state bounded by birth and death. Living organisms also are thought to require a degree of biochemical autonomy, carrying on the metabolic activities that produce the molecules and energy needed to sustain the organism. This level of autonomy is essential to most definitions.

Viruses, however, parasitize essentially all biomolecular aspects of life. That is, they depend on the host cell for the raw materials and energy necessary for nucleic acid synthesis, protein synthesis, processing and transport, and all other biochemical activities that allow the virus to multiply and spread. One might then conclude that even though these processes come under viral direction, viruses are simply nonliving parasites of living metabolic systems. But a spectrum may exist between what is certainly alive and what is not.

A rock is not alive. A metabolically active sack, devoid of genetic material and the potential for propagation, is also not alive. A bacterium, though, is alive. Although it is a single cell, it can generate energy and the molecules needed to sustain itself, and it can reproduce. But what about a seed? A seed might not be considered alive. Yet it has a potential for life, and it may be destroyed. In this regard, viruses resemble seeds more than they do live cells. They have a certain potential, which can be snuffed out, but they do not attain the more autonomous state of life.

Another way to think about life is as an emergent property of a collection of certain nonliving things. Both life and consciousness are examples of emergent complex systems. They each require a critical level of complexity or interaction to achieve their respective states. A neuron by itself, or even in a network of nerves, is not conscious-whole brain complexity is needed. Yet even an intact human brain can be biologically alive but incapable of consciousness, or "brain-dead." Similarly, neither cellular nor viral individual genes or proteins are by themselves alive. The enucleated cell is akin to the state of being braindead, in that it lacks a full critical complexity. A virus, too, fails to reach a critical complexity. So life itself is an emergent, complex state, but it is made from the same fundamental, physical building blocks that constitute a virus. Approached from this perspective, viruses, though not fully alive, may be thought of as being more than inert matter: they verge on life.

In fact, in October, French researchers announced fi ndings that illustrate afresh just how close some viruses might come. Didier Raoult and his colleagues at the University of the Mediterranean in Marseille announced that they had sequenced the genome of the largest known virus, Mimivirus, which was discovered in 1992. The virus, about the same size as a small bacterium, infects amoebae. Sequence analysis of the virus revealed numerous genes previously thought to exist only in cellular organisms. Some of these genes are involved in making the proteins encoded by the viral DNA and may make it easier for Mimivirus to co-opt host cell replication systems. As the research team noted in its report in the journal Science, the enormous complexity of the Mimivirus's genetic complement "challenges the established frontier between viruses and parasitic cellular organisms."

Impact on Evolution
Debates over whether to label viruses as living lead naturally to another question: Is pondering the status of viruses as living or nonliving more than a philosophical exercise, the basis of a lively and heated rhetorical debate but with little real consequence? I think the issue is important, because how scientists regard this question infl uences their thinking about the mechanisms of evolution.

Viruses have their own, ancient evolutionary history, dating to the very origin of cellular life. For example, some viral- repair enzymes-which excise and resynthesize damaged DNA, mend oxygen radical damage, and so on- are unique to certain viruses and have existed almost unchanged probably for billions of years.

Nevertheless, most evolutionary biologists hold that because viruses are not alive, they are unworthy of serious consideration when trying to understand evolution. They also look on viruses as coming from host genes that somehow escaped the host and acquired a protein coat. In this view, viruses are fugitive host genes that have degenerated into parasites. And with viruses thus dismissed from the web of life, important contributions they may have made to the origin of species and the maintenance of life may go unrecognized. (Indeed, only four of the 1,205 pages of the 2002 volume The Encyclopedia of Evolution are devoted to viruses.)

Of course, evolutionary biologists do not deny that viruses have had some role in evolution. But by viewing viruses as inanimate, these investigators place them in the same category of infl uences as, say, climate change. Such external infl uences select among individuals having varied, genetically controlled traits; those individuals most able to survive and thrive when faced with these challenges go on to reproduce most successfully and hence spread their genes to future generations.

But viruses directly exchange genetic information with living organisms-that is, within the web of life itself. A possible surprise to most physicians, and perhaps to most evolutionary biologists as well, is that most known viruses are persistent and innocuous, not pathogenic. They take up residence in cells, where they may remain dormant for long periods or take advantage of the cells' replication apparatus to reproduce at a slow and steady rate. These viruses have developed many clever ways to avoid detection by the host immune system- essentially every step in the immune process can be altered or controlled by various genes found in one virus or another.

