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What steps has our school district implemented?

What have we been asked to do?

Under what circumstances will school close?

What steps has Santa Clara county taken?

How many cases and how many deaths have happened so far in Santa Clara county?

Are cases increasing, staying the same, or going down?

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What is an epidemic curve?

What is "flattening the curve" and why is it so important?

What countries have been the hardest hit so far?

How does genetics help us trace the spread of the virus?

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What are some myths that have been repeated a lot about the coronavirus?

What evidence have people used to debunk these myths?

How can we recognize accurate vs. inaccurate or misleading statements?

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How worried should people be?

What should people be doing in response to this issue?

What would be over-reacting? What would be under-reacting?

How do emotions and management of emotions factor into this issue?

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Coronavirus genetics reveal global travels

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Coronavirus genetics reveal global travels

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Several years ago, Richard Neher, an evolutionary biologist at the University of Basel in Switzerland, and his colleagues wanted to monitor changes to the flu's genetic makeup to see if the data would help scientists build more-effective flu vaccines. They developed an online interface that integrated the latest viral sequencing data, analyzed it, and published the results in a publicly available interactive web browser.

"Then we thought, why just flu, why not other viruses?" Neher says. The team built a similar platform to chart the transmission of MERS and Ebola and called the site NextStrain.org. Now, they've adapted it to keep track of the genetic tweaks to SARS-CoV-2 as it spreads around the globe and chart the viral lineages on world maps to watch, in nearly real time, as the virus moves from major hotspots in China to smaller pockets in other countries.

Here, Neher talks with The Scientist about what NextStrain.org has uncovered about the transmission of SARS-CoV-2.

The Scientist: How do viral genomes' sequences from swabs taken from infected patients help you build a family tree of the virus?

Richard Neher: These coronavirsuses tend to change their genome, they mutate, at a fairly high rate. These mutations allow us to group viruses into more closely related viruses and less closely related viruses. All the sequences on the site are super similar because they were closely related. As time goes on, the lineages pick up independent mutations, and then they cause outbreaks in different parts of the world. You can group these sequences together by genetic makeup and reconstruct the transmission tree of the virus.

There are 70,000 reported cases so the number of infections could be 200,000. It could be 500,000.

TS: Can you estimate the number of infections from the tree?

RN: Yes, if you look at the viral tree you see different sequences. And the tree will have different shapes depending on if the outbreak it's staying the same size or growing. If it's growing, you see many, many lineages coming together very deep in the tree, and that's what we have here. That implies there was rapid expansion at the base of the tree that drove all of the lineages apart. You can estimate the rate of that expansion and if you know how old the outbreak is, you can estimate the number of infections.

TS: What kind of estimates do you get using this technique?

RN: It's a little difficult to interpret the numbers from China right now. The dynamics are changing; the cases are plateauing. We expect this to be a result of these draconian containment measures or quarantine measures that they imposed on half a billion people. There are 70,000 reported cases so the number of infections could be 200,000. It could be 500,000. We don't know because people may be sick at home and stay home because the hospitals are overcrowded and that's where you could get infected. I don't think we have a good handle on how many cases there were that simply don't show up in any statistic. I would [estimate] some three-fold underreporting at least.

TS: What can the data tell you about the virus's origins?

RN: The first takeaway is that all these sequences are very, very similar, about eight mutations different than the root. That's eight mutations in a 30,000-base sequence. What this tells us is that the virus came from one source, not too long ago, somewhere between mid-November and early December.

There's not much doubt it will become a pandemic.

TS: Can the mutation data tell you if the virus is becoming more virulent?

RN: We can see where the mutations change codons and where they change amino acids. Most of the mutations are probably completely inconsequential. They just happen; it's at a rate of about one mutation per month. But we are keeping an eye on mutations that might make a difference.

TS: How do the viral lineages help you track transmission of the disease?

RN: The mutations cluster similar transmissions together. So, families that had the virus tend to share a similar viral mutation because they had the same virus. They're a transmission cluster. So you can watch the clusters and see where they go around the world and map that spread. If you then sequence viral genomes in a new region, say, Italy, where the virus has spread, and they all were part of the same cluster, we could be reasonably confident that there was one introduction of the virus in the region. But if the viral genomes are from different clusters, that would mean there are lots of seeding events, which then make small clusters there.

TS: Does NextStrain give you any hints about the severity of outbreaks and whether the outbreaks will become a pandemic?

RN: It doesn't really give you information on severity of outbreaks. It does tell you how different outbreaks group together and how local different outbreaks are. And so if you ask me, there's not much doubt it will become a pandemic.
Editor's note: This interview has been edited for brevity.
Ashley Yeager is an associate editor at The Scientist. Email her at ayeager@the-scientist.com. Follow her on Twitter @AshleyJYeager.

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Coronavirus's Genetics Reveal Its Global Travels

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Several years ago, Richard Neher, an evolutionary biologist at the University of Basel in Switzerland, and his colleagues wanted to monitor changes to the flu's genetic makeup to see if the data would help scientists build more-effective flu vaccines.

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Where did the virus come from and when did it start spreading in humans?

How does genetics help us understand the origins of this virus?

What is a "zoonotic" disease and what are other examples?

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How is the coronavirus likely to play out, how does it end, and does our behaviour make a difference? Here infectious diseases expert Dr Siouxsie Wiles walks us through the epidemic curve, with illustrations by Toby Morris. The Spinoff's ongoing expert-led, evidence-based coverage of Covid-19 is funded by Spinoff Members. To support this work, join Spinoff Members here.
In a post last week, I showed you a picture of how the Covid-19 outbreak has played out in China. It was a graph of the number of cases reported each day, something we call an epidemic curve. It looked a bit like this. We can use the epidemic curve as a visual way to think about how Covid-19 could go, both here in Aotearoa New Zealand and globally.

But before we get to that, let me just explain epidemic curves in a little more detail. First, they have three parts: a start (phase one), a middle (phase two), and an end (phase three). Each of these phases is influenced by different things. Such as, how infectious is the virus or bacterium? How is it transmitted? Is it person-to-person, or from eating or drinking? If it's person-to-person, are people infectious before they have symptoms and don't know they are unwell? And if people do have symptoms, are they mild enough for people to go about their daily routine? Is everyone susceptible to the infection, or just some people? What resources do we need and have to contain the outbreak? The answers to these questions will influence the shape of the epidemic curve.

Phase one of the Covid-19 epidemic curve - containment

At the moment, Aotearoa and many other countries are in phase one for Covid-19. This is the start of the curve where cases pop up sporadically as people who have contracted the virus in one country travel to other countries.

Think of Covid-19 as several fires blazing away, with embers shooting off in all directions. Our goal is to stop those embers from turning into another blazing fire. It's beginning to look like anyone who has travelled overseas recently should think of themselves as a potential ember and be on the lookout for symptoms.

Sticking with the fire analogy, it's not unusual for embers to smoulder a little when they land. That's why public health officials are actively looking for people who have been in close contact with someone with Covid-19. This is called contact tracing. Anyone at high risk of having contracted the virus is then put into isolation. Here in New Zealand, two of the five people who have tested positive for the virus so far are partners or relatives of those "embers".
Covid-19 is now officially a pandemic. Do not panic. But do draft up a pandemic preparedness plan. Here's Siouxsie's step by step guide.
Our aim is to stay in phase one. The longer we can stay in phase one, the better we can prepare for phase two. If we can stay here for the next one to two years, then hopefully a vaccine will become available and we can avoid phases two and three altogether. One way to do that would be just to ban all international travel. No one in or out. Just to be clear, I don't think this is the right approach to take. One to two years is a long time.

Alternatively, we could just make everyone who travels here, Kiwis included, go into isolation for two weeks. Again, I'm not sure how well this would work in practice. My advice to everyone, even if you haven't travelled, is to be on the lookout for any of the symptoms of Covid-19. If you have a fever, or a cough, or shortness of breath, stay away from other people if you can. If you've a runny nose or sore throat this could be a really mild form of Covid-19 so I would also isolate yourself.

Phase two - community transmission

The way Covid-19 is playing out globally, we are going to enter phase two at some point. This will happen when people who don't realise they have contracted Covid-19 go about their daily lives rather than stay isolated. More and more cases will be reported each day as the virus transmits from person to person out in the community and outpaces our ability to keep up with the contact tracing. The quicker and higher the numbers rise, the more likely the outbreak will overwhelm us, making it harder to control.

The data so far suggests all of us are susceptible to the virus. It's clear from what's happened overseas that many people with Covid-19 spent many weeks being treated in hospital before they recovered. This isn't a trivial disease. China built two new hospitals in a matter of weeks to keep up with demand. Do we have the resources to do that if it came to it?

Flattening the curve

Our aim will be to keep phase two of the epidemic curve as flat as possible, keeping the number of cases reported each day as low as we can. If we can achieve that, it'll mean we'll be able to treat everyone who needs treating. We can all help with this by washing our hands regularly, avoiding touching our mouth, nose, and eyes, and staying away from other people when we are sick. This also means calling ahead if you feel sick and want to go to the doctor or hospital. The last thing we need is loads of our healthcare workers in isolation because they've been exposed to Covid-19. Forty-five staff from North Shore Hospital have been isolated as a precaution because of a probable case.

Another thing we are all going to need to start doing soon is minimising or avoiding contact with other people. This is called social distancing. If you are greeting people, don't hug, shake hands, hongi, or kiss. Bump elbows or feet instead. Work from home if you can. Much as it pains me to say it, social distancing also means avoiding public transport (get on your bicycle!). Similarly, it means avoiding gyms, churches, cinemas, concerts, and other events and places where people congregate. At the community level we may need to close schools, universities, museums, and workplaces, limit public transportation, and cancel public events. This is what China did so effectively and what Italy is currently implementing in some regions.
Read more After 'Flatten the Curve', we must now 'Stop the Spread'. Here's what that means
Moving into phase three

We move into phase three when the outbreak is either brought under control or everyone has been infected and there are no more susceptible people left to infect. Vaccination is one way we can stop people being susceptible, or at least enough people that the disease stops spreading from person-to-person - that's what herd immunity is all about.

Given we are one to two years away from a vaccine, bringing Covid-19 under control is obviously the goal here and what China has achieved. But if there are still susceptible people in a population and we stop taking all the right measures then we will see cases flare up again.

That's why what happens on the global scale is so important. Any "fires" left blazing threaten us all. At the moment, many of the new cases being reported in China are people who have contracted the virus while travelling outside of China. They are essentially back in phase one but with all the understanding of why it's so important to stay there. And all the expertise and public knowledge to make it happen.

While the coronavirus responsible for Covid-19 likely started out in bats, so far, it's not clear how it got from bats to people. SARS jumped from bats to humans via civet cats. With SARS once we managed to stop all human-to-human transmission, the disease then ran its course in those infected, and we haven't seen SARS since.

Hopefully, if we can stop all human-to-human transmission of Covid-19 that'll be the end of this coronavirus too. But it's clear that we'll all have to play our part to make that a reality.
Read all Dr Siouxsie Wiles' explainers on the Covid-19 outbreak here. Subscribe to Rec Room a weekly newsletter delivering The Spinoff's latest videos, podcasts and other recommendations straight to your inbox.

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The three phases of Covid-19 - and how we can make it manageable

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How is the coronavirus likely to play out, how does it end, and does our behaviour make a difference? Here infectious diseases expert Dr Siouxsie Wiles walks us through the epidemic curve, with illustrations by Toby Morris. The Spinoff's ongoing expert-led, evidence-based coverage of Covid-19

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How has coronavirus intersected with racism?

What can we do to stand up for victims of racist behavior?

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Coronavirus: From Bats to Humans to Epidemic

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Coronavirus: From Bats to Humans to Epidemic

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Click on "Start Pathway" to learn about the coronavirus

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A free online platform for science education from Harvard University

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World Health Organization (WHO) situation report

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World Health Organization (WHO) situation report

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Mercury News story about first death in Santa Clara county

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Mercury News story about first death in Santa Clara county

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Intro to exponential functions | Algebra (video) | Khan Academy

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In exponential functions the variable is in the exponent, like y=3ˣ. Here we introduce this concept with a few examples.

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This Quick Learn lesson will take approximately 10 minutes to complete.

When you are finished, you will be able to create an epidemic curve, or "epi curve."

You can move through this lesson by using the NEXT and BACK icons below.

What is an Epi Curve?

An epi curve is a visual display of the onset of illness among cases associated with an outbreak.

You can learn a lot about an outbreak from an epi curve, such as

The outbreak's time trend, that is, the distribution of cases over time

Outliers, that is, cases that stand apart from the overall pattern

General sense of the outbreak's magnitude

Inferences about the outbreak's pattern of spread

The most likely time period of exposure

X and Y Axes

An epi curve is represented by a graph with two axes that intersect at right angles.

The horizontal x-axis is the date or time of illness onset among cases.

The vertical y-axis is the number of cases.

Each axis is divided into equally spaced intervals, although the intervals for the two axes may differ.

Cases

Cases (represented by boxes) are placed along the x-axis according to the date when their earliest symptoms began.

If symptoms for more than one case began on the same date (or time), the boxes are stacked one above the other.

Time Intervals

The unit of time for the x-axis is based on the incubation period of the disease under investigation and the length of time over which cases are distributed.

As a general rule, the unit of time is set at roughly 1/4 (0.25) of the average incubation period for the illness under investigation.
Average incubation period
multiplied by .25 = Intervals
Time Intervals, continued

If the incubation period of an illness is short, the interval on the epi curve might be indicated in hours or even minutes.

View the example below

The incubation period for infection with E. coli O1257:H7 is usually 3-4 days. In this case, you would probably use an interval of one day on the x-axis.

4 days multiplied by 0.25 = 1 day
intervals (4 x 0.25 = 1)

Determining a Title

An epi curve should have a title that describes it, including the type of illness, the place where the outbreak occurred, and the time period.

Cases of [insert illness name] by date of onset, [insert location and time period]

View the example below.
Cases of E. coli O157:H7 by Date of Onset, Epps, Louisiana, February, 2012
Your Turn: Exercise 1

Seven cases of hepatitis A have been reported in Homer, Virginia. Construct the epi curve from the line list below.

Select the column heading that you would use to label the x-axis of the epi curve.

Your Turn: Exercise 2

Given that the average incubation period for hepatitis A is 28-30 days, what intervals would you use on the x-axis?

1-day intervals

7-day intervals

28-day intervals
Exercise 2: Incorrect Exercise 2: Correct Exercise 2: Incorrect
Your Turn: Exercise 3

What is the appropriate title for the epi curve?

Hepatitis A outbreak in Virginia

Outbreak in Homer, Virginia

Hepatitis A Cases by Date of Onset in Homer, Virginia, December 2011-January 2012
Exercise 3: Incorrect Exercise 3: Incorrect Exercise 3: Correct
Hepatitis A Cases by Date of Onset in Homer, Virginia, December 2011 - January 2012

Your Turn: Exercise 4

Using the following information from a line listing, which date from the Options below represents the Date of Onset for Case 1?
Options
Your Turn: Exercise 5

Using the following information from a line listing, which date from the Options below represents the Date of Onset for Case 5?
Options
Summary

Congratulations!

You have created a basic epi curve. The completed epi curve is below.
Hepatitis A Cases by Date of Onset in Homer, Virginia,
December 2011-January 2012
To view other Quick Learns, visit CDC Learning Connection.

Resources on Basic Epidemiology

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This Quick Learn lesson will take approximately 10 minutes to complete. When you are finished, you will be able to create an epidemic curve, or "epi curve." You can move through this lesson by using the NEXT and BACK icons below. An epi curve is a visual display of the onset of illness among cases associated with an outbreak.

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What groups of people are at higher risk of death from an infection?

Do people who are at low risk of death still catch and spread the virus?

How does the risk of death compare to other illnesses, like the seasonal flu or the Spanish flu?

Why are death rates for this illness difficult to estimate?

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What are the symptoms of a coronavirus infection? How do they differ from flu symptoms?

What should people do if they have symptoms that match those of coronavirus?

What is an "incubation period" and what is the incubation period for coronavirus?

What is a "secondary infection" and is this a concern with coronavirus?

What steps do doctors take to help people with severe cases of coronavirus? What factors might become limiting if a large number of cases happens in a short time?

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Incubation period definition is - the period between the infection of an individual by a pathogen and the manifestation of the illness or disease it causes. How to use incubation period in a sentence.

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Amidst the spread of the current coronavirus epidemic, it can be hard to find science-based advice, as so much of the information out there is either just cautionary, or downright wrong. Thankfully, we're getting more data on a daily basis.

Now, the latest research out of Johns Hopkins University has shown that COVID-19 has an average incubation period of 5.1 days, meaning that the 14-day quarantine period recommended by the CDC is bang on the money.

Health officials have to make important decisions based on limited information, and it's always good to have that decision backed up with science.

The Johns Hopkins team looked at 181 cases of COVID-19 outside of Hubei province in China before February 24 this year.

Recording the time of possible exposure, symptom onset, fever onset, and detection by authorities for each case, the team created a model of the incubation period distribution.

Put simply, the incubation period is the time between when you are exposed to the disease and when you start showing symptoms. This is usually before the contagious period, when you are likely to give the disease to others.

We don't yet know how contagious the coronavirus is when people aren't showing symptoms, however, there have been a few reports of people transmitting the virus without showing symptoms at all.

That being said, as with other coronaviruses (such as the common cold), you are much more likely to transmit the virus to someone else while you are coughing or sneezing.

The Johns Hopkins team found that less than 2.5 percent of those infected would show symptoms within 2.2 days; the estimated median incubation period was 5.1 days; and 97.5 percent will show symptoms within 11.5 days.

"Based on our analysis of publicly available data, the current recommendation of 14 days for active monitoring or quarantine is reasonable," says epidemiologist Justin Lessler from Johns Hopkins Bloomberg School of Public Health.

"Although with that period some cases would be missed over the long-term."

This sort of research is incredibly helpful for infectious disease specialists who are making policy decisions for coronavirus.

There has been worries that the incubation period isn't long enough, after other teams of researchers discovered incubation periods that lasted up to 19 and 24 days.

Extrapolating from the 181 cases, the Johns Hopkins team estimated that for every 10,000 people quarantined for 14 days, around 101 would develop symptoms after release.

More research - with larger groups of people - will have to be done to confirm whether the longer incubation periods might cause an issue for our current quarantine policies.

And for the rest of us, until a vaccine is developed created, the best way to deal with the virus is to keep calm, wash your hands (for 20 seconds!) and if you do feel sick - stay at home.

The research has been published in Annals of Internal Medicine.

