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The Spanish flu, also known as the 1918 flu pandemic, was an unusually deadly influenza pandemic. Lasting almost 36 months from January 1918 to December 1920, it infected 500 million people – about a third of the world's population at the time.The death toll is estimated to have been anywhere from 17 million to 50 million, and possibly as high as 100 million, making it one of the deadliest pandemics in human history

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Spanish flu

Disease
Influenza

Virus strain

Strains of A/H1N1

Location

Worldwide

First outbreak

Unknown

Date

February 1918 - April 1920[1]

Suspected cases‡

500 million (estimated)

25-50 million (generally accepted), other estimates range from 17 to 100 million[3][4][5]

‡Suspected cases have not been confirmed by laboratory tests as being due to this strain, although some other strains may have been ruled out.

The 1918-1920 flu pandemic, also known as the Great Influenza epidemic or by the common misnomer Spanish flu, was an exceptionally deadly global influenza pandemic caused by the H1N1 influenza A virus. The earliest documented case was March 1918 in the state of Kansas in the United States, with further cases recorded in France, Germany and the United Kingdom in April. Two years later, nearly a third of the global population, or an estimated 500 million people, had been infected in four successive waves. Estimates of deaths range from 17 million to 50 million, and possibly as high as 100 million, making it one of the deadliest pandemics in history.

The pandemic broke out near the end of World War I, when wartime censors in the belligerent countries suppressed bad news to maintain morale, but newspapers freely reported the outbreak in neutral Spain, creating a false impression of Spain as the epicenter and leading to the "Spanish flu" misnomer. Limited historical epidemiological data make the pandemic's geographic origin indeterminate, with competing hypotheses on the initial spread.

Most influenza outbreaks disproportionately kill the young and old, with a higher survival rate in-between, but this pandemic had unusually high mortality for young adults. Scientists offer several explanations for the high mortality, including a six-year climate anomaly affecting migration of disease vectors with increased likelihood of spread through bodies of water. The virus was particularly deadly because it triggered a cytokine storm, ravaging the stronger immune system of young adults, although the viral infection was apparently no more aggressive than previous influenza strains. Malnourishment, overcrowded medical camps and hospitals, and poor hygiene, exacerbated by the war, promoted bacterial superinfection, killing most of the victims after a typically prolonged death bed.

The 1918 Spanish flu was the first of three flu pandemics caused by H1N1 influenza A virus; the most recent one was the 2009 swine flu pandemic. The 1977 Russian flu was also caused by H1N1 virus.

Etymologies

El Sol (Madrid), 28 May 1918: "The three-day fever - In Madrid 80,000 Are Infected - H.M. the King is sick"

This pandemic was known by many different names-some old, some new-depending on place, time, and context. The etymology of alternative names historicises the scourge and its effects on people who would only learn years later that invisible viruses caused influenza. The lack of scientific answers led the Sierra Leone Weekly News ( Freetown) to suggest a biblical framing in July 1918, using an interrogative from Exodus 16 in ancient Hebrew: "One thing is for certain-the doctors are at present flabbergasted; and we suggest that rather than calling the disease influenza they should for the present until they have it in hand, say Man hu -'What is it?'"

Descriptive names

Outbreaks of influenza-like illness were documented in 1916-17 at British military hospitals in Étaples, France, and just across the English Channel at Aldershot, England. Clinical indications in common with the 1918 pandemic included rapid symptom progression to a "dusky" heliotrope cyanosis of the face. This characteristic blue-violet cyanosis in expiring patients led to the name 'purple death'.

The Aldershot physicians later wrote in , "the influenza pneumococcal purulent bronchitis we and others described in 1916 and 1917 is fundamentally the same condition as the influenza of this present pandemic." This " purulent bronchitis" is not yet linked to the same A/H1N1 virus, but it may be a precursor.