Furthermore, a virus genome (the entire complement of DNA or RNA) can permanently colonize its host, adding viral genes to host lineages and ultimately becoming a critical part of the host species' genome. Viruses therefore surely have effects that are faster and more direct than those of external forces that simply select among more slowly generated, internal genetic variations. The huge population of viruses, combined with their rapid rates of replication and mutation, makes them the world's leading source of genetic innovation: they constantly "invent" new genes. And unique genes of viral origin may travel, finding their way into other organisms and contributing to evolutionary change.

Data published by the International Human Genome Sequencing Consortium indicate that somewhere between 113 and 223 genes present in bacteria and in the human genome are absent in well-studied organisms-such as the yeast Saccharomyces cerevisiae, the fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans -that lie in between those two evolutionary extremes. Some researchers thought that these organisms, which arose after bacteria but before vertebrates, simply lost the genes in question at some point in their evolutionary history. Others suggested that these genes had been transferred directly to the human lineage by invading bacteria.

My colleague Victor DeFilippis of the Vaccine and Gene Therapy Institute of the Oregon Health and Science University and I suggested a third alternative: viruses may originate genes, then colonize two different lineages-for example, bacteria and vertebrates. A gene apparently bestowed on humanity by bacteria may have been given to both by a virus.

In fact, along with other researchers, Philip Bell of Macquarie University in Sydney, Australia, and I contend that the cell nucleus itself is of viral origin. The advent of the nucleus- which differentiates eukaryotes (organisms whose cells contain a true nucleus), including humans, from prokaryotes, such as bacteria-cannot be satisfactorily explained solely by the gradual adaptation of prokaryotic cells until they became eukaryotic. Rather the nucleus may have evolved from a persisting large DNA virus that made a permanent home within prokaryotes. Some support for this idea comes from sequence data showing that the gene for a DNA polymerase (a DNAcopying enzyme) in the virus called T4, which infects bacteria, is closely related to other DNA polymerase genes in both eukaryotes and the viruses that infect them. Patrick Forterre of the University of Paris-Sud has also analyzed enzymes responsible for DNA replication and has concluded that the genes for such enzymes in eukaryotes probably have a viral origin.

From single-celled organisms to human populations, viruses affect all life on earth, often determining what will survive. But viruses themselves also evolve. New viruses, such as the AIDS-causing HIV-1, may be the only biological entities that researchers can actually witness come into being, providing a real-time example of evolution in action.

Viruses matter to life. They are the constantly changing boundary between the worlds of biology and biochemistry. As we continue to unravel the genomes of more and more organisms, the contributions from this dynamic and ancient gene pool should become apparent. Nobel laureate Salvador Luria mused about the viral infl uence on evolution in 1959. "May we not feel," he wrote, "that in the virus, in their merging with the cellular genome and reemerging from them, we observe the units and process which, in the course of evolution, have created the successful genetic patterns that underlie all living cells?" Regardless of whether or not we consider viruses to be alive, it is time to acknowledge and study them in their natural context-within the web of life.

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Although viruses challenge our concept of what "living" means, they are vital members of the web of life

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What’s a virus, anyway? Part 1: The bare-bones basics

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What’s a virus, anyway? Part 1: The bare-bones basics

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As the coronavirus pandemic spreads across the globe, the term "virus" gets a lot of airplay. But what exactly are viruses, and how do they spread? Here's a primer, with a hat tip to Stanford virologist Jan Carette, PhD.

For starters, viruses are easily the most abundant life form on Earth, if you accept the proposition that they're alive. Try multiplying a billion by a billion, then multiply that by ten trillion, and that (10 to the 31st power) is the mind-numbing estimate of how many individual viral particles are estimated to populate the planet.

Is a virus a living thing? Maybe. Sometimes. It depends on location. "Outside of a cell, a viral particle is inert," Carette told me. On its own, it can't reproduce itself or, for that matter, produce anything at all. It's the ultimate parasite.

Or, you could say more charitably, very efficient. Viruses travel light, packing only the baggage they absolutely need to hack into a cell, commandeer its molecular machinery, multiply and make an escape.

When it comes to viruses, there are exceptions to nearly every rule. But they do have things in common, said Carette.

A virus's travel kit always includes its genome and a surrounding protein shell, or capsid, which keeps the viral genome safe, helps the virus latch onto cells and climb inside and, on occasion, abets its offspring's getaway. The capsid consists of identical protein subunits, whose unique shapes and properties determine the capsid's structure and function.