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Latest Research Says The Average Incubation Time For The New Coronavirus Is 5.1 Days

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Amidst the spread of the current coronavirus epidemic, it can be hard to find science-based advice, as so much of the information out there is either just cautionary, or downright wrong. Thankfully, we're getting more data on a daily basis.

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Scroll to the heading that says "clinical course" for some descriptions of treatments for severe cases of COVID-19. You will probably have to look up some words.

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Centers for Disease Control and Prevention

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This interim guidance is for clinicians caring for patients with confirmed infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease (COVID-19).

This update includes additional information from recent reports including:

Characteristics of patients with confirmed COVID-19 based on recent epidemiologic data from China, including characteristics of patients with COVID-19 admitted to the intensive care unit and data on pediatric cases

Data regarding SARS-CoV-2 viral shedding among asymptomatic persons, and data from a recent report of viable SARS-CoV-2 isolation from stool

Accessibility of investigational drug therapies for COVID-19 treatment through clinical trial enrollment in the United States

Recently published pediatric surviving sepsis guidance

CDC will update this interim guidance as more information becomes available.

Clinical Presentation

Among reports that describe the clinical presentation of patients with confirmed COVID-19, most are limited to hospitalized patients with pneumonia. The incubation period is estimated at 4 days (interquartile range: 2 to 7 days). [ 1] Some studies have estimated a wider range for the incubation period; data for human infection with other coronaviruses (e.g. MERS-CoV, SARS-CoV) suggest that the incubation period may range from 2-14 days. Frequently reported signs and symptoms of patients admitted to the hospital include fever (77-98%), cough (46%-82%), myalgia or fatigue (11-52%), and shortness of breath (3-31%) at illness onset. [ 2- 5] Among 1,099 hospitalized COVID-19 patients, fever was present in 44% at hospital admission, and developed in 89% during hospitalization. [ 6] Other less commonly reported respiratory symptoms include sore throat, headache, cough with sputum production and/or hemoptysis. Some patients have experienced gastrointestinal symptoms such as diarrhea and nausea prior to developing fever and lower respiratory tract signs and symptoms. The fever course among patients with COVID-19 is not fully understood; it may be prolonged and intermittent. A limited number of reports describe identification of asymptomatic or subclinical infection on the basis of detection of SARS-CoV-2 RNA or live virus from throat swab specimens of contacts of confirmed patients. [ 7- 8]

Risk factors for severe illness are not yet clear, although older patients and those with chronic medical conditions may be at higher risk for severe illness. Among more than 44,000 confirmed cases of COVID-19 in China as of Feb 11, 2020, most occurred among patients aged 30-69 years (77.8%), and approximately 19% were severely or critically ill [ 9]. Case-fatality proportion among cases aged ≥60 years was: 60-69 years: 3.6%; 70-79 years: 8%; ≥80 years: 14.8%. Patients who reported no underlying medical conditions had an overall case fatality of 0.9%, but case fatality was higher for patients with comorbidities: 10.5% for those with cardiovascular disease, 7% for diabetes, and 6% each for chronic respiratory disease, hypertension, and cancer. Case fatality for patients who developed respiratory failure, septic shock, or multiple organ dysfunction was 49%. [ 9]

Limited information is available about the clinical presentation, clinical course, and risk factors for severe COVID-19 in children. Of confirmed COVID-19 patients in China as of Feb 11, 2020, only 2.1% were aged <20 years, and no deaths were reported among those <10 years of age [ 9]. From limited published reports, signs and symptoms among children with COVID-19 may be more mild than adults, with most pediatric patients presenting with fever, cough, congestion, and rhinorrhea [ 10, 12- 13], and one report of primarily gastrointestinal symptoms (vomiting and diarrhea) [ 13]. Prolonged detection of SARS-CoV RNA has been reported in respiratory specimens (up to 22 days after illness onset) and stool specimens (at least 30 days after illness onset) [ 10- 11]. Severe complications of acute respiratory distress syndrome and septic shock were reported in a 13-month old with COVID-19 in China [ 13].

Clinical Course

Clinical presentation among reported cases of COVID-19 varies in severity from asymptomatic infection to mild illness to severe or fatal illness. Some reports suggest the potential for clinical deterioration during the second week of illness.[ 2, 5] In one report, among patients with confirmed COVID-19 and pneumonia, just over half of patients developed dyspnea a median of 8 days after illness onset (range: 5-13 days). [ 2] In another report, the mean time from illness onset to hospital admission with pneumonia was 9 days.[ 1] Acute respiratory distress syndrome (ARDS) developed in 17-29% of hospitalized patients, and secondary infection developed in 10%. [ 2, 4] In one report, the median time from symptom onset to ARDS was 8 days.[ 3]

Approximately 20-30% of hospitalized patients with COVID-19 and pneumonia have required intensive care for respiratory support.[ 2- 3] Compared to patients not admitted to an intensive care unit, critically ill patients were older (median age 66 years versus 51 years), and were more likely to have underlying co-morbid conditions (72% versus 37%). [ 3] Among critically ill patients admitted to an intensive care unit, 11-64% received high-flow oxygen therapy and 47-71% received mechanical ventilation; some hospitalized patients have required advanced organ support with endotracheal intubation and mechanical ventilation (4-42%).[ 3- 4, 9] A small proportion have also been supported with extracorporeal membrane oxygenation (ECMO, 3-12%).[ 3- 4, 9] Other reported complications include cardiac injury, arrhythmia, septic shock, liver dysfunction, acute kidney injury, and multi-organ failure. Post-mortem biopsies in one patient who died of ARDS reported pulmonary findings of diffuse alveolar damage. [ 14]

An overall case fatality proportion of 2.3% has been reported among confirmed cases of COVID-19 in China. [ 9] However, the majority of these cases were among hospitalized patients and therefore this estimate of mortality is likely biased upward. Among hospitalized patients with pneumonia, the case fatality proportion has been reported as 4-15%.[ 2- 4] Among critically ill COVID-19 patients in China, the reported case fatality proportion was 49%. In a report from one hospital, 61.5% of critically ill patients with COVID-19 had died by day 28 of ICU admission. [ 9, 15]

Diagnostic Testing

Information on specimen collection, handling, and storage is available at: Real-Time RT-PCR Panel for Detection 2019-Novel Coronavirus. After initial confirmation of COVID-10, additional testing of clinical specimens can help inform clinical management, including discharge planning.

Laboratory and Radiographic Findings

The most common laboratory abnormalities reported among hospitalized patients with pneumonia on admission included leukopenia (9-25%), leukocytosis (24-30%), lymphopenia (63%), and elevated alanine aminotransferase and aspartate aminotransferase levels (37%). [ 2, 4] Among 1,099 COVID-19 patients, lymphocytopenia was present in 83%; 36% had thrombocytopenia, and 34% had leukopenia. [ 6] Most patients had normal serum levels of procalcitonin on admission. Chest CT images have shown bilateral involvement in most patients. Multiple areas of consolidation and ground glass opacities are typical findings reported to date. [ 2- 4, 16- 24] However, one study that evaluated the time from symptom onset to initial CT scan found that 56% of patients who presented within 2 days had a normal CT. [ 20]

Limited data are available about the detection of SARS-CoV-2 RNA and infectious virus in clinical specimens. SARS-CoV-2 RNA has been detected from upper and lower respiratory tract specimens, and the virus has been isolated in cell culture from upper respiratory tract specimens and bronchoalveolar lavage fluid. In one case series SARS-CoV-2 viral RNA levels in the first 3 days after symptom onset were higher in specimens collected from the nose than from the throat (as demonstrated by lower cycle threshold values in the nose). [ 25] A similar time course and pattern of viral RNA detection was reported in one asymptomatic patient after exposure to a patient with confirmed COVID-19. [ 25]

SARS-CoV-2 RNA has been detected in blood and stool specimens and SARS-CoV-2 virus has been isolated in cell culture from the stool of a patient with pneumonia 15 days after symptom onset. [ 26- 29]. The duration of SARS-CoV-2 RNA detection in the upper and lower respiratory tracts and in extrapulmonary specimens is not yet known. It is possible that RNA could be detected for weeks, which has occurred in some cases of MERS-CoV or SARS-CoV infection. [ 30- 37] Viable SARS-CoV has been isolated from respiratory, blood, urine, and stool specimens. In contrast, viable MERS-CoV has been isolated only from respiratory tract specimens. [ 37- 39]

Clinical Management and Treatment

For information regarding infection prevention and control recommendations, please see Interim Infection Prevention and Control Recommendations for Patients with Confirmed Coronavirus Disease 2019 (COVID-19) or Persons Under Investigation for COVID-19 in Healthcare Settings.

Patients with a mild clinical presentation may not initially require hospitalization. However, clinical signs and symptoms may worsen with progression to lower respiratory tract disease in the second week of illness; all patients should be monitored closely. Possible risk factors for progressing to severe illness may include, but are not limited to, older age, and underlying chronic medical conditions such as lung disease, cancer, heart failure, cerebrovascular disease, renal disease, liver disease, diabetes, immunocompromising conditions, and pregnancy.

The decision to monitor a patient in the inpatient or outpatient setting should be made on a case-by-case basis. This decision will depend not only on the clinical presentation, but also on the patient's ability to engage in monitoring, home isolation, and the risk of transmission in the patient's home environment. For more information, see Evaluating and Reporting Persons Under Investigation (PUI)

No specific treatment for COVID-19 is currently available. Clinical management includes prompt implementation of recommended infection prevention and control measures and supportive management of complications, including advanced organ support if indicated.

Corticosteroids should be avoided, because of the potential for prolonging viral replication as observed in MERS-CoV patients, unless indicated for other reasons. [ 31, 40- 42] For example, for a chronic obstructive pulmonary disease exacerbation or for septic shock per Surviving Sepsis guidelines for adultsexternal icon and childrenexternal icon .

For more information, see: WHO interim guidance on clinical management of severe acute respiratory infection when novel coronavirus (nCoV) infection is suspectedpdf icon external icon , Diagnosis and Treatment of Adults with Community-acquired Pneumonia. An Official Clinical Practice Guideline of the American Thoracic Society and Infectious Diseases Society of Americaexternal icon , and Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Childrenexternal icon

Investigational Therapeutics

There are currently no antiviral drugs licensed by the U.S. Food and Drug Administration (FDA) to treat patients with COVID-19. In the United States, the National Institutes of Health (NIH) and collaborators are working on development of candidate vaccines and therapeutics for COVID-19. Some in-vitro or in-vivo studies suggest potential therapeutic activity of compounds against related coronaviruses, but there are no available data from randomized controlled trials in humans to support recommending any investigational therapeutics for patients with confirmed or suspected COVID-19 at this time.

Remdesivir is an investigational antiviral drug that was reported to have in-vitro activity against SARS-CoV-2. [ 43] Some patients with COVID-19 have received intravenous remdesivir for compassionate use outside of a clinical trial setting. In China, multiple clinical trials of investigational therapeutics have been implemented, including two clinical trials of remdesivir. An NIH adaptive randomized controlled clinical trial external icon of investigational therapeutics for hospitalized COVID-19 patients in the United States was approved by the Food and Drug Administration; the first investigational therapeutic to be studied is remdesivir. Other remdesivir trials for COVID-19 patients in the U.S. are available (participants with severeexternal icon and moderateexternal icon coronavirus disease). Some COVID-19 patients have received uncontrolled treatment with other investigational antivirals. [ 4, 28, 44] For information on specific clinical trials underway for treatment of patients with COVID-19, see clinicaltrials.govexternal icon , and www.chictr.org.cnexternal icon

In the absence of an approved vaccine, community mitigation measures are the primary way to reduce SARS-CoV-2 transmission among persons in the community, and adherence to recommended infection prevention and control measures can reduce the risk of SARS-CoV-2 spread in healthcare facilities. In the absence of an approved therapeutic with demonstrated safety and efficacy in patients with COVID-19, clinical management of COVID-19 patients includes avoidance of corticosteroids, and supportive care of complications, including advanced organ support.

Discontinuation of Transmission-Based Precautions or Home Isolation

For recommendations on discontinuation of transmission-based precautions or home isolation for patients who have recovered from COVID-19 illness, please see: Interim Guidance for Discontinuation of Transmission-Based Precautions and Disposition of Hospitalized Patients with COVID-19 and Interim Guidance for Discontinuation of In-Home Isolation for Patients with COVID-19

Additional resources:

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This interim guidance is for clinicians caring for patients with confirmed infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease (COVID-19).

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REQUIRED ACTIONS - CORONAVIRUS DISEASE 2019 (COVID-19)

The San José Unified School District, the Santa Clara County Office of Education, and the County of Santa Clara Public Health Department continue to work together in response to the Coronavirus Disease 2019 (COVID-19).
This is a critical moment in the growing outbreak of COVID-19 in Santa Clara County. The County of Santa Clara Public Health Department has issued updated recommendations that are meant to slow the spread of COVID-19 in our community, reduce the number of people infected, and protect those who are most vulnerable to severe illness.
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Health Information: Flu and Coronavirus Update

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REQUIRED ACTIONS - CORONAVIRUS DISEASE 2019 (COVID-19) The San José Unified School District, the Santa Clara County Office of Education, and the County of Santa Clara Public Health Department continue to work together in response to the Coronavirus Disease 2019 (COVID-19). This is a critical moment in the growing outbreak of COVID-19 in Santa Clara County.

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Editor's note, April 23: Since this piece was originally published in March, the "lab leak" theory has continued to spread in some circles. For Vox's latest reporting on why the scientific consensus rejects this theory, read this piece. For our most up-to-date coverage, visit our coronavirus hub.

There are more and more signs that the coronavirus outbreak in the United States is spiraling into a large-scale crisis. The decisions federal and local public health officials and individuals make right now - to test more people with symptoms, inform the public about the risk, isolate the sick, and institute social distancing measures like canceling events - are crucial. So will the speed at which they execute them.

Meanwhile, in some right-wing news outlets and on social media, a dangerous conspiracy theory about the origin of the health crisis won't die.

There are two main versions of the rumor, and they have one common thread: that the coronavirus, SARS-CoV-2, originated in a level 4 (the highest biosafety level) research laboratory in Wuhan.

In one version of the rumor, the virus was engineered in the lab by humans as a bioweapon. In another version, the virus was being studied in the lab (after being isolated from animals) and then "escaped" or "leaked" because of poor safety protocol.

The Wuhan Institute of Virology is a real place, and the exact origin of the novel coronavirus is still a mystery, with researchers racing since the outbreak began to figure it out. But already, virologists who've parsed the genome and infectious disease experts who study coronaviruses say they have enough evidence the virus is brand new and came from nature. A large group of them, citing genome analyses from multiple countries, recently affirmed in that the virus originated in wildlife.

The emergence of the virus in the same city as China's only level 4 biosafety lab, it turns out, appears to be pure coincidence.

Conspiratorial claims about the Wuhan lab are circulating on cable news and social media

Before we get to debunking, let's note who is spreading rumors about the origins of the virus.

First, several prominent US conservative pundits and politicians - known to regularly spew nonsense (and bash China) - have been politicizing the bioweapon rumorfor weeks.

"It probably is a ChiCom laboratory experiment that is in the process of being weaponized," right-wing radio host and Presidential Medal of Freedom recipient Rush Limbaugh said of the virus on February 24. "All superpower nations weaponize bioweapons."

Sen. Tom Cotton (R-AR) has repeatedly suggested before Congress and on Fox News that the virus could have come from the lab.

The Arkansas senator furthered "infodemic" by pushing debunked claim that the novel coronavirus may have been created in a Wuhan laboratory. https://t.co/oJvVzjOyxw
- Atlantic Council (@AtlanticCouncil) March 1, 2020

Former White House strategist Steve Bannon went on Fox News to defend Cotton and imply that the Chinese Communist Party was still hiding something about the origin of Covid-19. "The mainstream media and far left [are] saying, 'Oh, he's a conspiracy theorist,"' Bannon said. "All he's saying: It's incumbent upon the Chinese Communist Party and President Xi [Jinping] to come out and give all information ... this is all Cotton's saying."

In the New York Post, Steven Mosher, a regular critic of China's population control measures, has stoked the leakage rumor, using an array of circumstantial clues that Chinese labs' handling of deadly pathogens can't be trusted.

Similar rumors have also been running rampant in online forums in China. The South China Morning Post on February 20 debunked yet another rumor of the virus escaping from the lab in China:

More rumours swirled online over the weekend, this time that [Wuhan Institute of Virology] researcher Chen Quanjiao had reported the head of the institute, Wang Yanyi, claiming she had "sold experimental animals" to the live animal and seafood market and "leaked the virus" from the lab.

But Chen denied the claim, saying she was angry that her name had been used to fabricate information. "The recent rumours about the institute have affected the researchers as they try to tackle key problems," Chen said in a statement.

The scientific evidence disproving these rumors matters because the conspiracy theory could persist and undermine trust in public health authorities at this critical moment. As the Washington Post reported, the rumor that the virus came from a Chinese lab is one reason residents of one Alabama county are currently unnerved and distrustful of the response to Covid-19 in their state.

"Conspiracy theories about manmade viruses are not new. We saw this with HIV - the rumor that the US made it and introduced it into Africa. But they are really dangerous kinds of things to get spread around," Gerald Keusch, a professor of medicine and international health and associate director of Boston University's National Emerging Infectious Diseases Laboratories, told Vox.

So let's walk through what we know about the virus, and why it's time to put the lab rumor to rest.

The virus originated in bats and then jumped to humans, perhaps through other animals

Soon after the Chinese government acknowledged there was an outbreak of a mysterious new virus in late December in Wuhan, scientists raced to sequence its genome. By mid-January, they had it and shared it with the World Health Organization.

Soon after that, scientists saw that the virus closely resembled viruses that circulate in bats. "If you look at the genetic sequence of the virus, it's closely related to a bat virus, about 96 percent the same," Jim LeDuc, head of the Galveston National Laboratory, a level 4 biosafety lab in Texas, told Vox. "There's been talk about a pangolin intermediate host; that's probably not true."

Chinese officials also reported that several of the first cluster of cases had ties to a live animal market where both seafood and other wildlife were sold as food. (The market has since been closed.) The market soon became the leading hypothesis for how the virus made the leap into humans, where it's been able to spread efficiently ever since.

The genetic evidence and epidemiological information, according to three esteemed infectious disease researchers writing in the New England Journal of Medicine, "implicates a bat-origin virus infecting unidentified animal species sold in China's live-animal markets."

According to a genome analysis by Tanja Stadler from the Department of Biosystems Science and Engineering at ETH Zurich in Basel, the virus first began transmitting in humans in China as early as the first half of November 2019.