In 1918, ' epidemic influenza' ( Italian: influenza, influence), also known at the time as 'the grip' ( French: la grippe, grasp), appeared in Kansas in the U.S. during late spring, and early reports from Spain began appearing on 21 May. Reports from both places called it 'three-day fever' ( fiebre de los tres días).

Associative names

Front page of The Times (London), 25 June 1918: "The Spanish Influenza"

Many alternative names are exonyms in the practice of making new infectious diseases seem foreign. This pattern was observed even before the 1889-1890 pandemic, also known as the 'Russian flu', when the Russians already called epidemic influenza the 'Chinese catarrh', the Germans called it the 'Russian pest', while the Italians in turn called it the 'German disease'. These epithets were re-used in the 1918 pandemic, along with new ones.

'Spanish' influenza

Advertisement in The Times, 28 June 1918 for Formamint tablets to prevent "Spanish influenza"

Outside Spain, the disease was soon misnamed 'Spanish influenza'. In a 2 June 1918 of London dispatch titled, "The Spanish Epidemic," a correspondent in Madrid reported over 100,000 victims of, "The unknown disease...clearly of a gripal character," without referring to "Spanish influenza" directly. Three weeks later The Times reported that, "Everybody thinks of it as the 'Spanish' influenza to-day." Three days after that an advertisement appeared in The Times for Formamint tablets to prevent "Spanish influenza". When it reached Moscow, announced, " Ispánka (the Spanish lady) is in town," making 'the Spanish lady' another common name.

The outbreak did not originate in Spain (see below), but reporting did, due to wartime censorship in belligerent nations. Spain was a neutral country unconcerned with appearances of combat readiness, and without a wartime propaganda machine to prop up morale; so its newspapers freely reported epidemic effects, including King Alfonso XIII's illness, making Spain the apparent locus of the epidemic. The censorship was so effective that Spain's health officials were unaware its neighboring countries were similarly affected.

In an October 1918 "Madrid Letter" to the Journal of the American Medical Association, a Spanish official protested, "we were surprised to learn that the disease was making ravages in other countries, and that people there were calling it the 'Spanish grip'. And wherefore Spanish? ...this epidemic was not born in Spain, and this should be recorded as a historic vindication." But before this letter could be published, The Serbian Newspaper ( Corfu) said, "Various countries have been assigning the origin of this imposing guest to each other for quite some time, and at one point in time they agreed to assign its origin to the kind and neutral Spain..."

"Spanish influenza," "three-day fever," "the flu." by Rupert Blue, U.S. Surgeon General, 28 September 1918

Other exonyms

French press initially used 'American flu', but adopted 'Spanish flu' in lieu of antagonizing an ally. In the spring of 1918, British soldiers called it 'Flanders flu', while German soldiers used ' Flandern-Fieber' (Flemish fever), both after a famous battlefield in Belgium where many soldiers on both sides fell ill. In Senegal it was named 'Brazilian flu', and in Brazil, 'German flu'. In Spain it was also known as the 'French flu' ( gripe francesa), or the 'Naples Soldier' ( Soldado de Nápoles), after a popular song from a zarzuela. Spanish flu ( gripe española) is now a common name in Spain, but remains controversial there.

Other names derived from geopolitical borders and social boundaries. In Poland it was the ' Bolshevik disease', while the Bolsheviks referred to it as the ' Kirghiz disease'. Some Africans called it a 'white man's sickness', but in South Africa, white men also used the ethnophaulism 'kaffersiekte' (lit. negro disease). Japan blamed sumo wrestlers for bringing the disease home from a match in Taiwan by calling it 'sumo flu' ( Sumo Kaze), even though three top wrestlers died there.

World Health Organization 'best practices' first published in 2015 now aim to prevent social stigma by no longer associating culturally significant names with new diseases, listing "Spanish flu" under "examples to be avoided". Many authors now eschew calling this the Spanish flu, instead using variations of '1918-19/20 flu/influenza pandemic'.