Some viruses also wear greasy overcoats, called envelopes, made from stolen shards of the membranes of the last cell they infected. Influenza and hepatitis C viruses have envelopes, as do coronaviruses, herpesviruses and HIV. Rhinoviruses, which are responsible for most common colds, and polioviruses don't. Here's a practical takeaway: Enveloped viruses particularly despise soap because it disrupts greasy membranes. Soap and water are to these viruses what exhaling garlic is to a vampire, which is why washing your hands works wonders.

How do viruses enter cells, replicate and head for the exits?

For a virus to spread, it must first find a way into a cell. But, said Carette, "penetrating a cell's perimeter isn't easy." Cells' outer membranes are normally tough to penetrate without some kind of special pass. But viruses have ways of tricking cells into letting them in. Typically, a portion of the viral capsid will have a strong affinity to bind with one or another protein dotting the surfaces of one or another particular cell type. The binding of the viral capsid with that cell-surface protein serves as an admission ticket, easing the virus's invasion of the cell.

The viral genome, like ours, is an instruction kit for the production of proteins the virus needs. This genome can be made up of either DNA, as is the case with virtually all other creatures, or its close chemical relative RNA, which encodes genetic information just as DNA does but is much more flexible and somewhat less stable. Most mammal-infecting viruses' genomes are made of RNA. (Not herpesviruses, though.)

In addition to the gene coding for its capsid protein, every virus needs another gene for its own version of an enzyme known as a polymerase. Inside the cell, viral polymerases generate numerous copies of the invader's genes, from whose instructions the cell's obedient molecular assembly line produces capsid subunits and other viral proteins.

Capsids -- a virus's protein shell -- self-assemble from their subunits, often with help from proteins originally made by the cell for other purposes, but co-opted by the virus. These fresh copies of the viral genome are packaged inside newly-made capsids for export.

Viral genomes can also contain genes for proteins that can co-opt the cellular machinery to help viruses replicate and escape, or that can tweak the virus's own genome -- or ours. The genome can contain as few as two genes -- one for the protein from which the capsid is built, the other for the polymerase -- or as many as hundreds (as in herpesviruses, for example).

Often, the virus's plentiful progeny punish the good deed of the cell that produced them by lysing it -- punching holes in its outer membrane, busting out of it and destroying the cell in the process. But enveloped viruses can escape by an alternative process called budding, whereby they wrap themselves in a piece of membrane from the infected cell and, in these newly acquired greasy overcoats, diffuse through the cell's outer membrane without structurally damaging it. Even then, the cell, having birthed myriad baby viruses, is often left fatally weakened.
Up next: To learn more about how viruses including coronaviruses do what they do to us -- and about what we might be able to do to ward them off -- see "What's a virus, anyway? Part 2: How coronavirus infected us -- and how viruses made us"
Graphic illustration of a measles virus from the Centers for Disease Control and Prevention

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What's a virus, anyway? Part 1: The bare-bones basics - Scope

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As the coronavirus pandemic spreads across the globe, the term "virus" gets a lot of airplay. But what exactly are viruses, and how do they spread? Here's a primer, with a hat tip to Stanford virologist Jan Carette, PhD. For starters, viruses are easily the most abundant life form on Earth, if you accept the proposition that they're alive.

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Trump says US investigating if COVID-19 came from Wuhan lab

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Trump says US investigating if COVID-19 came from Wuhan lab

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15 Apr 2020

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WASHINGTON: US President Donald Trump said on Wednesday (Apr 15) that his government is trying to determine whether the coronavirus emanated from a lab in Wuhan, China, and Secretary of State Mike Pompeo said Beijing "needs to come clean" on what they know.

The source of the virus remains a mystery. General Mark Milley, chairman of the Joint Chiefs of Staff, said on Tuesday that US intelligence indicates that the coronavirus likely occurred naturally, as opposed to being created in a laboratory in China, but there is no certainty either way.

Fox News reported on Wednesday that the virus originated in a Wuhan laboratory not as a bioweapon, but as part of China's effort to demonstrate that its efforts to identify and combat viruses are equal to or greater than the capabilities of the United States.

This report and others have suggested the Wuhan lab where virology experiments take place and lax safety standards there led to someone getting infected and appearing at a nearby "wet" market, where the virus began to spread.

At a White House news conference Trump was asked about the reports of the virus escaping from the Wuhan lab, and he said he was aware of them.