"The widespread hypothesis that the first person was infected at an animal market in November is still plausible," Stadler said in a statement. "Our data effectively rule out the scenario that the virus circulated in humans for a long time before that."

LeDuc agrees with the hypothesis that the animal market played a role in the virus jumping to humans. "The linkage back to the market is pretty realistic, and consistent with what we saw with SARS," said LeDuc. "It's a perfectly plausible and logical explanation: The virus exists in nature and, jumping hosts, finds that it likes humans just fine, thank you."

Unfortunately, there's a long history of these "spillover" events, where an emerging disease jumps from wildlife to humans, turning into a pandemic. And scientists say we should expect them with more travel, trade, connectivity, urbanization, climate change, and ecological destruction, if we don't stop the drivers.

What researchers have to figure out now is how exactly the coronavirus jumped to humans: perhaps through a human eating an infected animal, or through humans being exposed to infected feces or urine. "All we know [is] its likely distant source was bats, but we don't know who was between bats and people," said Vincent Racaniello, a professor of microbiology and immunology at Columbia and host of the This Week in Virology podcast. "It could be a direct infection [between bats and humans] as well."

A scientific paper in a major journal shows this is a genuinely new virus, and there's no way it could have been engineered by humans

In a recent podcast episode, Racaniello discussed with two other researchers a fascinating paper about the virus origin. The key finding: that SARS-CoV-2 is "not a laboratory construct nor a purposefully manipulated virus."

The paper, published in Nature Medicine on March 17, is written by several leading microbiologists who closely examined the SARS-CoV-2 genome.

Specifically, they found theunusual biochemical features of the virus could only have come about two ways after the virus jumped from animal to humans, or what's called zoonotic transfer. The ways, they write, are: "1) natural selection in a non-human animal host prior to zoonotic transfer, and 2) natural selection in humans following zoonotic transfer."

In other words, nature came up with these weird characteristics in the genome, either in an intermediary animal between bats and people or in humans after the virus infected one. As Racaniello put it on his podcast: "Humans could never have dreamed this up."

What's more, he noted, no known lab anywhere in the world was working on a coronavirus like this one, and its closest relative is a bat virus found in a cave in 2013 in Yunnan, China, 1,000 miles from Wuhan."Presumably there's a common ancestor, most likely from a bat or an intermediary animal that was contaminated by that bat," Racaniello says.

The coronavirus would be a bad bioweapon

Several experts told me the theory that the virus was meant to be a bioweapon doesn't make sense, either. One big reason: Covid-19 isn't all that deadly or transmissible, compared to other potential pathogens out there.

"To make it as a bioweapon, if that's what you wanted to do, there are scarier and more virulent pathogens to work with," said Keusch of Boston University.

For instance, Ebola and the West African Lassa virus are deadly threats that can only be studied in biosafety level 4 labs, like Wuhan. Crimean-Congo hemorrhagic fever is a tick-borne disease that has a death rate of 30 to 50 percent. The global death rate for Covid-19, meanwhile, is around 3 percent at the moment, but it's expected to come down dramatically as more cases are discovered in the coming weeks. And even now, it varies widely by country and region.

Simply put, if you wanted to release a bioweapon to kill a lot of people, there are much deadlier pathogens you could use.

The Wuhan lab has the same safety protocols as top biosafety labs in the US and Europe

In his article in the New York Post, Mosher suggests that we shouldn't trust the officials who ran the Wuhan lab. "It sure sounds like China has a problem keeping dangerous pathogens in test tubes where they belong, doesn't it?" he says.

I asked LeDuc, who runs the Galveston biocontainment lab, if he has any experience with the Wuhan lab. Turns out he has a lot. He and his colleagues have worked for six years with the Chinese team there, both in advising them on building their lab and keeping it safe, and on scientific collaboration. "I can tell you that lab in Wuhan is equivalent to any lab here in the US and Europe," he said.

For instance, many labs now use radio waves to track and inventory vials containing dangerous pathogens.

Keusch agrees. "I don't think there's any likelihood that the lab is less prepared in terms of protocol and capability than any lab in the US. It's really good, though nothing is perfect," he said.

The rumors have also reportedly hurt the lab's ability to do its work.

"The rumours ... have caused severe damage to our researchers who have been dedicated to working on the front line, and seriously interrupted the emergency research we are doing during the epidemic," the lab said in a statement, according to the South China Morning Post.

Why we need to figure out all the details of where the virus came from

According to Bruce Aylward, an epidemiologist who led the World Health Organization's recent mission to China to assess its Covid-19 response, the investigation into where and how the virus jumped to people is ongoing. The focus remains on the (now closed) Huanan Wholesale Seafood Market, the wildlife market inside it, and other area markets.

"Ever since SARS, the market authorities now have to record which animals are sold by whom and where they come from in these markets. So now there's a list of 10 vendors from seven provinces," he told my colleague Julia Belluz in a recent interview. "Then China's CDC can do a case control study based on where in the market these animals were."

The focus in the past month has been on saving lives, he said, but as new cases and deaths decline, the investigators will eventually be able to turn back to getting animal info from the market vendors and testing the animals.

Racaniello says it's critical that the source is identified to eliminate the chance that the virus is introduced into people again.

For LeDuc, China's experience with the coronavirus should be a clear message of the great public health threat live animal markets post.

"The reason we're seeing [coronaviruses like SARS and SARS-CoV-2 emerge] in China is they have these live animal markets, where they bring in animals alive and co-house them, one cage on top of another, where there's an opportunity for transmission between atypical hosts," says LeDuc.

We'll need to be patient for Chinese investigators to get to the bottom of how the virus made the jump from animals to humans. In the meantime, remember that in a public health crisis, conspiracy theories are a distraction. Rather, it's our collective responsibility to stay focused on keeping each other safe.

Correction: An earlier version of this story misidentified Tom Cotton's position in Congress. He is a US senator.
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The conspiracy theories about the origins of the coronavirus, debunked

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Editor's note, April 23: Since this piece was originally published in March, the "lab leak" theory has continued to spread in some circles. For Vox's latest reporting on why the scientific consensus rejects this theory, read this piece. For our most up-to-date coverage, visit our coronavirus hub.

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Animation showing the spread of coronavirus

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Animation showing the spread of coronavirus

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Coronavirus genetics reveal global travels

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Coronavirus genetics reveal global travels

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Several years ago, Richard Neher, an evolutionary biologist at the University of Basel in Switzerland, and his colleagues wanted to monitor changes to the flu's genetic makeup to see if the data would help scientists build more-effective flu vaccines. They developed an online interface that integrated the latest viral sequencing data, analyzed it, and published the results in a publicly available interactive web browser.

"Then we thought, why just flu, why not other viruses?" Neher says. The team built a similar platform to chart the transmission of MERS and Ebola and called the site NextStrain.org. Now, they've adapted it to keep track of the genetic tweaks to SARS-CoV-2 as it spreads around the globe and chart the viral lineages on world maps to watch, in nearly real time, as the virus moves from major hotspots in China to smaller pockets in other countries.

Here, Neher talks with The Scientist about what NextStrain.org has uncovered about the transmission of SARS-CoV-2.

The Scientist: How do viral genomes' sequences from swabs taken from infected patients help you build a family tree of the virus?

Richard Neher: These coronavirsuses tend to change their genome, they mutate, at a fairly high rate. These mutations allow us to group viruses into more closely related viruses and less closely related viruses. All the sequences on the site are super similar because they were closely related. As time goes on, the lineages pick up independent mutations, and then they cause outbreaks in different parts of the world. You can group these sequences together by genetic makeup and reconstruct the transmission tree of the virus.

There are 70,000 reported cases so the number of infections could be 200,000. It could be 500,000.

TS: Can you estimate the number of infections from the tree?

RN: Yes, if you look at the viral tree you see different sequences. And the tree will have different shapes depending on if the outbreak it's staying the same size or growing. If it's growing, you see many, many lineages coming together very deep in the tree, and that's what we have here. That implies there was rapid expansion at the base of the tree that drove all of the lineages apart. You can estimate the rate of that expansion and if you know how old the outbreak is, you can estimate the number of infections.

TS: What kind of estimates do you get using this technique?

RN: It's a little difficult to interpret the numbers from China right now. The dynamics are changing; the cases are plateauing. We expect this to be a result of these draconian containment measures or quarantine measures that they imposed on half a billion people. There are 70,000 reported cases so the number of infections could be 200,000. It could be 500,000. We don't know because people may be sick at home and stay home because the hospitals are overcrowded and that's where you could get infected. I don't think we have a good handle on how many cases there were that simply don't show up in any statistic. I would [estimate] some three-fold underreporting at least.

TS: What can the data tell you about the virus's origins?

RN: The first takeaway is that all these sequences are very, very similar, about eight mutations different than the root. That's eight mutations in a 30,000-base sequence. What this tells us is that the virus came from one source, not too long ago, somewhere between mid-November and early December.

There's not much doubt it will become a pandemic.

TS: Can the mutation data tell you if the virus is becoming more virulent?

RN: We can see where the mutations change codons and where they change amino acids. Most of the mutations are probably completely inconsequential. They just happen; it's at a rate of about one mutation per month. But we are keeping an eye on mutations that might make a difference.

TS: How do the viral lineages help you track transmission of the disease?

RN: The mutations cluster similar transmissions together. So, families that had the virus tend to share a similar viral mutation because they had the same virus. They're a transmission cluster. So you can watch the clusters and see where they go around the world and map that spread. If you then sequence viral genomes in a new region, say, Italy, where the virus has spread, and they all were part of the same cluster, we could be reasonably confident that there was one introduction of the virus in the region. But if the viral genomes are from different clusters, that would mean there are lots of seeding events, which then make small clusters there.

TS: Does NextStrain give you any hints about the severity of outbreaks and whether the outbreaks will become a pandemic?

RN: It doesn't really give you information on severity of outbreaks. It does tell you how different outbreaks group together and how local different outbreaks are. And so if you ask me, there's not much doubt it will become a pandemic.
Editor's note: This interview has been edited for brevity.
Ashley Yeager is an associate editor at The Scientist. Email her at ayeager@the-scientist.com. Follow her on Twitter @AshleyJYeager.

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Coronavirus's Genetics Reveal Its Global Travels

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Several years ago, Richard Neher, an evolutionary biologist at the University of Basel in Switzerland, and his colleagues wanted to monitor changes to the flu's genetic makeup to see if the data would help scientists build more-effective flu vaccines.

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Filthy and frightened, the three young children staggered up the beach. Their tiny frames were feverish and behind them, on board the small sailboat they had drifted ashore upon, lay the bodies of two dead men.

The group had been attempting to flee an outbreak of disease that had devastated their small, isolated village further upstream from the spot where they run aground on the Naknek River in Bristol Bay, Alaska. The three young survivors were quickly taken to a hospital run by a salmon canning company.

Their unexpected arrival at the Alaska Packer Association's "Diamond O" cannery on the Naknek announced that "Spanish flu" had taken hold in this remote, largely ice-bound part of the world. The inhospitable winter weather conditions had prevented travel to the area between the months of September and May, meaning it had escaped the waves of influenza that swept the world during 1918.

By the time the pandemic had run its course, it claimed somewhere between 50 and 100 million lives - more than the total number of deaths from the terrors of World War One.

The arrival of the boat at the cannery on 4 June 1919 indicated the disease had finally found its way to the remote native Inuit communities that dotted the Alaskan coastline. The next day, the superintendent of the cannery dispatched a team to the children's village to see if they could help.
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What they discovered was horrifying.

Reports from the men on the expedition described the village of Savonoski as being in a "deplorable state" and " wretched". Nearly all of the adult population in the small cluster of around 10 houses were dead. Those still alive were gravely ill and told how their relatives had dropped even as they walked around. The team from the cannery buried the dead in a mass grave and brought those still alive back to the hospital in Naknek.

It was a picture that was repeated in villages all across Alaska. In just a few days nearly 200 people would die from the disease in the Bristol Bay area, leaving dozens of children orphaned. From some places, stories emerged of packs of stray dogs feasting on the bodies of the dead. In some communities, up to 90% of the population died and the mortality rates were some of the highest in the world.

Yet, just a few miles from some of the worst hit areas of Bristol Bay, one community in a tiny settlement called Egegak escaped the disease entirely.

"It is strange to relate that Egegak was the only village on Bristol Bay that was not troubled with the malady," the Alaska Packing Association's superintendent at Naknek station, JF Heinbockel was to say in his official report of the epidemic. "The natives there were apparently just as healthy when we left as they ever were."

Other medical reports stated that some villagers at Egegak showed only mild symptoms of the disease. It appears they were lucky.

"More people per capita died from influenza in Alaska than almost anywhere else in the world," says Katherine Ringsmuth, a historian who has been piecing together the story of the canneries in Bristol Bay. "Some places like Egegak escaped it and no one really knows why."

As the world tried to pick up the pieces in the aftermath of the global pandemic, stories began to emerge of similar places that had escaped the virus. There were not many - a handful of remote islands, rural towns, walled asylums and schools were left unaffected.

But the survival of these so-called "escape communities" could prove valuable today as public health officials look fearfully towards the next influenza pandemic.

The lessons they contain are considered so important that the US Department of Defense's Threat Reduction Agency investigated the handful of the places across the United States that were untouched by Spanish flu in the hope of gleaning some clues about how to keep military personnel safe in the future.

In all, the authors of the report focused on seven communities that they found had escaped the virus, although they say there may have been others they did not identify. Among them were the rural farming village of Fletcher, in northern Vermont, and Gunnison, Colorado, a remote town in the Rocky Mountains. Princeton University in New Jersey, Bryn Mawr College in Pennsylvania, the Western Pennsylvania Institution for the Blind in Pittsburgh and the Trudeau Tuberculosis Sanatorium in Saranac Lake, New York.

"These communities basically shut themselves down," explains Howard Markel, an epidemiological historian at the University of Michigan who was one of the authors of the study. "No one came in and no one came out. Schools were closed and there were no public gatherings. We came up with the term 'protective sequestration', where a defined and healthy group of people are shielded from the risk of infection from outsiders."

The people of Gunnison managed this by erecting guarded barricades on the main highways in and out of the surrounding county. Railway passengers were forced to submit to two days of quarantine upon arrival.

The sanatorium and school for the blind benefited from being relatively closed communities already, with walls to confine those who lived there also helping to protect those inside from the disease running rampant through the communities on the outside.

Being hard to reach also helped to protect other communities in 1918. The US naval base on the island of Yerba Buena, in San Francisco Bay, was only accessibly by boat. The base's 6,000 residents were confined to the island and no visitors were allowed ashore. The few arrivals allowed on the island were confined to quarantine, were given three times daily throat sprays, and had to maintain a distance of 20 feet from one another.

When these measures were lifted in November 1918, as reports of cases in San Francisco were on the decline, the base experienced only mild cases, but at least three people did die.

"The moment you open up the gates, the virus enters in the bodies of people who come in," says Markel. "Protective sequestration is only as good as long as you are doing it.

"The notion that you can shut down a modern city or even a university today is not very likely though. It is extremely expensive and disruptive."

But there may be some benefit to keeping the virus out for as long as is possible. American Samoa implemented a five-day quarantine for all boats that kept influenza from its shores until 1920. When it finally did arrive, the virus appears to have lost much of its sting and there were no deaths attributed to influenza in a population of more than 8,000. The main island of Samoa to the northwest, however, lost around a fifth of its population to the pandemic.

A similar story unfolded on the on the Australian island of Tasmania, which implemented strict quarantine measures for boats arriving on its shores that required all passengers and crew to be isolated for seven days. When the infection penetrated the island in August 1919, medical officers reported that it was a milder infection than that on the mainland. The death rate on Tasmania was one of the lowest recorded worldwide.

"For some islands, it might have been a mix of chance, remoteness and small numbers of travellers," says Nick Wilson, a professor of public health at the University of Otago in Wellington, New Zealand. "This experience has some modern relevance - for severe pandemics it might be cost beneficial for some islands to close their borders."

Other islands had similar success at keeping the pandemic at bay. The French territory of New Caledonia in the South Pacific did not experience an outbreak until July 1921, again escaping with just a mild form of the disease.

It's not clear why those attempts to delay the arrival of the disease reduced the mortality rates in these places. But research has suggested that over time, as the virus burned its way through populations, it accumulated mutations that naturally reduced its capacity to cause disease.

Another possibility could be that some populations may have acquired a degree of immunity against the pandemic strain from comparatively harmless seasonal flu strains that were circulating in the years running up to 1918.

In Denmark, for example, the pandemic claimed just 0.2% of the population while in Australia just 0.3% died. China also escaped lightly, with relatively few deaths - again something that has been attributed to some existing immunity within the population. Some large cities also reported lower mortality rates than might be expected in places where the risk of passing the virus from person to person is high, perhaps also due to immunity obtained in earlier less deadly outbreaks.

"This is known as the 'antigen recycling hypothesis'," says Professor Gerardo Chowell, an epidemiologist at Georgia State University who has been attempting to piece together the events that led to the 1918 pandemic. "In some areas, the older populations particularly were not as affected as much because they had some protection that they probably acquired when they were children."

While the idea is still debated, it has provided some clues that could help health officials in the fight against future pandemics. Today some countries offer annual vaccinations against seasonal flu strains that can help their populations build up temporary immunity. According to research by Jodie McVernon, an immunologist at the University of Melbourne, this could "provide important protection in the early stages of a new pandemic".

"The more times you get vaccinated, the more you are exposed to different versions of the flu virus," adds Markel.

But locations even with this potential immunity still saw people fall ill and some deaths. Just two small chains of remote volcanic islands in Fiji, in the South Pacific - the Lau and Yasawa islands - along with Marajo island on Brazil's Amazon delta, and a handful of tiny communities in Alaska and the Bering Strait could claim to have been left entirely untouched by the pandemic.

Their isolated locations and lack of outside visitors meant these island communities were never exposed to the virus.

"Transportation was much scarcer than nowadays and the population of Brazil was much smaller, so it is easy to see that Marajo might have got lucky," says Wladimir Alonso, a technical officer at the World Health Organization who has studied the patterns of the 1918 pandemic in Brazil. "But you would expect the population to remain immunologically susceptible to the pandemic virus."

This could mean that these remote locations were hit by the virus at a later date, but the very isolation that protected them from the waves of flu hitting other parts of the world meant these cases went unreported.

Blood tests conducted in Alaska, however, have confirmed that some remote populations were never exposed. People in the Yupik settlements of Gambell and Savoonga on St Lawrence Island in the Bering Strait and the even more remote Saint Paul Island further to the south, showed no trace of antibodies to the 1918 virus when they were tested in the 1950s.