Local names

Some language endonyms did not name specific regions or groups of people. Examples specific to this pandemic include: Northern Ndebele: 'Malibuzwe' (let enquiries be made concerning it), Swahili: 'Ugonjo huo kichwa na kukohoa na kiuno' (the disease of head and coughing and spine), Yao: 'chipindupindu' (disease from seeking to make a profit in wartime), Otjiherero: 'kaapitohanga' (disease which passes through like a bullet), and Persian: 'nakhushi-yi bad' (disease of the wind).

Other names

This outbreak was also commonly known as the 'great influenza epidemic', after the 'great war', a common name for World War I before World War II. French military doctors originally called it 'disease 11' ( maladie onze). German doctors downplayed the severity by calling it 'pseudo influenza' (Latin: pseudo, false), while in Africa, doctors tried to get patients to take it more seriously by calling it 'influenza vera' (Latin: vera, true).

A children's song from the 1889-90 flu pandemic was shortened and adapted into a skipping-rope rhyme popular in 1918. It is a metaphor for the transmissibility of 'Influenza', where that name was clipped to the apheresis 'Enza':

I had a little bird,
its name was Enza.
I opened the window,
and in-flu-enza.

First wave of early 1918

The pandemic is conventionally marked as having begun on 4 March 1918 with the recording of the case of Albert Gitchell, an army cook at Camp Funston in Kansas, United States, despite there having been cases before him. The disease had already been observed 200 miles (320 km) away in Haskell County as early as January 1918, prompting local doctor Loring Miner to warn the editors of the U.S. Public Health Service's academic journal Public Health Reports. Within days of the 4 March first case at Camp Funston, 522 men at the camp had reported sick. By 11 March 1918, the virus had reached Queens, New York. Failure to take preventive measures in March/April was later criticized.

As the U.S. had entered World War I, the disease quickly spread from Camp Funston, a major training ground for troops of the American Expeditionary Forces, to other U.S. Army camps and Europe, becoming an epidemic in the Midwest, East Coast, and French ports by April 1918, and reaching the Western Front by the middle of the month. It then quickly spread to the rest of France, Great Britain, Italy, and Spain and in May reached Wrocław and Odessa. After the signing of the Treaty of Brest-Litovsk (March 1918), Germany started releasing Russian prisoners of war, who then brought the disease to their country. It reached North Africa, India, and Japan in May, and soon after had likely gone around the world as there had been recorded cases in Southeast Asia in April. In June an outbreak was reported in China. After reaching Australia in July, the wave started to recede.

The first wave of the flu lasted from the first quarter of 1918 and was relatively mild. Mortality rates were not appreciably above normal; in the United States ~75,000 flu-related deaths were reported in the first six months of 1918, compared to ~63,000 deaths during the same time period in 1915. In Madrid, Spain, fewer than 1,000 people died from influenza between May and June 1918. There were no reported quarantines during the first quarter of 1918. However, the first wave caused a significant disruption in the military operations of World War I, with three-quarters of French troops, half the British forces, and over 900,000 German soldiers sick.

Deadly second wave of late 1918

American Expeditionary Force flu patients at U.S. Army Camp Hospital no. 45 in Aix-les-Bains, France, 1918

The second wave began in the second half of August 1918, probably spreading to Boston, Massachusetts and Freetown, Sierra Leone, by ships from Brest, where it had likely arrived with American troops or French recruits for naval training. From the Boston Navy Yard and Camp Devens (later renamed Fort Devens), about 30 miles west of Boston, other U.S. military sites were soon afflicted, as were troops being transported to Europe. Helped by troop movements, it spread over the next two months to all of North America, and then to Central and South America, also reaching Brazil and the Caribbean on ships. In July 1918, the Ottoman Empire saw its first cases in some soldiers. From Freetown, the pandemic continued to spread through West Africa along the coast, rivers, and the colonial railways, and from railheads to more remote communities, while South Africa received it in September on ships bringing back members of the South African Native Labour Corps returning from France. From there it spread around southern Africa and beyond the Zambezi, reaching Ethiopia in November. On 15 September, New York City saw its first fatality from influenza. The Philadelphia Liberty Loans Parade, held in Philadelphia, Pennsylvania, on 28 September 1918 to promote government bonds for World War I, resulted in 12,000 deaths after a major outbreak of the illness spread among people who had attended the parade.