"We are doing a very thorough examination of this horrible situation that happened," he said.

Asked if he had raised the subject in his conversations with Chinese President Xi Jinping, Trump said: "I don't want to discuss what I talked to him about the laboratory, I just don't want to discuss, it's inappropriate right now."

Trump has sought to stress strong US ties with China during the pandemic as the United States has relied on China for personal protection equipment desperately needed by American medical workers.

As far back as February, the Chinese state-backed Wuhan Institute of Virology pushed dismissed rumors that the virus may have been artificially synthesized at one of its laboratories or perhaps escaped from such a facility.

Pompeo, in a Fox News Channel interview after Trump's news conference, said "we know this virus originated in Wuhan, China," and that the Institute of Virology is only a handful of miles away from the wet market.

"We really need the Chinese government to open up" and help explain "exactly how this virus spread," said Pompeo.

"The Chinese government needs to come clean," he said.

The broad scientific consensus holds that SARS-CoV-2, the virus' official name, originated in bats.

Trump and other officials have expressed deep skepticism of China's officially declared death toll from the virus of around 3,000 people, when the United States has a death toll of more than 20,000 and rising.

He returned to the subject on Wednesday, saying the United States has more cases "because we do more reporting".
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"Do you really believe those numbers in this vast country called China, and that they have a certain number of cases and a certain number of deaths; does anybody really believe that?" he said.

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Trump says US investigating if COVID-19 came from Wuhan lab

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(Updated: ) Share this content WASHINGTON: US President Donald Trump said on Wednesday (Apr 15) that his government is trying to determine whether the coronavirus emanated from a lab in Wuhan, China, and Secretary of State Mike Pompeo said Beijing "needs to come clean" on what they know.

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Politics aside, US relies on China supplies to fight COVID-19: Experts

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Politics aside, US relies on China supplies to fight COVID-19: Experts

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3 Apr 2020

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WASHINGTON: US politicians have voiced fury over Beijing's handling of the coronavirus crisis but they face a harsh truth - the United States desperately needs China's supplies, some experts say.

China before the crisis produced nearly half of the face masks imported into the United States - which in normal times cost less than a dollar but have disappeared from shelves amid growing calls for ordinary Americans to wear them when outside.

As China appears to have contained its own outbreak of the disease, which has infected more than 1 million people worldwide since first emerging late last year in Wuhan, it is now the first resort for protective gear sought across the world.

"China is a massive source of supply for these products at a time of incredible need, both in the United States and globally," said Chad Bown, a senior fellow at the Peterson Institute for International Economics.

"So if you're not open to China and trying to buy these from China right now, you really have no hope," he said.

US manufacturers have stepped up, with 3M and Honeywell together raising production of masks to 70 million per month, but that's well below needs and the Department of Health and Human Services is seeking to buy 500 million masks for a strategic stockpile.

The health crisis has meant a seller's market for Chinese manufacturers of so-called N95 masks, which are designed to block out 95 per cent of very small particles.
TIME OF US-CHINA TENSION
Dan Harris, a Seattle lawyer who represents companies in emerging markets, wrote on his blog that he recently heard from three companies that were each scammed out of more than US$1 million after placing N95 mask orders from China - with one firm receiving "dusty, mouldy Halloween masks".

Bown found no evidence in the available early data that China has cut off supplies or diverted them to politically favoured partners such as hard-hit Italy.

Its exports of personal protective equipment declined in the first two months of the year - but by less than China's overall exports, he said.

Still, China exerts power as it supplies 48 per cent of personal protective equipment imported to the United States and 50 per cent to the European Union, according to Bown's calculations.

"When you start a trade war with a country that you deliberately antagonise while you're still reliant on them for certain things, you've sort of done this to yourself," Bown said.

President Donald Trump has veered from lashing out at Beijing to praising cooperation with President Xi Jinping.

Trump, who has slapped tariffs on billions of dollars of Chinese goods since taking office, said Wednesday that China's figures on the coronavirus outbreak "seem to be a little bit on the light side".

He appeared to be confirming a Bloomberg report that quoted US intelligence as saying China has deliberately downplayed its virus cases.

FOCUS ON PHARMACEUTICALS
Trump's former national security adviser John Bolton - who has himself faced criticism over preparations for a pandemic - on Thursday pointed to the alleged underreporting to call for the United States to pursue "new policies to prevent continued US over-reliance on China in our supply chain".