While it appears these places were largely protected by their geography alone, other communities took matters into their own hands. Villagers in Barrow and Wainwright in north Alaska posted armed guards around their villages and travel between settlements was prohibited. When scientists tested people living in a number of remote settlements in north Alaska, they found they too were free of antibodies, suggesting they had never been exposed.

It appears that many of these villages were given advanced warning of the oncoming virus as it spread across Alaska by dog sled teams that raced ahead of the infection to alert villages. It was an incredible gamble - mail delivery teams and seal hunters moving through the region were already spreading the virus from settlement to settlement - but one that paid off.

One native Inupiaq community called Shishmaref, situated on a barrier reef island to the north of the Bering Strait, received news in this way and were able to place armed guards eight miles south of the town with orders not to let anyone pass. It was among those villages to evade the flu completely.

"A few places had warning," says Nicole Braem, a cultural anthropologist with the Bering Land Bridge National Preserve, which is part of the US National Park Service. "Numerous settlements in Alaska were unaffected, largely because of quarantines established along travel routes or their remoteness. Communities at the time were very self-sufficient for food and clothing. They were not as dependent on food and goods imported from elsewhere in the United States [compared to today]."

In the modern world, shutting down settlements like this would be far harder. Few places are now not dependent on goods brought in from around the world. Global travel networks and supply chains could also mean few places would be remote enough to escape a modern pandemic.

"In 1918 they had very little idea about viruses or what caused the pandemic," says Howard Markel. "Today we would have a better shot at coping with it - we have antivirals, hospitals with intensive care units, respirators and much better surveillance. But we travel further and faster than we ever have before, so the spread could be much faster than we could cope with."

Some communities in 1918 also appear to have escaped the virus against all logic. The 737 people living in the town of Fletcher, Vermont, defied advice to avoid contact with the outside world, holding a dance and attending a county fair in a neighbouring town. The town even hosted a wedding for a soldier from a military camp in Massachusetts that saw 28% of its population hit by influenza and suffered 757 deaths in the same month as the wedding. Despite 120 guests attending the wedding, the residents of Fletcher appeared to have dodged a bullet.

And this good fortune is perhaps the greatest lesson that the escape communities of 1918 have to offer modern health officials. Many communities that implemented rigid protection and quarantine measures were still hit by the pandemic.

It was a lesson that the communities of Bristol Bay in Alaska learned the hard way.

"Although they knew about the flu and did what they could to prevent it from coming, it arrived anyway," says Katherine Ringsmuth. "The disease struck so quickly, most people didn't have a chance to respond." A fall in salmon stocks may have ultimately helped the Egegak village. "It was a terrible year for salmon as they had been producing so much canned salmon for the war effort in Europe, it caused the fish numbers to decline.

"It might have meant no one had any reason to visit the area. It was just chance."

Survival, it seems, can sometimes come down to blind luck.

--
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Filthy and frightened, the three young children staggered up the beach. Their tiny frames were feverish and behind them, on board the small sailboat they had drifted ashore upon, lay the bodies of two dead men.

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At this point, it's still difficult to predict the full effects of the novel coronavirus. Will efforts to contain the disease and cause its regression succeed, or will COVID-19 turn into a full-blown, worldwide pandemic?

"The coronavirus panic is dumb"

The coronavirus panic is dumb
-- Elon Musk (@elonmusk) March 6, 2020

"In the past week, COVID-19 has started to behave a lot like the once-in-a-century pathogen we've been worried about," writes Gates.

"I hope it's not that bad, but we should assume that it will be until we know otherwise."

You can really see how stark the contrast is of these two responses when you place them side by side:

Musk: "The coronavirus panic is dumb"

Gates: "I hope it's not that bad, but we should assume that it will be until we know otherwise."

Musk and Gates both possess brilliant minds. But while one of these responses is potentially dangerous, the other promotes a rational, "safety-first" mentality--and could possibly lead to saving millions of lives.

What's emotional intelligence got to do with it?

Emotional intelligence is the ability to identify, understand, and manage emotions--both in yourself and in others. This ability is important to develop in everyday life, but it can be lifesaving in the face of a panic-inducing situation like the coronavirus, because it allows you to keep emotions under control so you can make balanced, reasonable decisions.

In this case, Musk's and Gates's responses are important because they have colossal platforms, and each can influence the way millions of people view and respond to COVID-19.

Taken literally, of course, Musk's take on panic is correct. While the Centers for Disease Control and Prevention (CDC) have made it clear that "current circumstances suggest it is likely that this virus will cause a pandemic," experts also advise that one of the best things the public can do is to try and remain calm.

The problem with Musk's tweet is that its casual tone detracts from the seriousness of the situation. It also undermines the work of countless medical and scientific professionals.

And while Musk attempted to explain his reasoning through a follow-up tweet, the fact is very few people saw that explanation--as opposed to the almost two million reactions (1.6 million likes and over 334,000 retweets) the original five-word tweet has received to date.

Gates, on the other hand, provided a much more detailed and nuanced explanation for his reasoning. He spoke to the dangers presented by COVID-19, and why he believes the current situation is an "excellent case in point" of how the world needs to solve an immediate problem while also improving the way it responds to outbreaks in general.

This type of response not only shows the ability to balance emotions and rational thought, it inspires others to do the same.

But while Gates's words are important, it's his actions that speak the loudest.

How Gates is fighting the coronavirus

Last month, the Bill & Melinda Gates Foundation committed up to $100 million to the global effort to respond to COVID-19, and just last week the foundation announced it would commit an additional $5 million to assist public health agencies in the greater Seattle region to battle the coronavirus.

One project funded by Gates's foundation is especially noteworthy: providing at-home test kits for those who believe they are suffering from the virus.

According to the Seattle Times, people who fear they may be infected will be able to use a nose-swab to collect a sample, which they can then send in for analysis. Results should be available in one to two days and will be shared with local health officials, who will then notify patients who have tested positive.

Additionally, those who are infected will be able to provide information via online forms about their travel and contact with others. This will "[make] it easier for health officials to locate others who may need to be tested or quarantined, as well as to track the virus' spread and identify possible hot spots," says the Times.

Scott Dowell, leader of the coronavirus response at the Bill & Melinda Gates Foundation, says the eventual goal is to be able to process thousands of tests a day.

"Although there's a lot to be worked out, this has enormous potential to turn the tide of the epidemic," said Dowell.

This could be a game-changer--because one of the reasons it's so difficult to predict the eventual effects of the coronavirus is because of the lack of testing. For example, in the U.S., the actual number of cases is likely much higher then that of confirmed cases. And without knowing how extensively COVID-19 has already infiltrated the U.S., the less motivated people are to take appropriate measures in response.

For now, employers are struggling to determine a strategy for dealing with the potential effects of the coronavirus. For example, if an employee gets sick, should employers encourage them to stay home, even after they're feeling better, to avoid risking others? What if working from home is not an option, what then? There's just so much uncertainty involved. (For employers seeking helpful guidance on their sick day policy, check out this excellent piece from fellow Inc. columnist Suzanne Lucas.)

But if a person can get a confirmed diagnosis within two days, without even leaving home, employers can have more confidence when developing protective measures and putting them into practice. In addition, allowing patients to test at home reduces the need for visits to a hospital or clinic, lowering the chance of infecting others and potentially helping to prevent the epidemic from spiraling out of control.

The lesson for business owners

The question in the end is: Is it really worth it to invest this type of money in a potential problem?

In addressing what he believes is the new reality, Gates sums it up well:

"Obviously, billions of dollars for anti-pandemic efforts is a lot of money. But that's the scale of investment required to solve the problem. And given the economic pain that an epidemic can impose--just look at the way COVID-19 is disrupting supply chains and stock markets, not to mention people's lives--it will be a bargain."

In other words, when it comes to major risks, it pays to be prepared.

So, the next time you're faced with a problem that others are getting emotional about, resist the urge to downplay their feelings. Instead, work on understanding and relating to those feelings.

Doing so will help you to see the bigger picture--and may even allow you to become part of the solution.

Like this column? Sign up to subscribe to email alerts and you'll never miss a post.

The opinions expressed here by Inc.com columnists are their own, not those of Inc.com.

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Bill Gates and Elon Musk Just Issued Very Different Responses to the Coronavirus. It's a Lesson in Emotional Intelligence

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At this point, it's still difficult to predict the full effects of the novel coronavirus. Will efforts to contain the disease and cause its regression succeed, or will COVID-19 turn into a full-blown, worldwide pandemic?

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As a team, we're fielding a lot of questions about COVID-19 and how individuals and families should be preparing. We compiled a list of the most common question. In this document we answer them with information and recommendations from resources that we trust.

It is important to note that COVID-19 is a novel virus; We are still learning about disease characteristics including who is most likely to become infected or experience serious illness as a result of it. Current clinical knowledge is based primarily on data from the China outbreak. We believe everyone should be taking steps to protect themselves and their families. We hope the resources below will help you to do that.

COVID-19 is a respiratory virus, and nonpharmaceutical interventions are the most effective tool we currently have to prevent and slow the spread of COVID-19 at this time. There is not currently a vaccine or specific treatment for COVID-19. Some key ways to implement nonpharmaceutical interventions are to:

Practice social distancing, such as limiting attendance at events with large groups of people

Stay home, especially if you are feeling ill

Implement good hand washing practices - it is extremely important to wash your hands regularly and thoroughly (see below for how-tos!)

Cover coughs and sneezes with your elbow or tissue

Avoid touching your eyes, nose, and mouth with unwashed hands

Disinfect frequently touched surfaces, such as doorknobs

Begin to take your temperature every day, if you develop a fever, stay home (if possible, separated from other people you live with) and call your doctor

Start preparations in anticipation of social distancing and potential supply chain shortages. This includes ensuring you have sufficient supplies of prescription medicine and have about a 2-week supply of food and other necessary household goods

If possible, discuss a plan to work from home with your employer or how classes could be attended remotely

With these steps in mind, it is important to not panic and panic buy. Panic buying unnecessarily increases strain on supply chains and can make it difficult to ensure that everyone is able to get supplies that they need. For an excellent explanation on why we should all be having a proactive, but measured response to the situation, we recommend reading this twitter thread by Nextstrain team member, Emma Hodcroft, PhD.

Some other resources and articles we have found extremely useful during our own preparations are:
Past Time to Tell the Public: "It Will Probably Go Pandemic, and We Should All Prepare Now" by Jody Lanard and Peter M. Sandman
Ready - Pandemic Preparedness Page - a helpful public service campaign on disaster preparedness from the US Department of Homeland Security
So you think you're about to be in a pandemic? by Ian McKay, PhD and Katherine E Arden, PhD US CDC - Preventing COVID-19 Spread in Communities US CDC - When & How to Wash Your Hands US CDC - Nonpharmaceutical Interventions US CDC - What to Do if You are Sick US CDC - Coronavirus Disease 2019 (COVID-19)
COVID-19 is a respiratory virus, which spread in 3 main ways:

1. Between people who are in close contact with each other (within about 6 feet, or 2 metres), through small aerosolized particles that can be produced when a person talks, coughs, or sneezes.

2. In (relatively) larger droplets that are produced someone coughs or sneezes (these can travel over similar distances).

3. Contact with surfaces or objects infected with the virus (also known as fomites). If a person touches an infected surface and then touches their eyes, nose, or mouth without washing their hands, they may become sick by introducing the virus into their body.

For COVID-19 there is evidence of transmission in clinically mild and asymptomatic cases. This means that people who are infected with COVID-19 and able to transmit the virus to others may not appear, or even feel, sick.

Though there is not yet clear evidence on how long the COVID-19 virus can survive on surfaces, we expect it to be similar to other coronaviruses. Coronaviruses can live on surfaces for anywhere from a couple hours to several days, depending on the surface and the climate. The US CDC recommends disinfecting frequently touched areas often.

Based on disease modeling estimates and phylodynamic analysis, the current epidemic doubling time is about 7 days. There is uncertainty with these estimates and this rate will vary based on community contact patterns. Nonpharmaceutical interventions can be effective in reducing this rate, as we have seen in China. Sudden jumps in case counts are likely due to increases in testing capacity catching cases that were previously missed by surveillance systems.

Current case counts, deaths, and recoveries are being tracked in a number of places. These are updated as regularly as possible, but may not always be immediately up to date. One dashboard that we particularly like is from the Johns Hopkins Center for Systems Science and Engineering:
Johns Hopkins CSSE Dashboard
Studies of patients in China have shown that most COVID-19 cases are adults. Just 2.1% of 44,672 cases in China were in individuals below 20 years of age and just 1% of those were in children under 10 years of age. Approximately 80% of people experience mild illness, 14% experience severe disease, and 5% experience critical illness (meaning the patient experienced respiratory failure requiring mechanical ventilation, shock, or other organ failure that required intensive care). Overall, 20% of Chinese cases required hospitalization.

The WHO currently estimates the overall case-fatality rate at 3.4%, but says that it can range from 0.7% to 4% depending on the quality of the healthcare system where the case is treated. Based on data from China, the case-fatality rate was 14.8% in patients aged ≥80 year, 8.0% in patients aged 70-79 years, and 49.0% in critical cases. The WHO-China CDC Joint Report found that while women and men were infected at similar rates, COVID-19 infections seem to be more severe in men. Only 2.8% of Chinese women who were infected died from the disease, while 4.7% of infected men died.

Based on the WHO-China CDC Joint Report, individuals over 60 and those who have weakened immune systems or underlying health conditions like hypertension, diabetes, cardiovascular disease, chronic respiratory disease and cancer are at a higher risk for severe disease.

Children do not seem to be at a high risk for either contracting COVID-19 or having severe disease as a result of an infection. A great graphic by Jesse Bloom, PhD and his team illustrates this point and compares case fatality across age groups; it be viewed here. Additionally, we'd recommend looking at this graphic from Claus Wilke, PhD, which re-plots the same data on a log-scale and highlights that, with the exception of children, COVID-19 is consistently worse than the seasonal flu, across all age groups. With both these graphics, it's important to note that all statistics are subject to error and biases, but these do give a ballpark idea of the risk of COVID-19 among different age groups.

At this time, little evidence exists on the risk of COVID-19 to pregnant women, fetuses, and newborns. More detailed information on this can be found on the US CDC's page, Coronavirus Disease 2019 (COVID-19): Pregnant Women. That being said, Public Health - Seattle King & County (the local public health authority in Seattle, WA where many of our team members are based) has recommended that pregnant women and membesr of other high risk groups stay home and away from larger groups of people as much as possible.

More detailed information on outcomes and clinical characteristics can be found in the original journal article summarizing the WHO-CHina Joint Mission Report and the report itself: Characteristics of and Important Lessons From the Coronavirus Disease 2019 (COVID-19) Outbreak in China by Zunyou Wu, MD, PhD and Jennifer M. McGoogan, PhD.

Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19O).

Based on the data from China, the most commonly reported symptoms are fever (88%), dry cough (68%), exhaustion (38%), wet cough (33%) and shortness of breath (18%). About 14% of people also experience sore throat, headaches, and muscle aches. Again, these symptoms will be mild in about 80% of cases. COVID-19 is a lower respiratory infection (so most symptoms will appear "below" the voicebox) but is a flu-like illness and how its symptoms present varies from person to person. If you are concerned about symptoms you or someone else may be having, in line with US CDC recommendations, we suggest calling your doctor or local health department to discuss next steps.

More detailed information on outcomes and clinical characteristics can be found in the original journal article summarizing the WHO-CHina Joint Mission Report and the report itself: Characteristics of and Important Lessons From the Coronavirus Disease 2019 (COVID-19) Outbreak in China by Zunyou Wu, MD, PhD and Jennifer M. McGoogan, PhD.

Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19O).

At the time of publication, the US CDC recommends to "Call ahead to a healthcare professional if you develop a fever and symptoms of respiratory illness, such as cough or difficulty breathing, and have been in close contact with a person known to have COVID-19 or if you live in or have recently traveled to an area with ongoing spread. Tell your healthcare professional about your recent travel or contact. Your healthcare professional will work with your state's public health department and CDC to determine if you need to be tested for COVID-19."

For more detailed information on what to do if you are concerned that you or someone you know might have COVID-19, please review the US CDC page, What to Do if You are Sick. This page includes information for individuals who may be sick, as well as information for their family members, caregivers, and intimate partners.

At the time of publication, the US CDC has "established geographic risk-stratification criteria for the purpose of issuing travel health notices for countries with COVID-19 transmission and guiding public health management decisions for people with potential travel-related exposures to COVID-19." A listing of risk assessments for different countries and what this means for traveler's can be found on the US CDC's Coronavirus Disease 2019 (COVID-19): Travel Information page.

Coronaviruses (CoV) are members of a diverse species of positive-sense single-stranded RNA ((+)ssRNA) viruses which have a history of causing respiratory infections in humans. Some variants of coronaviruses are associated with outbreaks, others are continuously circulating and cause mostly mild respiratory infections (e.g. the common cold). Their name comes from the Latin word for crown or halo, Corona, which references the club-shaped protein spikes that the surface of coronaviruses are covered in. More information about coronaviruses can be found on our Human Coronavirus page.

SARS-CoV-2 is the specific coronavirus that causes Coronavirus Disease 2019, which is abbreviated to COVID-19. SARS-CoV-2 is the cause of the ongoing COVID-19 outbreak. A bit more about SARS-CoV-2 can be found on our SARS-CoV-2 page.

The origin of the virus is still unclear, however genomic analysis suggests the COVID-19 virus is most closely related to viruses previously identified in bats. It is plausible that there were other intermediate animal transmissions before the introduction into humans.

There is not evidence of snakes as an intermediary. A good, though technical, explanation of why there is not evidence of snakes as an intermediary was written by Kristian Andersen, PhD, at the Scripps Research Institute. This article was posted on Virological and can be found here.

There is not evidence that the COVID-19 outbreak is the result of a lab escape. The data we have on the COVID-19 outbreak is consistent with a zoonotic origin and inconsistent with a lab escape scenaria (where a virus being used for research "escapes" from the laboratory and causes an outbreak). The WHO-China Joint Report noted that "since the COVID-19 virus has a genome identity of 96% to a bat SARS-like coronavirus and 86%-92% to a pangolin SARS-like coronavirus, an animal source for COVID-19 is highly likely." For a full analysis of the evidence supporting a zoonotic origin over a lab escape origin, please read this twitter thread by Nextstrain team member, Trevor Bedford, PhD, which discusses this issue in-depth.

There is not evidence that the COVID-19 virus was genetically engineered with HIV sequences. This theory was based on a pre-print paper that has since been thoroughly debunked and the article has been withdrawn. A non-technical discussion of why this theory had no ground can be found in this article in Forbes, which links out to Nextstrain team member, Trevor Bedford's, twitter thread on the same topic.