From Europe, the second wave swept through Russia in a southwest-northeast diagonal front, as well as being brought to Arkhangelsk by the North Russia intervention, and then spread throughout Asia following the Russian Civil War and the Trans-Siberian railway, reaching Iran (where it spread through the holy city of Mashhad), and then later India in September, as well as China and Japan in October. The celebrations of the Armistice of 11 November 1918 also caused outbreaks in Lima and Nairobi, but by December the wave was mostly over.

The second wave of the 1918 pandemic was much more deadly than the first. The first wave had resembled typical flu epidemics; those most at risk were the sick and elderly, while younger, healthier people recovered easily. October 1918 was the month with the highest fatality rate of the whole pandemic. In the United States, ~292,000 deaths were reported between September-December 1918, compared to ~26,000 during the same time period in 1915. The Netherlands reported over 40,000 deaths from influenza and acute respiratory disease. Bombay reported ~15,000 deaths in a population of 1.1 million. The 1918 flu pandemic in India was especially deadly, with an estimated 12.5-20 million deaths in the last quarter of 1918 alone.[page needed ]

Third wave of 1919

Pandemic activity persisted, in general, into 1919 in many places. This persistence in activity is possibly attributable to climate, specifically in the Northern Hemisphere, where it was winter and thus the usual time for influenza activity. The pandemic nonetheless continued into 1919 largely independent of region and climate.

Cases began to rise again in some parts of the United States as early as late November 1918, with the Public Health Service issuing its first report of a "recrudescence of the disease" being felt in "widely scattered localities" in early December. This resurgent activity varied across the country, however, possibly on account of differing restrictions. Michigan, for example, experienced a swift resurgence of influenza that reached its peak in December, possibly as a result of the lifting of the ban on public gatherings. Pandemic interventions, such as bans on public gatherings and the closing of schools, were reimposed in many places in an attempt to suppress the spread.

There was "a very sudden and very marked rise in general death rate" in most cities in January 1919; nearly all experienced "some degree of recrudescence" of the flu in January and February. Significant outbreaks occurred in cities including Los Angeles, New York City, Memphis, Nashville, San Francisco, and St. Louis. By 21 February, with some local variation, influenza activity was reported to have been declining since mid-January in all parts of the country. Following this "first great epidemic period" that had commenced in October 1918, deaths from pneumonia and influenza were "somewhat below average" in the large cities of the United States between May 1919 and January 1920. Nonetheless, nearly 160,000 deaths were attributed to these causes in the first six months of 1919.

It was not until later in the winter and into the spring that a clearer resurgence appeared in Europe. A significant third wave had developed in England and Wales by mid-February, peaking in early March, though it did not fully subside until May. France also experienced a significant wave that peaked in February, alongside the Netherlands. Norway, Finland, and Switzerland saw recrudescences of pandemic activity in March, and Sweden in April.

Much of Spain was affected by "a substantial recrudescent wave" of influenza between January and April 1919. Portugal experienced a resurgence in pandemic activity that lasted from March to September 1919, with the greatest impact being felt on the west coast and in the north of the country; all districts were affected between April and May specifically.

Influenza entered Australia for the first time in January 1919 after a strict maritime quarantine had shielded the country through the latter part of 1918. It assumed epidemic proportions first in Melbourne, peaking in mid-February. The flu soon appeared in neighboring New South Wales and South Australia and then spread across the country throughout the year. New South Wales experienced its first wave of infection between mid-March and late May, while a second, more severe wave occurred in Victoria between April and June.