Yanzhong Huang, a global health expert at the Council on Foreign Relations and Seton Hall University, said face mask manufacturing has grown in China for the same reasons as many export industries - production is low-tech and labour-intensive.

Potentially more problematic, Huang said, is the supply of active pharmaceutical ingredients.

A Senate hearing last year heard that more than 80 per cent of the key ingredients in drugs in the United States originated abroad - mostly in China or in India, which by contrast has warm relations with the United States.

Huang expected the United States after the crisis would move to shorten or diversify the supply chain for active pharmaceutical ingredients.

But he also noted that the United States dominated in plenty of vital drugs, including in treating non-communicable diseases of rising concern in China.

"China has leverage but we should just keep in mind that it is not a one-way street. The US also has its own leverage," he said.

"I don't think it would be wise for any country to use this, really, as a weapon."

Senator Tom Cotton, a Republican outspoken in his criticism of Beijing, has proposed a complete ban on buying active pharmaceutical ingredients from China in 2022.

Bown, the economist, said countries should not aim for self-sufficiency in medical supplies but rather seek a diverse global supply.
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"The point is, with a pandemic like this, nowhere geographically is safe anywhere in the world," Bown said.

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Politics aside, US relies on China supplies to fight COVID-19: Experts

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(Updated: ) Share this content WASHINGTON: US politicians have voiced fury over Beijing's handling of the coronavirus crisis but they face a harsh truth - the United States desperately needs China's supplies, some experts say.

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Spain COVID-19 death count 'may be thousands short'

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Spain COVID-19 death count 'may be thousands short'

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17 Apr 2020

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MADRID: Spain's coronavirus death toll soared past 19,000 on Thursday (Apr 16) with another 551 deaths, but questions over the counting method have raised some regional concerns the real figure is much higher.

After nearly five weeks of confinement, the rise in deaths and infections has slowed over the past fortnight, with the overnight fatalities taking the toll to 19,130.

But regional authorities in Madrid and Catalonia said they each had thousands more victims than the official count.

"The real number of deaths is difficult to know," said Fernando Simon, the health ministry's emergencies coordinator.

The daily figure was compiled from information provided by regional authorities concerning deaths among patients who "had tested positive for coronavirus", he said.

Between them, Madrid and Catalonia account for 56 per cent of the national toll, but some officials say the numbers are flawed for not including all those who have died outside of hospital.

Madrid has counted 6,877 deaths but on Wednesday a top official said the true figure was likely to be more than 10,000.
DEATHS OUTSIDE OF HOSPITAL
In Catalonia, where 3,855 people have died, the real number could be higher than 7,000 -- prompting the regional government to announce changes to its counting method.

"Until now, the official figures were supplied by Catalan hospitals counting people who died there," it said in a statement late on Wednesday.

"But as of today.. figures on deaths at (old people's) residences and homes throughout Catalonia will also be collected following an order to funeral services to provide this information," it said, giving a new figure of 7,097.

The funeral homes based their numbers on a count of those who died with COVID-19 and others who died while showing symptoms compatible with infection without having being tested, the Catalan government said.

But Simon said it was important to verify whether or not those victims "had tested positive or not".

Among the latest wave of victims was best-selling Chilean writer Luis Sepulveda, who died at a hospital in the northern city of Oviedo, his publishing house said.

Spain also recorded 5,183 new cases of COVID-19, taking the overall figure to 182,816 - officially second highest in the world behind the United States.

Spanish officials say the virus has steadied since a daily toll of 950 was recorded on Apr 2 but they have insisted on maintaining the Mar 14 lockdown that is likely to be extended into mid-May.
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One of the tightest lockdowns in Europe, the restrictions allow just essential workers out, otherwise the rest of the population can only leave home to buy food and medicine, to attend a medical emergency or to briefly walk the dog.

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Spain COVID-19 death count 'may be thousands short'

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(Updated: ) Share this content MADRID: Spain's coronavirus death toll soared past 19,000 on Thursday (Apr 16) with another 551 deaths, but questions over the counting method have raised some regional concerns the real figure is much higher.

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COVID-19 cases in Indonesia could cross 100,000 mark, says national taskforce expert

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COVID-19 cases in Indonesia could cross 100,000 mark, says national taskforce expert

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16 Apr 2020

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JAKARTA: Indonesia's COVID-19 cases is predicted to exceed 100,000, an expert with the government pandemic task force said on Thursday (Apr 16).