For a less technical discussion of why the COVID-19 outbreak is not the result of a lab escape and why the virus was not genetically engineered, we recommend this VOX article, which discusses both points.

There is not evidence that any strain of the COVID-19 virus, SARS-CoV-2, is more severe. A recent paper has claimed that SARS-CoV-2 has split into two strains, "L" and "S", with the "L" strain causing a more severe version of COVID-19. This theory was used to try to explain the higher case fatality ratio that has been seen in Wuhan, China, the epicenter of the outbreak as compared to other parts of China. Nextstrain team member, Richard Neher, PhD, summed up why this theory is inaccurate in this twitter thread. In short, this difference in case fatality rates is likely a statistical artifact due to the way that "genomes are sampled extremely heterogeneously in time and space. Rapidly growing local outbreaks get sampled intensively and result in overrepresentation of some variants."

A more detailed discussion of why there is not evidence for this claim was written by posted on Virological by Oscar A. MacLean et al., at the MRC-University of Glasgow Centre for Virus Research.

# data[].attributes.attachment_link.description
As a team, we're fielding a lot of questions about COVID-19 and how individuals and families should be preparing. We compiled a list of the most common question. In this document we answer them with information and recommendations from resources that we trust.

# data[].attributes.attachment_link.readable_text
attaaaggtt tataccttcc caggtaacaa accaaccaac tttcgatctc ttgtagatct ...

That string of apparent gibberish is anything but: It's a snippet of a DNA sequence from the viral pathogen, dubbed 2019 novel coronavirus (2019-nCoV), that is overwhelming China and frightening the entire world. Scientists are publicly sharing an ever-growing number of full sequences of the virus from patients-53 at last count in the Global Initiative on Sharing All Influenza Data database. These viral genomes are being intensely studied to try to understand the origin of 2019-nCoV and how it fits on the family tree of related viruses found in bats and other species. They have also given glimpses into what this newly discovered virus physically looks like, how it's changing, and how it might be stopped.

"One of the biggest takeaway messages [from the viral sequences] is that there was a single introduction into humans and then human-to-human spread," says Trevor Bedford, a bioinformatics specialist at the University of Washington and Fred Hutchinson Cancer Research Center. The role of Huanan Seafood Wholesale Market in Wuhan, China, in spreading 2019-nCoV remains murky, though such sequencing, combined with sampling the market's environment for the presence of the virus, is clarifying that it indeed had an important early role in amplifying the outbreak. The viral sequences, most researchers say, also knock down the idea the pathogen came from a virology institute in Wuhan.

In all, 2019-nCoV has nearly 29,000 nucleotides bases that hold the genetic instruction book to produce the virus. Although it's one of the many viruses whose genes are in the form of RNA, scientists convert the viral genome into DNA, with bases known in shorthand as A, T, C, and G, to make it easier to study. Many analyses of 2019-nCoV's sequences have already appeared on virological.org, nextstrain.org, preprint servers like bioRxiv, and even in peer-reviewed journals. The sharing of the sequences by Chinese researchers allowed public health labs around the world to develop their own diagnostics for the virus, which now has been found in 18 other countries. ( Science's news stories on the outbreak can be found here.)

When the first 2019-nCoV sequence became available, researchers placed it on a family tree of known coronaviruses-which are abundant and infect many species-and found that it was most closely related to relatives found in bats. A team led by Shi Zheng-Li, a coronavirus specialist at the Wuhan Institute of Virology, reported on 23 January on bioRxiv that 2019-nCoV's sequence was 96.2% similar to a bat virus and had 79.5% similarity to the coronavirus that causes severe acute respiratory syndrome (SARS), a disease whose initial outbreak was also in China more than 15 years ago. But the SARS coronavirus has a similarly close relationship to bat viruses, and sequence data make a powerful case that it jumped into people from a coronavirus in civets that differed from human SARS viruses by as few as 10 nucleotides. That's one reason why many scientists suspect there's an "intermediary" host species-or several-between bats and 2019-nCoV.

According to Bedford's analysis, the bat coronavirus sequence that Shi Zheng-Li's team highlighted, dubbed RaTG13, differs from 2019-nCoV by nearly 1100 nucleotides. On nextstrain.org, a site he co-founded, Bedford has created coronavirus family trees (example below) that include bat, civet, SARS, and 2019-nCoV sequences. (The trees are interactive -by dragging a computer mouse over them, it's easy to see the differences and similarities between the sequences.)

Bedford's analyses of RaTG13 and 2019-nCoV suggest that the two viruses shared a common ancestor 25 to 65 years ago, an estimate he arrived at by combining the difference in nucleotides between the viruses with the presumed rates of mutation in other coronaviruses. So it likely took decades for RaTG13-like viruses to mutate into 2019-nCoV.

Middle East respiratory syndrome (MERS), another human disease caused by a coronavirus, similarly has a link to bat viruses. But studies have built a compelling case it jumped to humans from camels. And the phylogenetic tree from Shi's bioRxiv paper (below) makes the camel-MERS link easy to see.

The longer a virus circulates in a human populations, the more time it has to develop mutations that differentiate strains in infected people, and given that the 2019-nCoV sequences analyzed to date differ from each other by seven nucleotides at most, this suggests it jumped into humans very recently. But it remains a mystery which animal spread the virus to humans. "There's a very large gray area between viruses detected in bats and the virus now isolated in humans," says Vincent Munster, a virologist at the U.S. National Institute of Allergy and Infectious Diseases who studies coronaviruses in bats, camels, and others species.

Strong evidence suggests the marketplace played an early role in spreading 2019-nCoV, but whether it was the origin of the outbreak remains uncertain. Many of the initially confirmed 2019-nCoV cases-27 of the first 41 in one report, 26 of 47 in another-were connected to the Wuhan market, but up to 45%, including the earliest handful, were not. This raises the possibility that the initial jump into people happened elsewhere.

According to Xinhua, the state-run news agency, "environmental sampling" of the Wuhan seafood market has found evidence of 2019-nCoV. Of the 585 samples tested, 33 were positive for 2019-nCoV and all were in the huge market's western portion, which is where wildlife were sold. "The positive tests from the wet market are hugely important," says Edward Holmes, an evolutionary biologist at the University of Sydney who collaborated with the first group to publicly release a 2019-nCoV sequence. "Such a high rate of positive tests would strongly imply that animals in the market played a key role in the emergence of the virus."

Yet there have been no preprints or official scientific reports on the sampling, so it's not clear which, if any, animals tested positive. "Until you consistently isolate the virus out of a single species, it's really, really difficult to try and determine what the natural host is," says Kristian Andersen, an evolutionary biologist at Scripps Research.

One possible explanation for the confusion about where the virus first entered humans is if there was a batch of recently infected animals sold at different marketplaces. Or an infected animal trader could have transmitted the virus to different people at different markets. Or, Bedford suggests, those early cases could have been infected by viruses that didn't easily transmit and sputtered out. "It would be hugely helpful to have just a sequence or two from the marketplace [environmental sampling] that could illuminate how many zoonoses occurred and when they occurred," Bedford says.

In the absence of clear conclusions about the outbreak's origin, theories thrive, and some have been scientifically shaky. A sequence analysis led by Wei Ji of Peking University and published online by the Journal of Medical Virology received substantial press coverage when it suggested that "snake is the most probable wildlife animal reservoir for the 2019‐nCoV." Sequence specialists, however, pilloried it.

Conspiracy theories also abound. A CBC News report about the Canadian government deporting Chinese scientists who worked in a Winnipeg lab that studies dangerous pathogens was distorted on social media to suggest that they were spies who had smuggled out coronaviruses. The Wuhan Institute of Virology, which is the premier lab in China that studies bat and human coronaviruses, has also come under fire. "Experts debunk fringe theory linking China's coronavirus to weapons research," read a headline on a story in The Washington Post that focused on the facility.

Concerns about the institute predate this outbreak. Nature ran a story in 2017 about it building a new biosafety level 4 lab and included molecular biologist Richard Ebright of Rutgers University, Piscataway, expressing concerns about accidental infections, which he noted repeatedly happened with lab workers handling SARS in Beijing. Ebright, who has a long history of raising red flags about studies with dangerous pathogens, also in 2015 criticized an experiment in which modifications were made to a SARS-like virus circulating in Chinese bats to see whether it had the potential to cause disease in humans. Earlier this week, Ebright questioned the accuracy of Bedford's calculation that there are at least 25 years of evolutionary distance between RaTG13-the virus held in the Wuhan virology institute-and 2019-nCoV, arguing that the mutation rate may have been different as it passed through different hosts before humans. Ebright tells Science Insider that the 2019-nCoV data are "consistent with entry into the human population as either a natural accident or a laboratory accident."

Shi did not reply to emails from Science, but her longtime collaborator, disease ecologist Peter Daszak of the EcoHealth Alliance, dismissed Ebright's conjecture. "Every time there's an emerging disease, a new virus, the same story comes out: This is a spillover or the release of an agent or a bioengineered virus," Daszak says. "It's just a shame. It seems humans can't resist controversy and these myths, yet it's staring us right in the face. There's this incredible diversity of viruses in wildlife and we've just scratched the surface. Within that diversity, there will be some that can infect people and within that group will be some that cause illness."

Daszak and Shi's group have for 8 years been trapping bats in caves around China to sample their feces and blood for viruses. He says they have sampled more than 10,000 bats and 2000 other species. They have found some 500 novel coronaviruses, about 50 of which fall relatively close to the SARS virus on the family tree, including RaTG13-it was fished out of a bat fecal sample they collected in 2013 from a cave in Moglang in Yunnan province. "We cannot assume that just because this virus from Yunnan has high sequence identity with the new one that that's the origin," Daszak says, noting that only a tiny fraction of coronaviruses that infect bats have been discovered. "I expect that once we've sampled and sampled and sampled across southern China and central China that we're going to find many other viruses and some of them will be closer [to 2019-nCoV]."

It's not just a "curious interest" to figure out what sparked the current outbreak, Daszak says. "If we don't find the origin, it could still be a raging infection at a farm somewhere, and once this outbreak dies, there could be a continued spillover that's really hard to stop. But the jury is still out on what the real origins of this are."

doi:10.1126/science.abb1256

Jon is a staff writer for Science.

More from News

# data[].attributes.attachment_link.title
Mining coronavirus genomes for clues to the outbreak's origins

# data[].attributes.attachment_link.description
attaaaggtt tataccttcc caggtaacaa accaaccaac tttcgatctc ttgtagatct ... That string of apparent gibberish is anything but: It's a snippet of a DNA sequence from the viral pathogen, dubbed 2019 novel coronavirus (2019-nCoV), that is overwhelming China and frightening the entire world.

# data[].attributes.attachment_link.readable_text
attaaaggtt tataccttcc caggtaacaa accaaccaac tttcgatctc ttgtagatct ...

That string of apparent gibberish is anything but: It's a snippet of a DNA sequence from the viral pathogen, dubbed 2019 novel coronavirus (2019-nCoV), that is overwhelming China and frightening the entire world. Scientists are publicly sharing an ever-growing number of full sequences of the virus from patients-53 at last count in the Global Initiative on Sharing All Influenza Data database. These viral genomes are being intensely studied to try to understand the origin of 2019-nCoV and how it fits on the family tree of related viruses found in bats and other species. They have also given glimpses into what this newly discovered virus physically looks like, how it's changing, and how it might be stopped.

"One of the biggest takeaway messages [from the viral sequences] is that there was a single introduction into humans and then human-to-human spread," says Trevor Bedford, a bioinformatics specialist at the University of Washington and Fred Hutchinson Cancer Research Center. The role of Huanan Seafood Wholesale Market in Wuhan, China, in spreading 2019-nCoV remains murky, though such sequencing, combined with sampling the market's environment for the presence of the virus, is clarifying that it indeed had an important early role in amplifying the outbreak. The viral sequences, most researchers say, also knock down the idea the pathogen came from a virology institute in Wuhan.

In all, 2019-nCoV has nearly 29,000 nucleotides bases that hold the genetic instruction book to produce the virus. Although it's one of the many viruses whose genes are in the form of RNA, scientists convert the viral genome into DNA, with bases known in shorthand as A, T, C, and G, to make it easier to study. Many analyses of 2019-nCoV's sequences have already appeared on virological.org, nextstrain.org, preprint servers like bioRxiv, and even in peer-reviewed journals. The sharing of the sequences by Chinese researchers allowed public health labs around the world to develop their own diagnostics for the virus, which now has been found in 18 other countries. ( Science's news stories on the outbreak can be found here.)

When the first 2019-nCoV sequence became available, researchers placed it on a family tree of known coronaviruses-which are abundant and infect many species-and found that it was most closely related to relatives found in bats. A team led by Shi Zheng-Li, a coronavirus specialist at the Wuhan Institute of Virology, reported on 23 January on bioRxiv that 2019-nCoV's sequence was 96.2% similar to a bat virus and had 79.5% similarity to the coronavirus that causes severe acute respiratory syndrome (SARS), a disease whose initial outbreak was also in China more than 15 years ago. But the SARS coronavirus has a similarly close relationship to bat viruses, and sequence data make a powerful case that it jumped into people from a coronavirus in civets that differed from human SARS viruses by as few as 10 nucleotides. That's one reason why many scientists suspect there's an "intermediary" host species-or several-between bats and 2019-nCoV.

According to Bedford's analysis, the bat coronavirus sequence that Shi Zheng-Li's team highlighted, dubbed RaTG13, differs from 2019-nCoV by nearly 1100 nucleotides. On nextstrain.org, a site he co-founded, Bedford has created coronavirus family trees (example below) that include bat, civet, SARS, and 2019-nCoV sequences. (The trees are interactive -by dragging a computer mouse over them, it's easy to see the differences and similarities between the sequences.)

Bedford's analyses of RaTG13 and 2019-nCoV suggest that the two viruses shared a common ancestor 25 to 65 years ago, an estimate he arrived at by combining the difference in nucleotides between the viruses with the presumed rates of mutation in other coronaviruses. So it likely took decades for RaTG13-like viruses to mutate into 2019-nCoV.

Middle East respiratory syndrome (MERS), another human disease caused by a coronavirus, similarly has a link to bat viruses. But studies have built a compelling case it jumped to humans from camels. And the phylogenetic tree from Shi's bioRxiv paper (below) makes the camel-MERS link easy to see.

The longer a virus circulates in a human populations, the more time it has to develop mutations that differentiate strains in infected people, and given that the 2019-nCoV sequences analyzed to date differ from each other by seven nucleotides at most, this suggests it jumped into humans very recently. But it remains a mystery which animal spread the virus to humans. "There's a very large gray area between viruses detected in bats and the virus now isolated in humans," says Vincent Munster, a virologist at the U.S. National Institute of Allergy and Infectious Diseases who studies coronaviruses in bats, camels, and others species.

Strong evidence suggests the marketplace played an early role in spreading 2019-nCoV, but whether it was the origin of the outbreak remains uncertain. Many of the initially confirmed 2019-nCoV cases-27 of the first 41 in one report, 26 of 47 in another-were connected to the Wuhan market, but up to 45%, including the earliest handful, were not. This raises the possibility that the initial jump into people happened elsewhere.

According to Xinhua, the state-run news agency, "environmental sampling" of the Wuhan seafood market has found evidence of 2019-nCoV. Of the 585 samples tested, 33 were positive for 2019-nCoV and all were in the huge market's western portion, which is where wildlife were sold. "The positive tests from the wet market are hugely important," says Edward Holmes, an evolutionary biologist at the University of Sydney who collaborated with the first group to publicly release a 2019-nCoV sequence. "Such a high rate of positive tests would strongly imply that animals in the market played a key role in the emergence of the virus."

Yet there have been no preprints or official scientific reports on the sampling, so it's not clear which, if any, animals tested positive. "Until you consistently isolate the virus out of a single species, it's really, really difficult to try and determine what the natural host is," says Kristian Andersen, an evolutionary biologist at Scripps Research.

One possible explanation for the confusion about where the virus first entered humans is if there was a batch of recently infected animals sold at different marketplaces. Or an infected animal trader could have transmitted the virus to different people at different markets. Or, Bedford suggests, those early cases could have been infected by viruses that didn't easily transmit and sputtered out. "It would be hugely helpful to have just a sequence or two from the marketplace [environmental sampling] that could illuminate how many zoonoses occurred and when they occurred," Bedford says.

In the absence of clear conclusions about the outbreak's origin, theories thrive, and some have been scientifically shaky. A sequence analysis led by Wei Ji of Peking University and published online by the Journal of Medical Virology received substantial press coverage when it suggested that "snake is the most probable wildlife animal reservoir for the 2019‐nCoV." Sequence specialists, however, pilloried it.

Conspiracy theories also abound. A CBC News report about the Canadian government deporting Chinese scientists who worked in a Winnipeg lab that studies dangerous pathogens was distorted on social media to suggest that they were spies who had smuggled out coronaviruses. The Wuhan Institute of Virology, which is the premier lab in China that studies bat and human coronaviruses, has also come under fire. "Experts debunk fringe theory linking China's coronavirus to weapons research," read a headline on a story in The Washington Post that focused on the facility.

Concerns about the institute predate this outbreak. Nature ran a story in 2017 about it building a new biosafety level 4 lab and included molecular biologist Richard Ebright of Rutgers University, Piscataway, expressing concerns about accidental infections, which he noted repeatedly happened with lab workers handling SARS in Beijing. Ebright, who has a long history of raising red flags about studies with dangerous pathogens, also in 2015 criticized an experiment in which modifications were made to a SARS-like virus circulating in Chinese bats to see whether it had the potential to cause disease in humans. Earlier this week, Ebright questioned the accuracy of Bedford's calculation that there are at least 25 years of evolutionary distance between RaTG13-the virus held in the Wuhan virology institute-and 2019-nCoV, arguing that the mutation rate may have been different as it passed through different hosts before humans. Ebright tells Science Insider that the 2019-nCoV data are "consistent with entry into the human population as either a natural accident or a laboratory accident."

Shi did not reply to emails from Science, but her longtime collaborator, disease ecologist Peter Daszak of the EcoHealth Alliance, dismissed Ebright's conjecture. "Every time there's an emerging disease, a new virus, the same story comes out: This is a spillover or the release of an agent or a bioengineered virus," Daszak says. "It's just a shame. It seems humans can't resist controversy and these myths, yet it's staring us right in the face. There's this incredible diversity of viruses in wildlife and we've just scratched the surface. Within that diversity, there will be some that can infect people and within that group will be some that cause illness."