Land quarantine measures hindered the spread of the disease, resulting in varied experiences of exposures and outbreaks among the various states. Queensland was not infected until late April; Western Australia avoided the disease until early June, and Tasmania remained free from it until mid-August. Out of the six states, Victoria and New South Wales experienced generally more extensive epidemics. Each experienced another significant wave of illness over the winter. The second epidemic in New South Wales was more severe than the first, while Victoria saw a third wave that was somewhat less extensive than its second, more akin to its first.

The disease also reached other parts of the world for the first time in 1919, such as Madagascar, which saw its first cases in April; the outbreak had spread to practically all sections of the island by June. In other parts, influenza recurred in the form of a true "third wave". Hong Kong experienced another outbreak in June, as did South Africa during its fall and winter months in the Southern Hemisphere. New Zealand also experienced some cases in May.

Parts of South America experienced a resurgence of pandemic activity throughout 1919. A third wave hit Brazil between January and June. Between July 1919 and February 1920, Chile, which had been affected for the first time just in October 1918, experienced a severe second wave, with mortality peaking in August 1919. Montevideo similarly experienced a second outbreak between July and September.

The third wave particularly affected Spain, Serbia, Mexico and Great Britain, resulting in hundreds of thousands of deaths. It was in general less severe than the second wave but still much more deadly than the initial first wave.

Fourth wave of 1920

Public health recommendations from the Illustrated Current News

In the Northern Hemisphere, fears of a "recurrence" of the flu grew as fall approached. Experts cited the history of past flu epidemics, such as that of 1889-1890, to predict that such a recurrence a year later was not unlikely, though not all agreed. In September 1919, U.S. Surgeon General Rupert Blue said a return of the flu later in the year would "probably, but by no means certainly," occur. France had readied a public information campaign before the end of the summer, and Britain began preparations in the fall with the manufacture of vaccine.

In Japan, the flu broke out again in December and spread rapidly throughout the country, a fact attributed at the time to the coming of cold weather. Pandemic-related measures were renewed to check the spread of the outbreak, and health authorities recommended the use of masks. The epidemic intensified in the latter part of December before swiftly peaking in January.

Between October 1919 and 23 January 1920, 780,000 cases were reported across the country, with at least 20,000 deaths recorded by that date. This apparently reflected "a condition of severity three times greater than for the corresponding period of" 1918-1919, during Japan's first epidemic. Nonetheless, the disease was regarded as being milder than it had been the year before, albeit more infectious. Despite its rapid peak at the beginning of the year, the outbreak persisted throughout the winter, before subsiding in the spring.

In the United States, there were "almost continuously isolated or solitary cases" of flu throughout the spring and summer months of 1919. An increase in scattered cases became apparent as early as September, but Chicago experienced one of the first major outbreaks of the flu beginning in the middle of January. The Public Health Service announced it would take steps to "localize the epidemic", but the disease was already causing a simultaneous outbreak in Kansas City and quickly spread outward from the center of the country in no clear direction. A few days after its first announcement, PHS issued another assuring that the disease was under the control of state health authorities and that an outbreak of epidemic proportions was not expected.

It became apparent within days of the start of Chicago's explosive growth in cases that the flu was spreading in the city at an even faster rate than in winter 1919, though fewer were dying. Within a week, new cases in the city had surpassed its peak during the 1919 wave. Around the same time, New York City began to see its own sudden increase in cases, and other cities around the country were soon to follow. Certain pandemic restrictions, such as the closing of schools and theaters and the staggering of business hours to avoid congestion, were reimposed in cities like Chicago, Memphis, and New York City. As they had during the epidemic in fall 1918, schools in New York City remained open, while those in Memphis were shuttered as part of more general restrictions on public gatherings.