In a press briefing, Professor Wiku Adisasmito said the number of cases is predicted to peak between early May and the beginning of June. This is based on predictions by experts, scientific institutions and individuals.

"We have reviewed and combined all the predictions ... The number of cases during the peak cumulative is 95,000. Whereas in June and July, the confirmed cases cumulative will be reaching 106,000," he said.

He noted, however, that the number is not a rigid figure, and the government hopes that the number of cases will be lower.

As of Thursday afternoon, there were 5,516 COVID-19 cases reported in the country with 496 deaths and 548 recovered cases.
ATTEMPTS UNDERWAY TO INTEGRATE DATA NATIONALLY
Indonesia has one of the highest fatality rates in the world, between 8 per cent and 9 per cent.

Since Indonesia announced its first COVID-19 cases on Mar 2, observers have criticised the government for not announcing details of the cases and providing reliable as well as coherent data.

The government had initially explained that this was to avoid causing public panic. Earlier this week, however, President Joko Widodo instructed officials to provide transparent data.

Prof Adisasmito said the government is working on this as quickly as possible.

"We are now integrating the data in the COVID-19 task force. We are working very hard to make sure that there is data integration at all levels within Indonesia, from the district level, provincial level, and national level," he said, adding that there are efforts to improve the validity of the data.

"As soon as we have all the data integrated and valid, we will be informing the public on the situation."
BANNING IDUL FITRI EXODUS WOULD HURT THE UNEMPLOYED: TASK FORCE HEAD

Questions have also been asked over the central government's decision to stop short of barring movement of people during the upcoming Idul Fitri holidays, where many would usually leave the big cities to go back to their hometowns, potentially leading to the virus spreading further.

Only civil servants, military, police as well as employees of state-owned enterprises are barred from participating in the Idul Fitri exodus.

The head of the COVID-19 task force, Mr Doni Monardo said during the Thursday briefing that the decision was taken because the government wanted to protect those who have lost their livelihoods in the cities.

"Those who lost their jobs entirely and those who have been made redundant .... cannot sustain their life for the next three to six months ... If they remain in the capital city, it's almost impossible for them to get assistance (as their official place of residence is in the other provinces)," he noted.

"If they return to their hometowns, they will be able to obtain that (assistance) because they have their own agriculture ... This will provide a bit of sustenance for them," said Mr Monardo.

During the press briefing, it was also mentioned that the government is targeting to increase the polymerase chain reaction (PCR) tests to 10,000 tests a day, in order to enhance detection of COVID-19 cases.
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As of Thursday, the Indonesian government has tested about 35,000 individuals nationwide.

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COVID-19 cases in Indonesia could cross 100,000 mark, says national taskforce expert

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(Updated: ) Share this content JAKARTA: Indonesia's COVID-19 cases is predicted to exceed 100,000, an expert with the government pandemic task force said on Thursday (Apr 16). In a press briefing, Professor Wiku Adisasmito said the number of cases is predicted to peak between early May and the beginning of June.

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Respirators and Surgical Masks - A Comparison

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Respirators and Surgical Masks - A Comparison

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Respirators and Surgical Masks - A Comparison

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Why washing hands with soap is critical in battling Covid-19

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Why washing hands with soap is critical in battling Covid-19

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14 Apr 2020

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SINGAPORE - Masks are now a must for anyone stepping out, and safe distancing measures are in full throttle, but washing your hands properly remains a cornerstone of the battle against the coronavirus.

An experiment conducted by The Straits Times has shown that doing this thoroughly with soap makes a critical difference. It can reduce the amount of germs picked up on the hands by 45 per cent compared to just rinsing them with water.

Even as the multi-ministry task force tackling Covid-19 announced on Tuesday (April 14) that masks would be compulsory for those leaving home, Health Minister Gan Kim Yong stressed the importance of personal hygiene, particularly during the current period of enhanced safe distancing.

"I would continue to encourage Singaporeans to wash your hands, observe personal hygiene, which is a very critical factor in disrupting the transmission chain," he said.

An effective way of washing hands involves a seven-step process that ensures a thorough cleansing as it covers the base of one's palms to the tip of their fingers - all of which should take approximately the time needed to sing 'Happy Birthday' twice.

ST worked with professional cleaning company Cleaning Express, to see how easily germs can get on hands after touching common surfaces, and how thorough hand washing may help to dispel these germs, which include bacteria and viruses, among them Covid-19.