Daszak and Shi's group have for 8 years been trapping bats in caves around China to sample their feces and blood for viruses. He says they have sampled more than 10,000 bats and 2000 other species. They have found some 500 novel coronaviruses, about 50 of which fall relatively close to the SARS virus on the family tree, including RaTG13-it was fished out of a bat fecal sample they collected in 2013 from a cave in Moglang in Yunnan province. "We cannot assume that just because this virus from Yunnan has high sequence identity with the new one that that's the origin," Daszak says, noting that only a tiny fraction of coronaviruses that infect bats have been discovered. "I expect that once we've sampled and sampled and sampled across southern China and central China that we're going to find many other viruses and some of them will be closer [to 2019-nCoV]."

It's not just a "curious interest" to figure out what sparked the current outbreak, Daszak says. "If we don't find the origin, it could still be a raging infection at a farm somewhere, and once this outbreak dies, there could be a continued spillover that's really hard to stop. But the jury is still out on what the real origins of this are."

doi:10.1126/science.abb1256

Jon is a staff writer for Science.

More from News

# data[].attributes.attachment_link.title
Mining coronavirus genomes for clues to the outbreak's origins

# data[].attributes.attachment_link.description
attaaaggtt tataccttcc caggtaacaa accaaccaac tttcgatctc ttgtagatct ... That string of apparent gibberish is anything but: It's a snippet of a DNA sequence from the viral pathogen, dubbed 2019 novel coronavirus (2019-nCoV), that is overwhelming China and frightening the entire world.

# data[].attributes.attachment_link.readable_text
The outbreak of the novel coronavirus is like a real-life sci-fi movie, except we don't know yet whether it's The Hitchhiker's Guide to the Galaxy or Alien.

At least that's how I feel, as I find myself in a state of anxiety in which "oh my god" can mean everything from "what a hype" to "this is it: the apocalypse."

Arguably, the effects of the continued spread of COVID-19 are palpable, not only for those who fell ill or even died, but also for the global psyche. Work is perhaps where we feel it the most. COVID-19 is disrupting many businesses, most prominently among them the tourism and travel industry (Lufthansa announced it was going to temporarily suspend 25 percent of all its flight operations), and of course the event sector: Mobile World Congress was the first major show to be canceled, and many others have now followed suit. Yesterday, The Next Web, a leading European conference for the digital economy, postponed its June event. And one of my clients canceled a dinner that was planned for tomorrow-for 12 guests.

Conferences and speakers alike are looking into virtual gatherings as alternatives. Piers Fawkes has a great piece on how the outbreak will push some fringe technologies into the mainstream. Azeem Azhar connects all the dots and projects the long-term implications of COVID-19 on business models and the economy overall.

In the short term, it's clear what companies can do: limit travel (Amazon, Facebook, Google, L'Oreal, Nestle, SAP, and Twitter, among many others, have all put non-essential travel on hold and canceled their own events), encourage and enable employees to work from home, implement generous sick policies, and help staff cope with the new reality both physically - and emotionally.

The emotional side

The emotional side is often overlooked, but it's the ultimate battlefield in our fight against the outbreak, which, even though not officially labeled as one yet by the WHO, bears all the characteristics of a pandemic.

I'm feeling it myself. I'm torn between mocking those who buy everything off the shelves of grocery stories as if WWIII was about to start, and disinfecting my hands every time I touch my face-and being, ever so slightly, freaked out. The words of M. Leavitt from the DHHS are wise and ever more relevant: "Everything we do before a pandemic will seem alarmist. Everything we do after will seem inadequate."

The outbreak of the new coronavirus is hitting close to home. This week, my daughter's school in Berlin was closed because a parent had been in contact with an infected person. And my father, whose immune system is severely compromised after several rounds of chemotherapy, is a high-risk person these days.

As much as I'm feeling uneasy about the health of my loved ones and my own, as well as the possibility of mass infections and quarantines, I am also secretly enjoying the new constraints that reduce my life to more essential things, appreciating the mundane errands, and the time I have won back due to events and travel being canceled. Being bound to one place by superior force is a blessing in disguise. At the same time, I feel for all the pain and suffering the virus has inflicted on many, and I feel ashamed of my privilege to even consider COVID-19 a luxury that is replenishing my time stock.

Polarized, but now all in this together

We live in a bipolar world, in so many ways: liberal and open societies, allowing the rise of fluid identities and progressive social policies on the one hand, and on the other hand, neo-conservative, nativist movements that want to bring us back to the stone age. AI that can paint, write, and beat humans in the game Go is a strange juxtaposition with the archaic nature of an epidemic and humankind struggling to find an adequate response.

The coronavirus outbreak has brought all these paradoxes to the fore. It is hyper-global and hyper-local at the same time. Abstract and only one wrong touch away. Enabled by technological connectivity and transmitted through physical proximity and social intimacy.

The virus brings out the worst and best of us.

As for the worst, there have been incidents of Sinophobia and attacks against the infected, and everyone is racing to put on their own (oxygen) mask first.

But as The Atlantic reminded us (with an admittedly sensationalist headline, " You're Likely to Get the Coronavirus"), we are all susceptible. I had the pleasure of speaking with special pathogens expert Dr. Syra Madad last week as part of an online lecture I co-hosted with my colleague Monika Jiang. Madad, who is currently featured in Netflix's eerily timely docu-series, Pandemic: How to Prevent an Outbreak, is in charge of preparedness efforts for NYC Health and Hospitals, the largest municipal system in the U.S.

She told us:
"This particular virus seems like it is highly transmissible and is certainly acting a lot like the flu in terms of its ability to infect a large number of individuals. From that standpoint, I think that it is certainly plausible that 40 to 70% of the world's population could become infected with coronavirus disease, but a large number of cases are [expected to be] mild."
Madad warned of spreading contagious misinformation and looking for scapegoats: "Implicating a particular community is very unfortunate, because viruses don't respect boundaries. When you're marginalizing a particular community or society, or group of people, you then instill more fear in that particular group and then they are more reluctant to come and seek healthcare services. We should not fear individuals, but the virus itself."

She insists that everyone has a role to play, as we struggle to contain or mitigate the virus, and while it may seem like common sense, these are still excellent and timely reminders and simple actions we can all take:
"While you may not be a public health practitioner, or a healthcare provider, or even in the healthcare field, every single person has a role to play. This includes our own human behavior. If you know you are sick and can infect others, don't go out to public places. If you know you are sick and you need to see a healthcare provider, let them know ahead of time so that they can bring you in through an entrance where there's not a lot of people. Additionally, the everyday preventative measures that we constantly talk about like washing your hands, not touching your mucous membranes - things like that go a long way."
Stories of hope

This is our test, and while there are examples of how the virus can dehumanize us, there are also countless examples of how we can respond with the best of our humanity.

Monika Jiang posted stories shared with her by her Tianjin-born mother, who since the outbreak had been keeping in close contact with relatives and friends whose worlds have shrunk to their own four walls, sharing compassionate words and "quirky jokes with one laughing and one weeping eye." She told Monika of a daughter who witnessed her father carrying her infected mother on a bicycle around a local hospital for 14 days, until one bed finally was available. Unfortunately, his efforts were in vain. It was already too late. Or the young marathon runner who turned his room into a training ground, accomplishing 6250 laps in his winning time! Or how animal lovers, vegans, and vegetarians buried their differences and shared cooking recipes among each other, as all restaurants had been shut down.

There is also this video of Wuhan residents cheering each other on, from window to window.

Last week, we concluded our lecture with a brief video message we had received from Hong Kong-based Chinese journalist Yuli Yang who has family in Wuhan, the original epicenter of the outbreak. She asked the world to send messages of encouragement and support to the people in Wuhan through social media, so they know they're not alone:
"When people in Wuhan have more hope and strength in their hearts, their immune systems improve. It literally makes them stronger," she said, "and if Wuhan becomes stronger, we're all one step closer to winning this fight against COVID-19. That's just the simple logic of our oneness as a species."
And further: "What gives me hope is that we are human beings, and the year right now is 2020. We have shocking, amazing powers. This virus might not know this, but we have walked on the moon, we can speak to one another instantaneously, even if we are on two sides of the planet. We have cured and gotten rid of so many diseases on the face of this planet. We can definitely defeat this virus. It's just a matter of time. But exactly because of our powers as a species, we need to be cautious in how we use our strengths. We absolutely cannot allow fear, hate, or anger lead our actions, because whenever that happened, horrible things followed."

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The Coronavirus Crisis Is a Test of Our Humanity

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The outbreak of the novel coronavirus is like a real-life sci-fi movie, except we don't know yet whether it's The Hitchhiker's Guide to the Galaxy or Alien. At least that's how I feel, as I find myself in a state of anxiety in which "oh my god" can mean everything from "what a hype" to "this is it: the apocalypse."

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This story is part of a group of stories called

Finding the best ways to do good.

As of Monday, March 9, cases of the novel coronavirus have passed 110,000 worldwide, with outbreaks worsening in the US, Italy, and Iran (though easing in China and South Korea) - and more countries around the world announcing cases. In the US, there are now more than 600 confirmed cases, with numbers rising in Washington state, California, Boston, New York, and elsewhere as more and more states report cases within their borders.

The head of the World Health Organization said that the world is in "uncharted territory" with a dangerous and rapidly spreading disease that has caused serious outbreaks around the world. But there's one word the World Health Organization has yet to use to describe the outbreak: "pandemic."

"The threat of a pandemic has become very real," WHO Director General Tedros Adhanom Ghebreyesus said in a briefing Monday - but still stopped just short of calling the situation an actual pandemic.

The WHO says that since there's still uncertainty about the disease's impact, most countries still have only a few cases, and containment is not yet hopeless, the word "pandemic" isn't appropriate yet. But many observers have disagreed with the WHO's decision, believing that what we're seeing unfold now fits the definition of the word.

As the novel coronavirus continues its global spread, with cases in more than 100 countries and regions, and 20 countries reporting more than 100 cases, experts have drawncomparisons -some of them reassuring, some of them alarming - to past major disease outbreaks, public health emergencies, and pandemics, from SARS and MERS to the 1918-'19 Spanish influenza that was one of the biggest catastrophes of the past 200years.

So: What makes a pandemic? Or an epidemic? And what's the difference? This explainer will catch you up on the terminology and the history behind global disease scares.

What is a pandemic?

To define a pandemic, we need to first define a few other terms.

First, when a disease infects a lot of people in one area in a short period of time, that's an outbreak. For example, the US has experienced a series of measles outbreaks over the past few years, with 2019 the worst year for measles since 1992.

The measles outbreaks were quite different from a global public health perspective than the coronavirus outbreak. Measles was introduced by travelers from other countries and spread in populations with low vaccination rates, instead of jumping from animals. Since there is a vaccine, and since some people have had exposure and immunity, the measles outbreaks - while a serious public health crisis - didn't present a risk on the scale of the coronavirus outbreak.

The novel coronavirus crisis began with an outbreak of 41 identified cases inWuhan, China, in December that began spreading rapidly in January.

That brings us to a term you might have seen thrown around: epidemic.The World Health Organization defines an epidemic as "the occurrence in a community or region of cases of an illness ... clearly in excess of normal expectancy." The CDC defines it as "an increase, often sudden, in the number of cases of a disease above what is normally expected" in a region. You may have heard the term used to refer to the "opioid epidemic," or other instances of a long-existing harm becoming rapidly more deadly or more widespread.

By that definition, the coronavirus outbreak has certainly reached "epidemic" status in a number of regions, most notably China, South Korea, Iran, and Italy. In a briefing last week, Ghebreyesus referred to it in those terms. "This epidemic is a threat for every country, rich and poor," he said, calling on governments around the world to respond with the strongest measures available.

When it comes to defining a pandemic, things get a little more complicated.

According to A Dictionary of Epidemiology, the standard reference for epidemiologists,a pandemic is "an epidemic occurring worldwide, or over a very wide area, crossing international boundaries and usually affecting a large number of people."

A "pandemic" disease sounds much scarier than a mere "outbreak." But it's important to remember that "pandemic" refers to how many parts of the world are dealing with an elevated rate of the disease - and, in theory, says nothing about how serious the disease is.

In 2009, the H1N1 influenza was deemed a pandemic. One in five people worldwide caught the disease. But it was not very deadly, with an overall mortality rate estimated at 0.02 percent, so the societal disruption was limited and the loss of lives, while tragic, didn't overwhelm medical systems.

Past coronaviruses have been dangerous, but they have not gone pandemic around the globe. The 2002-'03 SARS outbreak - primarily in China and Hong Kong, though with cases around the world - had about a 10 percent mortality rate. But as the disease was swiftly contained, it was never a pandemic, and no cases have been reported anywhere in the world since 2004.

Similarly, the even deadlier MERS coronavirus - with an approximately 35 percent mortality rate - was not very contagious and circulated only slowly. MERS originated in Saudi Arabia, and nearly all transmission has been there, though a traveler from the Middle East spurred a 2015 outbreak in South Korea. It has not been entirely eliminated, but it has never been a pandemic.

Sometimes, though, diseases have both a high mortality rate and enough transmissibility to become a pandemic. That's the worst-case scenario for public health. The best example is the 1918-'19 influenza pandemic, which - aided by the troop movements of World War I - travelled all around the world and struck an estimated 500 million people.

At the time, that represented 25 percent of the population of the world. There are varying estimates for its lethality, but it was likely lower than that of SARS or MERS and may even have been as low as a few percentage points. That's still high enough to have had a devastating effect on society. The death toll is estimated to have been 40 million to 50 million, though some estimates are higher.

When public health experts talk about their fear of another global pandemic, they have in mind the possibility of something like the 1918-'19 influenza. That said, it's worth noting that even a "mild" pandemic like H1N1 in 2009 is estimated to have caused up to 575,000 deaths, because when a disease infects the whole world the death toll will be very high even if the disease is fairly mild.

So is the new coronavirus a pandemic?

By that standard, the novel coronavirus outbreak seems at first glance like it really ought to be considered a pandemic. It is an epidemic in China, Italy, South Korea, and Iran, and it is occurring in more than 80 countries, with some devastating effects. More than 100,000 people have been affected so far (and millions more have been affected by travel restrictions and quarantines).

Indeed, many global health experts have called it a pandemic. The outbreak "has become a global pandemic," German health minister Jens Spahn said Wednesday.

"Personally, I think we're doing everyone a disservice by continuing this debate [over whether it's time to call the situation a pandemic]," Lauren Sauer, director of operations for the Johns Hopkins Office of Critical Event Preparedness, told the Washington Post. "It is creating more panic than just declaring it and moving on."

But the World Health Organization has still not used the word "pandemic" for the outbreak. Ghebreyesus, the WHO's director general, has said the decision will be based on "an ongoing assessment" of how widely the virus has spread and how badly it is affecting people. He cited the fact that most cases have been in China and that case counts have been very limited in most countries.

"Although a few countries are reporting large numbers of cases, 115 countries have not reported any cases. Twenty-one countries have reported only one case. And five countries that had reported cases have not reported new cases in the past 14 days," Ghebreyesus argued Thursday, although those numbers have since changed.

So according to the WHO, the coronavirus spread isn't a pandemic yet - though it may become one if things get worse.

The WHO has held off before onusing the word "pandemic," even once it was applicable. In 2009, with the spread of H1N1, the WHO was reluctant to declare the situation a global pandemic, despite the fact that the disease ended up infecting between 10 percent and 20 percent of the world in both hemispheres, which clearly qualifies it as an "epidemic occurring worldwide, or over a very widearea."

Experts observed at the time that the WHO's guidance on categorizing epidemics seemingly had political considerations. The "complicated pandemic definitions" that the WHO and the CDC had deployed seemed crafted "in a deliberate attempt to garner political attention and financial support for pandemic preparedness," researcher Heath Kelly argued in the Bulletin of the World Health Organization.

In other words, rather than using the classic definition of a pandemic, the WHO found itself leaning on its a definition that mixed severity and spread. The WHO was aware that people associated the word with disease severity, and wanted to be using language that reflected that so the WHO would be taken seriously in requests for pandemic preparedness.

It seems likely that there's something similar isgoing on right now. The word "pandemic" has profound implications for how we think about a disaster, and the World Health Organization is wary of them.

"Using the word pandemic carelessly has no tangible benefit, but it does have significant risk in terms of amplifying unnecessary and unjustified fear and stigma, and paralyzing systems," Ghebreyesus argued last week.

Other organizations have mostly followed the WHO's lead.In some cases, the situation has been further complicated by local political constraints on how to talk about the virus. Earlier this week, Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, said the virus would reach "likely pandemic proportions," reportedly angering the White House.

Why it matters that something is called a pandemic

So if the distinction between a pandemic and an epidemic isn't how severe they are or how scared we should be, what is the distinction? Why bother categorizing diseases by how many countries are affected?

One answer is that pandemics must be battled, at the international level, significantly differently than epidemics.

When one region of the world experiences an epidemic, the rest of the world is on the sidelines. They may shut their borders to the affected region, or send help, or both. They may start making preparations in case the disease affects their own country. When coronavirus broke out in Wuhan, many of China's neighbors sent masks. In a now-retracted Lancet paper, health workers in Wuhan asked if they'd consider sending volunteer nurses and doctors, too.

When there's a global pandemic, there largely are no sidelines. It no longer makes sense for countries to shut their borders against the affected countries, as the disease is present everywhere. Public health officials might recommend shifting to social distancing measures - which reduce spread within a country - instead of screening efforts that try to keep the disease out of the country at all. Countries still must share medical knowledge and expertise with one another, but directing supplies to affected areas is more complicated when affected areas are everywhere. A world fighting a pandemic is not focused on containment to a distant elsewhere but on harm-reduction at home.

By that definition of a pandemic, we're at a tipping point. Some experts say it's already too late for containment, but not all experts agree. The WHO does not, arguing in Monday's press conference that "the threat of a pandemic has become very real. But it would be the first pandemic in history that could be controlled. The bottom line is: we are not at the mercy of this virus."

This is why we're seeing disagreement on whether we've now reached pandemic stage with the novel coronavirus.
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The first two months of the coronavirus's spread have been full of surprises. It makes sense the World Health Organization wants to choose its words carefully - and that it's still holding out hope that containment can be achieved.

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Why the WHO won't call the coronavirus a pandemic

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Finding the best ways to do good. As of Monday, March 9, cases of the novel coronavirus have passed 110,000 worldwide, with outbreaks worsening in the US, Italy, and Iran (though easing in China and South Korea) - and more countries around the world announcing cases.

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In recent weeks, China has faced an unprecedented public health challenge. The novel coronavirus that causes COVID-19 has taken more than 3,000 lives and infected more than 80,000 people on the Chinese mainland.

Confronted with the sudden outbreak of the previously unknown virus, the Chinese government, led by President Xi Jinping, moved ahead with the most comprehensive and rigorous public health effort ever mounted in response to an epidemic. Despite disruption to economic activities and personal life, the Chinese people came together to contain the spread of the virus.