The experiment, conducted using common touch-points such as computers, door handles and light switches, involved three people, an optics solution as a stand-in for the germs on a surface, and an ATP meter to measure the cleanliness of a surface.

The device detects biological contamination by measuring adenosine triphosphate (ATP), the molecule found in cells.

While it does not specifically indicate the presence of viruses, it highlights where they may lurk.

The optics solution is typically used in hygiene training to demonstrate correct hand-washing techniques. When under UV light, darkened parts show unwashed areas, signalling that this was not done correctly.

Microbes such as the coronavirus are able to remain on some surfaces for days, and can be transferred onto each subsequent person touching the same lift button or ATM machine, for instance.

In the experiment, the first person touched various surfaces with unwashed hands.

Two others then touched the same items.

Afterwards, one rinsed her hands with water, while the other used soap.

The results were telling: water alone gave a cleanliness reading of 47 - her hands remained dirty, and the UV light highlighted visible stains.

The one who used soap, in contrast, got a score of 26, which is considered generally clean, and her hands were stain-free.

But her hands were still not 100 per cent germ-free.

Infectious diseases expert Leong Hoe Nam explained that to kill all the microbes on one's hands, skin disinfectants containing chlorhexidine or iodine agents - the kind used by doctors before surgery - have to be used.

To maintain one's hygiene amid the Covid-19 pandemic, however, he added that washing hands thoroughly with soap and water would be sufficient, and suggested that antibacterial soap has an added advantage.

"As viruses require physical flushing and soap detergent to break its structure, regular soap will suffice- as long as we practise the seven-step hand-washing process," he said.

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Why washing hands with soap is critical in battling Covid-19

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SINGAPORE - Masks are now a must for anyone stepping out, and safe distancing measures are in full throttle, but washing your hands properly remains a cornerstone of the battle against the coronavirus. An experiment conducted by The Straits Times has shown that doing this thoroughly with soap makes a critical difference.

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How soap absolutely annihilates the coronavirus

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How soap absolutely annihilates the coronavirus

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27 Mar 2020

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As Covid-19 cases in the US surge, there's one consumer product critical to our great national battle to "flatten the curve," or slow the pandemic: soap. Humble, ancient, cheap, effective soap.

Respiratory viruses - like the novel coronavirus, the flu, and the common cold - can be spread via our hands. If someone is sick, a hand can touch some mucus and viral particles will stick to the hand. If someone is well, hands act like sticky traps for viruses. We can pick up droplets that contain the virus, and they'll stay on our hands, and perhaps enter our bodies if we touch our hands to our faces.

That's why our hands are the front lines in the war against Covid-19. The Centers for Disease Control and Prevention (CDC) recommends washing hands with soap and water as the top way to clean our hands. "But if soap and water are not available, using a hand sanitizer with at least 60% alcohol can help," the CDC says.

The CDC prioritizes soap. Yet, per news reports, people have been stocking up and hoarding sanitizer. The sanitizer situation has grown absurd: The Atlantic reported on a man who sold a bottle of Purell on eBay for $138. Hand sanitizer containing over 60 percent alcohol works against Covid-19 and is a good option when you're not near a sink. But it's getting harder to find than a hypodermic needle in a haystack.

Sanitizer might feel like a modern-day, scientific, and more clinical upgrade to soap. But I'm here to tell you that soap - all sorts of it: liquid, solid, honeysuckle-scented, the versions inexplicably only marketed to men or women - is a badass, and even more routinely effective than hand sanitizer. We should be excited to use it, as much as possible.

In a recent phone call, he explained why soap is such an effective Covid-19 killer and why it's so important to soap your hands for at least 20 seconds.

First up: What is soap?

Soap, Thordarson explains, is common phrase for what chemists call "amphiphiles." These are molecules that have a dual nature. One end of the molecule is attracted to water and repelled by fats and proteins. The other side of the molecule is attracted to fats and is repelled by water. (If you're looking out for product labels, the most common soap is "sodium laureth sulfate" - it's a detergent that's often mixed with other chemicals to both clean our hands and not damage our skin.)

It's this dual-nature chemical construction that makes soap so effective. "When you buy a conventional soap, it consists of a mixture of these amphiphiles," Thordarson explains. And they all do the same thing.

Think about what happens when you pour some olive oil into water. The oil pools up in a mass that floats. "That's because fats don't mix with water," he says. But mix some soap into the oil and water and the oil will disperse. Basically, that happens because the soap is attracted to the grease, via its fat-loving side, but then tears it up, pulling it into the water via its water-loving side. It's a one-two punch. Surround the oil particles and move them away from one another.

Now, lucky for us, coronaviruses are a bit like the oil mentioned in the above example: bits of genetic information - encoded by RNA - surrounded by a coat of fat and protein. Thordarson likes to call viruses "nano-sized grease balls." And grease balls, no matter the size, are the exact type of thing soap loves to annihilate.

1/25 Part 1 - Why does soap work so well on the SARS-CoV-2, the coronavirus and indeed most viruses? Because it is a self-assembled nanoparticle in which the weakest link is the lipid (fatty) bilayer. A two part thread about soap, viruses and supramolecular chemistry #COVID19 pic.twitter.com/OCwqPjO5Ht
- Palli Thordarson (@PalliThordarson) March 8, 2020

How soap destroys viruses

The soap takes care of the virus much like it takes care of the oil in the water. "It's almost like a crowbar; it starts to pull all the things apart," Thordarson says.

One side of the soap molecule (the one that's attracted to fat and repelled by water) buries its way into the virus's fat and protein shell. Fortunately, the chemical bonds holding the virus together aren't very strong, so this intrusion is enough to break the virus's coat. "You pull the virus apart, you make it soluble in water, and it disintegrates," he says.

Then the harmless shards of virus get flushed down the drain. And even if it the soap doesn't destroy every virus, you'll still rid them from your hands with soap and water, as well as any grease or dirt they may be clinging to. Soap will also wash away bacteria and other viruses that may be a bit tougher than coronavirus, and harder to disintegrate.

The trick is this all takes a little time to happen, and that's why you need to take at least 20 seconds to wash your hands.

First off, your skin is wrinkly, and it takes time for soap to penetrate into all the tiny folds and demolish the viruses that lurk within. Then the soap needs a few moments to do its chemical work. "You do need a bit of time for all the soap to interact back and forth with the virus particle," he says. Twenty seconds should do the trick just fine.

Alcohol, the main ingredient in hand sanitizer, can destroy viruses, too. Sanitizers "actually work in a similar way, the alcohol molecules are somewhat amphiphiles," he says. The thing is, you need a very high concentration of alcohol to achieve the same effect. (Chemicals called quaternary ammonium compounds - the main ingredient in Lysol - kill viruses too but can be a bit harsher on the skin.)

The CDC recommends a sanitizer that's 60 percent alcohol, so beware of sanitizers or wipes on the market that don't meet this standard (or contain alcohol at all). Hand sanitizer is useful, but it can fail in un-ideal situations. If your hands are wet or sweaty when you use the sanitizer, that can dilute it and diminish its effectiveness. Also, sanitizer doesn't clean your hands of sticky grease to which viruses can also adhere.

"Soap doesn't really fail easily," Thordarson says. It doesn't really matter the formulation of soap, either. You don't need "antibacterial soap" - which the Food and Drug Administration advises to skip altogether due to a lack of evidence of its usefulness. And you don't need a super-harsh detergent like you'd put in your dishwasher or laundry machine. Simple soap works fine. "As long as you give it a little bit of time, it will do its job."

All of this, at least, makes me excited to wash my hand more. As I'm washing with soap and water and counting to 20, I'm going to imagine a battle being waged on the nano-scale in the teeny-tiny folds of my skin. The soap is charging in, sticking to viruses (as well as dirt and other grease), and tearing them apart in brutal, heroic fashion. It's almost like the Avengers, but better. Because it's real. And it can help stop the spread of this outbreak.

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How soap absolutely annihilates the coronavirus

# data[].attributes.attachment_link.description
As Covid-19 cases in the US surge, there's one consumer product critical to our great national battle to "flatten the curve," or slow the pandemic: soap. Humble, ancient, cheap, effective soap. Respiratory viruses - like the novel coronavirus, the flu, and the common cold - can be spread via our hands.

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World Health Organization

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Studies: Hand sanitizers kill COVID-19 virus, e-consults appropriate

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Studies: Hand sanitizers kill COVID-19 virus, e-consults appropriate

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14 Apr 2020

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Mary Van Beusekom | News Writer | CIDRAP News April 14, 2020

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Studies: Hand sanitizers kill COVID-19 virus, e-consults appropriate

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In a study today in Emerging Infectious Diseases, Swiss and German researchers found that alcohol-based hand sanitizers recommended by the World Health Organization (WHO) are effective in killing the novel coronavirus.