Stringent quarantine measures were imposed in many cities, including a complete lockdown of the city of Wuhan, the epicenter of the outbreak. People were required to stay at home to minimize the risk of virus transmission. Great efforts were made to identify all the suspected cases, enhance treatment of the confirmed cases and reduce the fatality rate. In Wuhan, two hospitals were constructed within two weeks, and a number of public facilities were converted into makeshift hospitals to admit all those patients with a positive diagnosis.

These efforts have yielded positive progress. Over the last few days, new confirmed cases and suspected cases have begun to decline both inside and outside the epicenter. The latest report, issued on Thursday, showed no new infections in 26 out of 31 province-level regions in China. Overall, the daily number of patients cured and discharged now surpasses that of new confirmed cases.

China's actions were not simply to benefit our own people. By imposing stringent and forceful measures at home and working closely with the international community, including the World Health Organization, China served as a strong line of defense against the rapid spread of the epidemic, buying precious time for other countries to enhance preparedness. By providing timely updates on the epidemic and sharing information about our sequencing of the virus, we made it easier for other countries to tackle the virus on their shores. WHO Director-General Tedros Adhanom Ghebreyesus commended China for "the extraordinary measures it has taken to contain the outbreak" and for "setting a new standard" for epidemic response.

New viruses like this one are a reminder that in the globalized era, epidemics know no borders. As Tedros noted, "This is time for solidarity, not stigma."

Yet despite our need to work together, there have been disturbing reports from around the world about discrimination and stigmatization of the Chinese community. Xenophobia has gone rampant on social media. People who appear to be of Chinese descent have been physically and verbally attacked, and patients have shunned doctors of Chinese descent. And despite its unparalleled response to the crisis, the Chinese government has been attacked by some people out of ideological prejudice. The virus is understandably a source of concern, but it should not be exploited as an excuse for xenophobia or advancing a political agenda. At a time when the world is working hard to contain the spread of the coronavirus, we should guard against the spread of political and racist viruses as well.

What is gratifying is that there has also been an outpouring of support. We have received messages of empathy as well as donations of money and medical supplies, and these things have warmed the hearts of Chinese people and boosted the strength and confidence of those fighting at frontline.

At present, with about 90 countries reporting confirmed cases of COVID-19 and some still seeing a rapid increase of new infections, the global situation remains grim. It continues to demand international coordination and cooperation.

The outbreak is a reminder that, in the globalized era, we all live in a community with a shared future. China is committed to cooperating across borders on a worldwide response to the virus. While continuing to fight the epidemic at home, we will do as much as we can to assist those countries and regions experiencing a spread of the infections. We will further participate in global health governance and work together with international community to better address non-traditional security challenges.

COVID-19 won't be the last international health crisis, and the bonds we forge today in coping with it will serve us well in the future.
Zhang Ping is consul general of the People's Republic of China in Los Angeles.

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Op-Ed: In the global response to COVID-19, there's no room for racism

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In recent weeks, China has faced an unprecedented public health challenge. The novel coronavirus that causes COVID-19 has taken more than 3,000 lives and infected more than 80,000 people on the Chinese mainland.

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"If you're scared of me, get up and leave."

By

Ms. Tien is an entrepreneur.

Because of misplaced fear, Asians may be facing something more contagious than Covid-19: harassment and racism. Credit... Nicole Bengiveno/The New York Times

LOS ANGELES - I turned 24 last month. The day before my birthday, I walked into a nail salon to get myself a birthday manicure. After I was seated, a nail technician walked over. She was an Asian woman in her 50s. She sat down and I smiled at her. I couldn't see if she smiled back because she was wearing a face mask.

The technician looked at my hands, as if considering their shape, and then suddenly asked, "Are you Chinese?"

"I am," I responded. "Are you?"

"No," she said quickly, "I am Vietnamese. We all are in the salon. But are you from-China Chinese?" She raised an eyebrow, her tone like the edge of a blade, sharp and cold.

I shifted uncomfortably in the seat, suddenly very aware she was holding my hands. "I'm from mainland China and Taiwan."

"You know, we are scared of you Chinese people," she said loudly, because you eat "weird" food "and bring it here. Chinese people, I don't like you, you are so bad, so bad and so gross."

There was a moment when I couldn't even hear what she was saying anymore. I could only focus on the slight shifts in her face mask as she continued to rant.

Finally, my voice cracking, I said: "I just came back from China in January. If you're scared of me, get up and leave." The technician went silent. The manager, who had been listening nearby, ran over to intervene. When I looked up, I realized everyone in the salon had been listening. I turned to the woman on my right, then to the other workers who were to my left. Each person I turned to looked away. The room was silent.

The manager made my nail technician leave and apologized quietly, offering a free manicure. I bit my lips to stop the trembling.

This past month, I've made less eye contact with people when I've walked outside. When I felt like coughing, I smothered the urge by biting my tongue. When I went to shake someone's hand at a party, I instinctively scanned their arm for the tiniest jerk back, a moment of hesitation. When I went to a restaurant in Santa Monica, Calif., the awareness of my being the only Chinese person sat heavier in my gut than anything I ate at lunch.

All the while, I watched news headlines snowball from unforgiving takedowns about Chinese people and their supposed " hygiene problems" to random pictures of Asian-Americans walking down the street splayed as cover art for articles about non-Asian coronavirus patients.

It dawned on me: Sensational reporting and social media were making fear more contagious than the virus itself.

I realized my friends in the United States read only the headlines about the coronavirus but knew nothing about the stories behind them. They didn't hear from our family friend whose mother, a doctor, flew from Guangdong Province to Wuhan to volunteer with thousands of other hospital workers. They didn't see the lines etched into doctors' and nurses' faces from wearing face masks and goggles nonstop for weeks.

My non-Asian friends don't have friends in China who carefully ration their meals into daily slivers because supermarket shelves are empty. They don't see the internet activity in cities across Asia, where people come together to comfort one another during quarantine, to be together even when they are apart.

People in America aren't sharing enough of these stories because what they really want to share is fear. Fear generated by the headlines that my friends whisper about over every meal.

Fear arouses us more. Fear is viral. When fear is coursing through every group chat, Instagram story, news headline, people don't stop to ask: Are we hurting anyone by perpetuating it?

After I rushed home from the nail salon that day, my mother and I called the owner. We asked her to let us come into her store and speak to her staff. The owner agreed.

The next morning, my mother, two friends and I gathered in a circle with the entire salon staff of Asian women. At first, no one said anything. But slowly, one by one, they started asking questions that revealed their foremost fear: the coronavirus death rate.

I brought up a report by the Chinese Center for Disease Control and Prevention: It had the Covid-19 fatality rate at 2.3 percent. The latest report from the World Health Organization shows the global fatality rate at 3.4 percent, but the rate varies from country to country. In South Korea, where thousands have been tested and 35 have died, the rate is currently about 0.6 percent.

And considering that the number of cases that are not reported - because of mild symptoms - is probably high, epidemiologists believe that the death rate could be under 1 percent, and even lower in China once you look outside of Wuhan. About 80 percent of Covid-19 cases appear to be mild and do not require medical treatment. They resolve on their own. Chinese analysts have found that 1.2 percent of Covid-19 cases are completely asymptomatic.

We also talked about how perpetuating harmful stereotypes that Chinese people eat "weird" food can be detrimental not just to Chinese people but also to all Asians. After all, to many Americans, we all look the same.

My voice a little unsteady, I shared with the women that the incident in the salon left me shaky for the rest of the day. That by nighttime, my anger had melted away to tears, leaving me collapsed on the couch.

But something haunted me more than the nail technician's rant: The silence in the room when everyone heard it.

Silence is deafening. Silence is enabling. In my family people call me the pit bull because I'm the first to fight back if someone attacks my people. In the one moment I tried and failed to be my own pit bull, no one stepped in to be mine.

At the end of our conversation, there was a brief silence, and then a woman stepped forward. She said quietly: "This has happened to me too. People said bad things to me, too, because of virus." The manager, who had been profusely apologizing, stopped. Her face softened to sadness.

"Customers come in and ask me again and again, am I Chinese, have I been to China, do I have the virus," she said. "I didn't know what to say before when people say bad things. Now I know."

The coronavirus is serious. It is worth taking protective measures against. I am also wary of it. But in the past few weeks, I've learned to be fearful of things possibly more contagious than Covid-19: racism and the silence of those who witness it.

If you see someone like me being harassed or attacked, step in. Say something. If you can't say something, at least check on the person afterward. Share factson social media about Covid-19, not fear.

I have a little brother I want to protect and parents who I hope can walk into a store and not be made to feel inhuman. With every word I write, I think: We cannot forsake love even in fear, because that's when we need it most.

Celine Tien is the founder and chief executive of Flowly: Relaxation Training, a mobile virtual reality app for chronic pain and anxiety management.
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Opinion | I'm Chinese. That Doesn't Mean I Have Coronavirus.

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"If you're scared of me, get up and leave." By Ms. Tien is an entrepreneur. LOS ANGELES - I turned 24 last month. The day before my birthday, I walked into a nail salon to get myself a birthday manicure. After I was seated, a nail technician walked over.

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My freshman year in high school, I was playing an improv game in my theatre class. Everyone stood in a circle; one person began acting out what object or noun they were and then someone else jumped into the circle, acting as another object or noun that was subsequently added to the scenario. Usually, if people's instinctive responses to playful prompts are not racist, the game is light-hearted. For instance, if one person jumps in acting like a dog, the next person jumps in acting like a fire hydrant.

But alas, as the second round of the improv game progressed, it quickly turned volatile: One person jumped in saying they were a police officer and immediately after, the next person said they were "an african american" and then the following person jumped in with wide eyes and waving hands, exclaiming that he was "Ebola." I left the room after this, so I am not sure how the game continued.

Conversations surrounding Ebola a few years ago were certainly racially charged; however, apart from that improv game, I was not particularly tuned into the discourse. But that was my first experience with racialized pathology. Now, with the spread of Coronavirus, I have employed the help of several of my friends to discuss the impact of the prejudicial and ignorant rhetoric that has proliferated alongside the virus.

Gracie Lu '21 expressed her thoughts, saying that she feels the current situation is just "another reminder that when people see Chinese/other Eastern Asian people we are still viewed as un-American." She continues, pointing out how nonsensical it is to associate Asian Americans with Coronavirus: "Because obviously, if we are all in America, Asian people and white people have the same likelihood of contracting the disease because they are offered the same exposure."

Feelings of being "othered" and feared have affected another friend of mine. Jerry Ahn '20 voiced: "I am worried about the coming months since I have a pollen allergy, and I don't want to be sneezing everywhere and freaking people out."

Jerry's concern of other people's uneducated and prejudicial misdiagnosis of his seasonal allergies as COVID-19 actually transpired for Cat Huang '21, who, a few weeks ago, got sick with the flu. She shared: "A facetious rumor spread that I had the Coronavirus." Though she was not bothered, because she knew it wasn't true, at the same time she said: "I kind of realized that this rumor would have never spread in the same way if I had been white ... This rumor only held ground because it was attached to my Asian face."

Jonathan Zheng '22 agrees, saying that despite the racial "face" the virus has taken, "coronavirus sees no race." And though "confronting acts of racism isn't as easy as washing your hands, the implications of containing xenophobia is just as important as containing coronavirus."

While in many ways the public's dread of contracting Coronavirus is misguided, the dread Yuan Chen '22 feels about going back home is not. Yuan relayed a conversation she and a friend were having: "We are scared to go back to NYC because of all the xenophobic attacks that [have] happened." Jerry expressed similar worries, saying: "The main thing is that I'm sad my parents probably won't be able to attend my graduation since they live in South Korea."

Italy - as of now - has the second highest record of COVID-19 cases, and while many Chinese restaurants have become financially decimated, Niko Nguyen '22 points out, "Olive Garden is still doing well." Though he says this in jest, he expands on his point, saying, "there should be an awareness of who you are thinking of when you are thinking about Coronavirus." In a Code Switch podcast episode focused on Coronavirus, historian Erika Lee discusses the weaponizing power of xenophobia. Since this weaponization is compounded by stereotypes and prejudices attributed to "threatening" races, she doubts "that we're going to see the same types of exclusions or informal acts of discrimination targeting Italians or Italian restaurants or Italian communities in the same way that we're seeing this with China." Italians, unlike the Asian community, are white, and - historically, presently and continually - are thus, harmless.

There is a double crisis happening in this world, of both health and injustice. Because while a global viral outbreak is distressing and scary, so too is the profound racism and xenophobia that it has unmasked.

There is a double crisis happening in this world, of both health and injustice.

Sidney Malia Waite is a sophomore in the School of Industrial and Labor Relations. She can be reached at swaite@cornellsun.com. Waite, What? runs every other Monday this semester.

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WAITE | Unmasking the Racist Infection of the Coronavirus

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My freshman year in high school, I was playing an improv game in my theatre class. Everyone stood in a circle; one person began acting out what object or noun they were and then someone else jumped into the circle, acting as another object or noun that was subsequently added to the scenario.

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he new coronavirus is not an equal-opportunity killer: Being elderly and having other illnesses, for instance, greatly increases the risk of dying from the disease the virus causes, Covid-19. It's also possible being male could put you at increased risk.

For both medical and public health reasons, researchers want to figure out who's most at risk of being infected and who's most at risk of developing severe or even lethal illness. With that kind of information, clinicians would know whom to treat more aggressively, government officials would have a better idea of steps to take, and everyone would know whether they need to take special, additional precautions.

Here's what research has shown three months into the outbreak:

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Old and young
The vast majority of cases in China - 87% - were in people ages 30 to 79, the China Center for Disease Control reported last month based on data from all 72,314 of those diagnosed with Covid-19 as of Feb. 11. That probably reflects something about biology more than lifestyle, such as being in frequent contact with other people. Teens and people in their 20s also encounter many others, at school and work and on public transit, yet they don't seem to be contracting the disease at significant rates: Only 8.1% of cases were 20-somethings, 1.2% were teens, and 0.9% were 9 or younger. The World Health Organization mission to China found that 78% of the cases reported as of Feb. 20 were in people ages 30 to 69.

The death toll skews old even more strongly. Overall, China CDC found, 2.3% of confirmed cases died. But the fatality rate was 14.8% in people 80 or older, likely reflecting the presence of other diseases, a weaker immune system, or simply worse overall health. By contrast, the fatality rate was 1.3% in 50-somethings, 0.4% in 40-somethings, and 0.2% in people 10 to 39.

The age-related death risk probably reflects the strength, or weakness, of the respiratory system. About half of the 109 Covid-19 patients (ages 22 to 94) treated at Central Hospital of Wuhan, researchers there reported, developed acute respiratory distress syndrome (ARDS), in which fluid builds up in the small air sacs of the lungs. That restricts how much air the lungs can take in, reducing the oxygen supply to vital organs, sometimes fatally; half of the ARDS patients died, compared to 9% of patients who did not develop the syndrome.

The ARDS patients had an average age of 61, compared to an average age of 49 for those who did not develop ARDS. Elderly patients "were more likely to develop ARDS," the researchers wrote, suggesting how age can make Covid-19 more severe and even fatal: age increases the risk that the respiratory system will basically shut down under viral assault.

Youth, in contrast, seems to be protective. The WHO mission reported a relatively low incidence in people under 18, who made up only 2.4% of all reported cases. In fact, through mid-January, zero children in Wuhan, the epicenter of the outbreak, had contracted Covid-19. It's not clear whether that's because children do not show signs of illness even if infected.

Even cases among children and teens aged 10 to 19 are rare. As of Feb. 11 there were 549 cases in that age group, 1.2% of the total, China CDC found. Only one had died.

One intriguing explanation for the apparent resilience of youth: in regions near Hubei province, young children seem especially likely to be exposed to other coronaviruses, scientists in China reported in 2018. That might have given them at least partial immunity to this one.
Men and women
The effect of sex on susceptibility to Covid-19 is less clear than the age effect, but preliminary data suggest men might be more susceptible. China CDC found that 106 men had the disease for every 100 women, while the WHO mission found that men make up 51% of cases. A study of 1,099 Covid-19 patients in Wuhan through Jan. 29 found a greater imbalance: 58% were male, the China Medical Treatment Expert Group for Covid-19 reported last week in the New England Journal of Medicine.

It's possible the apparent sex imbalance reflects patterns of travel and contacts that make men more likely to be exposed to carriers of the virus, not any inherent biological differences. It's also possible the apparent worse disease severity in men could skew the data. Among hospitalized patients, there is "a slight predominance of men," U.S. researchers wrote last week in JAMA. If the virus hits men harder than women, health care systems will see, test, and count more men.

To determine if there are sex differences in susceptibility to infection would require an unethical experiment: expose 1,000 otherwise similar men and women to the virus and see who gets sick.

The difference is fatality rates, however, is real: 1.7% for women and 2.8% for men, China CDC reported.
Sick or healthy
The male-female difference in fatality rates, and perhaps in reported incidence, may arise from differences in underlying health. People with pre-existing illness are more likely to get seriously ill from Covid-19, and men have a higher incidence of such chronic illnesses as cardiovascular disease.

In the first large study of the effect of underlying illness, researchers in China analyzed 1,590 patients from throughout the country with laboratory-confirmed disease. They calculated how "co-morbidities" - existing illnesses - affected the risk of being admitted to intensive care, being put on a ventilator, or dying.

After taking into account the patients' ages and smoking status, the researchers found that the 399 patients with at least one additional disease (including cardiovascular diseases, diabetes, hepatitis B, chronic obstructive pulmonary disease, chronic kidney diseases, and cancer) had a 79% greater chance of requiring intensive care or a respirator or both, or of dying, they reported last week in a paper posted to medRxiv, a preprint site that posts research before it has been peer-reviewed. The 130 with two or more additional diseases had 2.5 times the risk of any of those outcomes.

That fits with what's known about other respiratory viruses. People with a single co-morbidity who catch avian flu (H7N9) are 3.4 times more likely than otherwise-healthy flu patients to require ventilators and other intensive care. SARS and MERS, which are also caused by coronaviruses, are more severe in patients with underlying illnesses, too.

Breaking down the Covid-19 risk with the most common co-morbidities, the scientists found that cancer raises the risk 3.5-fold, COPD 2.6-fold, and diabetes and hypertension by about 60%. Because it isn't unusual for someone to have an underlying disease (especially diabetes and hypertension) but not know it, the last figure is likely an underestimate.

Co-morbidities also raise the risk of dying from Covid-19. China CDC's analysis of 44,672 patients found that the fatality rate in patients who reported no other health conditions was 0.9%. It was 10.5% for those with cardiovascular disease, 7.3% for those with diabetes, 6.3% for people with chronic respiratory diseases such as COPD, 6.0% for people with hypertension, and 5.6% for those with cancer.

Underlying disease might change the course of Covid-19. During the height of the epidemic in Wuhan, 37 of 230 patients receiving dialysis for kidney failure at Remnin Hospital developed the disease. Even though none were sick enough to require intensive care or a mechanical ventilator, six of them died, for a very high fatality rate of 16%. Oddly, however, none of the six died of pneumonia, Remnin researchers reported. Instead, the causes of death were heart disease, stroke, and high blood levels of potassium (a result of kidney failure). The high fatality rate of Covid-19 in already-sick people might result not from the virus but from an exacerbation of existing disease.

About 60% of U.S. adults have at least one underlying health condition, Tom Frieden, former director of the U.S. Centers for Disease Control and Prevention, told reporters on Monday.
Pregnancy
In early February, Chinese state media reported that a woman infected with the virus gave birth to a baby who later tested positive for it. Newborns might become infected because of close proximity to a patient, like anyone else, but the case raised fears that a pregnant woman can transmit the virus to her fetus via the placenta.

Only one small study has investigated such "vertical transmission." Scientists at Wuhan University found that, of nine pregnant patients infected with the virus (all had a caesarean section) in their third trimester, none seemed to pass the virus to their babies, all of whom scored at the top of the Apgar scale of newborn health.

As for the mothers, "Covid-19 seems not to be especially severe in pregnant women, at least based on the small number in this study," the scientists wrote. That was somewhat surprising because pregnancy suppresses the immune system (so it doesn't attack the fetus); pregnant women are more susceptible to respiratory pathogens than non-pregnant women. Nevertheless, none of the nine women developed severe Covid-19 pneumonia.

It may be that immuno-suppression is actually helpful. Some of the most serious symptoms of Covid-19 result from an immune system on the rampage rather than a lethargic one, Chinese scientists found: An extreme immune response called cytokine storm, a flood of immune cells and the biochemicals they produce, tears through lung tissue.

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Who is getting sick? A look at coronavirus risk by age, gender, and more

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he new coronavirus is not an equal-opportunity killer: Being elderly and having other illnesses, for instance, greatly increases the risk of dying from the disease the virus causes, Covid-19. It's also possible being male could put you at increased risk.

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On Monday, Donald Trump held a meeting in the White House to discuss his Administration's response to COVID-19, the novel coronavirus that has spread to every continent except Antarctica. At the time there had been more than a hundred and five thousand cases reported in at least eighty-three countries, leading to more than thirty-five hundred deaths. Seated around an oval table in the Cabinet Room were health experts from the Centers for Disease Control and Prevention, the Food and Drug Administration, and the National Institutes of Health, as well as pharmaceutical executives from Pfizer, Johnson & Johnson, Sanofi, and others. With more than a hundred cases already discovered in the U.S., which had resulted in six deaths (the virus has since infected nearly four hundred people in the U.S., and killed at least nineteen of them), Trump was concerned. But he was also confused, despite having had several previous briefings with the Administration's top health officials. Grasping for some good news, he pressed the executives to deliver a vaccine within a few months, at which point Anthony Fauci, the longtime director of the National Institute of Allergy and Infectious Diseases (N.I.A.I.D.), spoke up. "A vaccine that you make and start testing in a year is not a vaccine that's deployable," he said. The earliest it would be deployable, Fauci added, is "in a year to a year and a half, no matter how fast you go."

The virus seems to have been circulating in the United States, particularly in Washington State, for the past month, and more cases are expected. A person can be infected but asymptomatic, and therefore unknowingly infect other people. This limits the ability of public-health tools to contain its spread. Even still, a COVID-19 vaccine developed, licensed, and manufactured at a global scale in twelve months would be an unprecedented, remarkable, even revolutionary achievement. No other vaccine has come close to being developed that quickly. The fastest effort to date was during the Zika outbreak, in 2015, when one was ready for testing in about seven months, but the epidemic fizzled out before an approved vaccine could be sent through clinical trials. At the meeting on Monday, Trump said, "I like the sound of a couple months better, if I must be honest."

John Shiver, the global head of vaccine research and development at the multinational pharmaceutical company Sanofi, which is developing a COVID-19 vaccine, was at the meeting with Trump. "There was some confusion there," Shiver said, that certain officials did not understand that "being in people," as in human trials, is not the same as having a product. Clinical trials are conducted on healthy people, which is inherently challenging. "You certainly don't want a vaccine that can make it worse," Shiver said. "There have been some vaccine candidates historically that could actually enhance the disease." Sanofi is working with the United States Biomedical Advanced Research and Development Authority, a sort of biomedical DARPA, to advance a COVID-19 vaccine based largely on the vaccine candidate it had developed for SARS. Shiver told me that the authority doesn't expect to have anything ready for human trials until much later this year. "It's difficult," Shiver said, "to see how, even in the case of an emergency, a vaccine could be fully ready for licensure in a year and a half."

The Coalition for Epidemic Preparedness Innovations ( CEPI), an Oslo-based nonprofit organization, was established at Davos, in 2017, to help the world prepare for a "disease X" pandemic. One of its aims is to dramatically hasten the process of vaccine development. To create a viable, scalable vaccine "takes vast amounts of funding and R. & D.," Rachel Grant, the advocacy and communications director at CEPI, told me. "It is a long and complex business. It's all doable, science can meet the challenges, but there is lots of attrition" before any vaccine gets to the point of licensure. The problem is twofold. First, there may never be a market for a vaccine at the end of the development process, because the epidemic is contained, or never comes to pass. Then, traditionally, if there is an epidemic, it may take hold in a developing country where the costs of research and development cannot be recouped. "The resources and expertise sit in biotech and pharma, and they've got their business model," Grant said. "They're not charities. They can't do this stuff for free."

CEPI, with funding from the government of Norway, the Gates Foundation, the Wellcome Trust, and several other countries (the United States is not among them), is trying to bridge the gap. The challenge of vaccine development is "what CEPI was set up to solve," Grant told me, "played out writ large in an episode like this." Since the novel coronavirus emerged, CEPI has ramped up its grant-making expenditures to more than nineteen million dollars. Two grant recipients-a Massachusetts-based biotech startup named Moderna and a lab at the University of Queensland, in Brisbane, Australia-have, remarkably, already developed a vaccine candidate that they will start testing in human trials in the next few months, and another biotech startup supported by CEPI is not far behind. But, ultimately, to get three different vaccines through the final phase of clinical testing, Nick Jackson, CEPI 's head of programs and innovative technology, told me, will require an estimated two billion dollars.

Barney Graham is the deputy director of the Vaccine Research Center, at the N.I.A.I.D., in Bethesda, Maryland, which is collaborating with Moderna and other academic labs on a possible vaccine. Graham is one of the world's experts on the structure of viruses and how they interact with human cells to make us sick. In the seven years before the COVID-19 virus appeared, one of Graham's projects had involved understanding the MERS coronavirus, in order to potentially develop a vaccine. ( MERS, which can be transmitted from camels to humans, has been contained to the Middle East, and seems to spread mostly in confined spaces, like hospitals.) "There's several ways of delivering a protein to a human body that will make a vaccine-type response," he told me. Certain proteins, when injected into a human, are antigenic, provoking the body's immune system to create antibodies. Traditionally, proteins are made "in a microbrewery type of bioreactor," Graham said-a common flu-virus vaccine, for instance, is grown in chicken eggs-and it "takes up to two years to get that protein ready. That is not fast enough if you're in a pandemic situation." Researchers have long been working on so-called vaccine-platform manufacturing technologies for future use. The idea is akin to creating a frozen-yogurt maker for vaccines-same machine, different flavors. With vaccine-platform technologies, the hope is that the way in which the vaccine is manufactured and delivered to the body-such as Moderna's messenger-RNA (mRNA) technology-will transport any antigen and, therefore, theoretically protect against any infectious disease. "You can make the RNA in the same way, purify it in the same way, release it in the same way, and yet make many different proteins," Graham said.

In Moderna's case, the vaccine contains a synthetic version of mRNA. When injected into a muscle cell, the mRNA acts like a drill sergeant, ordering the cell to create a doppelgänger of one of the coronavirus's surface proteins-known as "spikes," which, together, decorate the surface of the virus, giving the appearance of a crown. The spike protein is only part of the virus and therefore won't make a person sick. But it is a crucial component of how the virus infects a human cell. In a sense, the Moderna technology outsources the labor of building these spike proteins to our own bodies. Once our muscle cells follow the vaccine's mRNA orders, and manufacture loads of these spike-protein doppelgängers, our immune system recognizes them as foreign objects and learns how to fight them by creating antibodies.

Moderna has done several different vaccine trials with its mRNA "platform," a few in partnership with Graham and the Vaccine Research Center. Among other things, they have tested MERS coronavirus vaccines in mice.. (There are now, including COVID-19, seven known coronaviruses that infect humans, and many more carried by animals; four of them circulate in the population and are responsible for common colds, and the other two are SARS and MERS.) "The early data we already have with the mice shows it is working the way it should," Graham said. "If this was a virus from a different family, we would not be nearly as prepared."

On the other side of the world, at the University of Queensland, Keith Chappell is working on what he and his two co-inventors call a "molecular clamp," a different type of rapid-response vaccine platform, also funded in part by CEPI. The molecular-clamp vaccine uses a more traditional method compared to what Moderna is making; its shot would already contain the spike protein. The big difference is that Chappell's team has found a way to incorporate a lab-created polypeptide (or sequence of amino acids)-"the clamp"-into the spike protein, to insure that the protein remains stable, folded like origami, in precisely the right configuration, thereby provoking a strong, accurate immune response (i.e., lots of appropriate antibodies). After years of working in cell cultures (Chinese-hamster ovaries, or CHO, the standard mammalian cell line used in therapeutic biomedical research), Chappell's team plans to start testing its vaccine on about a hundred healthy adult volunteers, and he estimates that a trial will begin sometime this summer. "It's a terrifying prospect, what's occurring currently," Chappell told me, by phone, from his lab in Brisbane. "It's a lot of weight on our shoulders, and a lot of pressure."

Even if the virus wanes in the warmer months, as does influenza, it will have circulated in the population already, and could reëmerge in the fall. For now, although the total number of infections worldwide is unknown, experts estimate, crudely, that the virus has a mortality rate between 0.5 per cent and two per cent. The flu, which kills, on average, between twenty thousand and forty thousand people each year in this country alone, has a mortality rate of 0.1 per cent. "We're still learning a lot about the virus, what we were all watching for, and what has emerged is that it is readily spread person to person in a community setting, more so than SARS or MERS," John Mascola, the director of the Vaccine Research Center at the N.I.A.I.D., told me. "That is not surprising, but it is concerning. There is the potential for the virus to really establish itself in a human population, and not go away quickly."

On Tuesday, Trump toured Mascola's Vaccine Research Center, where about five hundred scientists are at work. (On Friday, the President signed an $8.3 billion emergency-aid package to counter the virus; some of the funds will go toward the Vaccine Research Center's work.) Kizzmekia Corbett, the research fellow leading the COVID-19 vaccine team, explained the basics of virology to Trump-a student whom she had not anticipated-and other researchers showed off jumbo models of the coronavirus's spike protein as Trump looked on, nonplussed. "The environment here is one of a lot of excitement," Mascola later told me. "It's gratifying to be recognized by the leadership, but, honestly, a lot of what we do is not recognized at that kind of level, and that really doesn't matter. We do what we do because of the love of the science and our commitment to public health."

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How Long Will It Take to Develop a Coronavirus Vaccine?

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On Monday, Donald Trump held a meeting in the White House to discuss his Administration's response to COVID-19, the novel coronavirus that has spread to every continent except Antarctica. At the time there had been more than a hundred and five thousand cases reported in at least eighty-three countries, leading to more than thirty-five hundred deaths.

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Vaccines contain the same germs that cause disease. (For example, measles vaccine contains measles virus, and Hib vaccine contains Hib bacteria.) But they have been either killed or weakened to the point that they don't make you sick. Some vaccines contain only a part of the disease germ.

A vaccine stimulates your immune system to produce antibodies, exactly like it would if you were exposed to the disease. After getting vaccinated, you develop immunity to that disease, without having to get the disease first.

This is what makes vaccines such powerful medicine. Unlike most medicines, which treat or cure diseases, vaccines prevent them.

For more than the basics, see:

See also:

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Vaccines contain the same germs that cause disease. (For example, measles vaccine contains measles virus, and Hib vaccine contains Hib bacteria.) But they have been either killed or weakened to the point that they don't make you sick. Some vaccines contain only a part of the disease germ.

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As the number of coronavirus infections approaches 100,000 people worldwide, researchers are racing to understand what makes it spread so easily.

A handful of genetic and structural analyses have identified a key feature of the virus - a protein on its surface - that might explain why it infects human cells so readily.

Other groups are investigating the doorway through which the new coronavirus enters human tissues - a receptor on cell membranes. Both the cell receptor and the virus protein offer potential targets for drugs to block the pathogen, but researchers say it is too early to be sure.

"Understanding transmission of the virus is key to its containment and future prevention," says David Veesler, a structural virologist at the University of Washington in Seattle, who posted his team's findings about the virus protein on the biomedical preprint server bioRxiv on 20 February.

The new virus spreads much more readily than the one that caused severe acute respiratory syndrome, or SARS (also a coronavirus), and has infected more than ten times the number of people who contracted SARS.

Spiky invader

To infect a cell, coronaviruses use a 'spike' protein that binds to the cell membrane, a process that's activated by specific cell enzymes. Genomic analyses of the new coronavirus have revealed that its spike protein differs from those of close relatives, and suggest that the protein has a site on it which is activated by a host-cell enzyme called furin.

This is significant because furin is found in lots of human tissues, including the lungs, liver and small intestines, which means that the virus has the potential to attack multiple organs, says Li Hua, a structural biologist at Huazhong University of Science and Technology in Wuhan, China, where the outbreak began. The finding could explain some of the symptoms observed in people with the coronavirus, such as liver failure, says Li, who co-authored a genetic analysis of the virus that was posted on the ChinaXiv preprint server on 23 February. SARS and other coronaviruses in the same genus as the new virus don't have furin activation sites, he says.

The furin activation site "sets the virus up very differently to SARS in terms of its entry into cells, and possibly affects virus stability and hence transmission", says Gary Whittaker, a virologist at Cornell University in Ithaca, New York. His team published another structural analysis of the coronavirus's spike protein on bioRxiv on 18 February.

Several other groups have also identified the activation site as possibly enabling the virus to spread efficiently between humans. They note that these sites are also found in other viruses that spread easily between people, including severe strains of the influenza virus. On these viruses, the activation site is found on a protein called haemagglutinin, not on the spike protein.

Urging caution

But some researchers are cautious about overstating the role of the activation site in helping the coronavirus to spread more easily. "We don't know if this is going to be a big deal or not," says Jason McLellan, a structural biologist at the University of Texas at Austin, who co-authored another structural analysis of the coronavirus, which was published in Science on 20 February.

Other scientists are wary of comparing furin activation sites on flu viruses to those on the new coronavirus. The haemagglutinin protein on the surface of flu viruses isn't similar or related to the spike protein in coronaviruses, says Peter White, a virologist at the University of New South Wales in Sydney, Australia.

And the flu virus that caused the deadliest recorded pandemic, the 1918 Spanish flu pandemic, doesn't even have a furin activation site, says Lijun Rong, a virologist at the University of Illinois in Chicago.

Whittaker says studies in cell or animal models are needed to test the activation site's function. "Coronaviruses are unpredictable, and good hypotheses often turn out to be wrong," he says. His team is currently testing how removing or modifying the site affects the spike protein's function.

Drug targets

Li's team are also looking at molecules that could block furin, which could be investigated as possible therapies. But their progress is slow because of the outbreak. Li lives on campus and is currently the only member able to access his team's laboratory.

McLellan's group in Texas has identified another feature that could explain why the new coronavirus infects human cells so successfully. Their experiments have shown that the spike protein binds to a receptor on human cells - known as angiotensin-converting enzyme 2 (ACE2) - at least ten times more tightly than does the spike protein in the SARS virus.

Veesler's team also found that the spike protein binds with high affinity to the ACE2 receptor, which suggests that the receptor is another potential target for vaccines or therapies. For example, a drug that blocks the receptor might make it harder for coronavirus to enter cells.
doi: https://doi.org/10.1038/d41586-020-00660-x
Updates & Corrections

Correction 11 March 2020: An earlier version of this story misstated a result from David Vessler's study on ACE2.

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Why does the coronavirus spread so easily between people?

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Researchers have identified microscopic features that could make the pathogen more infectious than the SARS virus - and serve as drug targets. Researchers have identified microscopic features that could make the pathogen more infectious than the SARS virus - and serve as drug targets.

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Centers for Disease Control and Prevention

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COVID-19 is a new disease and we are still learning how it spreads, the severity of illness it causes, and to what extent it may spread in the United States.

How COVID-19 Spreads

Person-to-person spread

The virus is thought to spread mainly from person-to-person.

Between people who are in close contact with one another (within about 6 feet).

Through respiratory droplets produced when an infected person coughs or sneezes.

These droplets can land in the mouths or noses of people who are nearby or possibly be inhaled into the lungs.

Can someone spread the virus without being sick?

People are thought to be most contagious when they are most symptomatic (the sickest).

Some spread might be possible before people show symptoms; there have been reports of this occurring with this new coronavirus, but this is not thought to be the main way the virus spreads.

Spread from contact with contaminated surfaces or objects

It may be possible that a person can get COVID-19 by touching a surface or object that has the virus on it and then touching their own mouth, nose, or possibly their eyes, but this is not thought to be the main way the virus spreads.

How easily the virus spreads

How easily a virus spreads from person-to-person can vary. Some viruses are highly contagious (spread easily), like measles, while other viruses do not spread as easily. Another factor is whether the spread is sustained, spreading continually without stopping.

The virus that causes COVID-19 seems to be spreading easily and sustainably in the community ("community spread") in some affected geographic areas.

Community spread means people have been infected with the virus in an area, including some who are not sure how or where they became infected.

International Areas with Sustained (Ongoing) Transmission
Last updated February 28, 2020

Related Links

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how is coronavirus disease 2019 (covid-19) spread

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transmission of coronavirus disease 2019 (covid-19)

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COVID-19 is a new disease and we are still learning how it spreads, the severity of illness it causes, and to what extent it may spread in the United States. The virus is thought to spread mainly from person-to-person. Between people who are in close contact with one another (within about 6 feet).