American Red Cross nurses tend to flu patients in temporary wards set up inside the Oakland Municipal Auditorium

The fourth wave in the United States subsided as swiftly as it had appeared, reaching a peak in early February. "An epidemic of considerable proportions marked the early months of 1920", the U.S. Mortality Statistics would later note; according to data at this time, the epidemic resulted in one third as many deaths as the 1918-1919 experience. New York City alone reported 6,374 deaths between December 1919 and April 1920, almost twice the number of the first wave in spring 1918. Other U.S. cities including Detroit, Milwaukee, Kansas City, Minneapolis, and St. Louis were hit particularly hard, with death rates higher than all of 1918. The Territory of Hawaii experienced its peak of the pandemic in early 1920, recording 1,489 deaths from flu-related causes, compared with 615 in 1918 and 796 in 1919.

Poland experienced a devastating outbreak during the winter months, with its capital Warsaw reaching a peak of 158 deaths in a single week, compared to the peak of 92 reached in December 1918; however, the 1920 epidemic passed in a matter of weeks, while the 1918-1919 wave had developed over the entire second half of 1918. By contrast, the outbreak in western Europe was considered "benign", with the age distribution of deaths beginning to take on that of seasonal flu. Five countries in Europe (Spain, Denmark, Finland, Germany and Switzerland) recorded a late peak between January-April 1920.

Mexico experienced a fourth wave between February and March. In South America, Peru experienced "asynchronous recrudescent waves" throughout the year. A severe third wave hit Lima, the capital city, between January and March, resulting in an all-cause excess mortality rate approximately four times greater than that of the 1918-1919 wave. Ica similarly experienced another severe pandemic wave in 1920, between July and October. A fourth wave also occurred in Brazil, in February.

Korea and Taiwan, both colonies of Japan at this time, also experienced pronounced outbreaks in late 1919 and early 1920.

Post-pandemic

By mid-1920, the pandemic was largely considered to be "over" by the public as well as governments. Though parts of Chile experienced a third, milder wave between November 1920 and March 1921, the flu seemed to be mostly absent through the winter of 1920-1921. In the United States, for example, deaths from pneumonia and influenza were "very much lower than for many years".

Influenza began to be reported again from many places in 1921. The pandemic continued to be felt in Chile, where a fourth wave affected seven of its 24 provinces between June and December 1921. The winter of 1921-1922 was the first major reappearance of influenza in the Northern Hemisphere, in many parts its most significant occurrence since the main pandemic in late 1918. Northwestern Europe was particularly affected. All-cause mortality in the Netherlands approximately doubled in January 1922 alone. In Helsinki, a major epidemic (the fifth since 1918) prevailed between November and December 1921. The flu was also widespread in the United States, its prevalence in California reportedly greater in early March 1922 than at any point since 1920.

In the years after 1920, the disease, a novel one in 1918, assumed a more familiar nature, coming to represent at least one form of the "seasonal flu". The virus, H1N1, remained endemic, occasionally causing more severe or otherwise notable outbreaks as it gradually evolved over the years. The period since its initial appearance in 1918 has been termed a "pandemic era", in which all flu pandemics since its emergence have been caused by its own descendants. Following the first of these post-1918 pandemics, in 1957, the virus was totally displaced by the novel H2N2, the reassortant product of the human H1N1 and an avian influenza virus, which thereafter became the active influenza A virus in humans.

In 1977, an influenza virus bearing a very close resemblance to the seasonal H1N1, which had not been seen since the 1950s, appeared in Russia and subsequently initiated a "technical" pandemic that principally affected those 26 years of age and younger. While some natural explanations, such as the virus remaining in some frozen state for 20 years, have been proposed to explain this unprecedented phenomenon, the nature of influenza itself has been cited in favor of human involvement of some kind, such as an accidental leak from a lab where the old virus had been preserved for research purposes. Following this miniature pandemic, the reemerged H1N1 became endemic once again but did not displace the other active influenza A virus, H3N2 (which itself had displaced H2N2 through a pandemic in 1968). For the first time, two influenza A viruses were observed in cocirculation. This state of affairs has persisted even after 2009, when a novel H1N1 virus emerged, sparked a pandemic, and thereafter took the place of the seasonal H1N1 to circulate alongside H3N2.

Potential origins

United States

The first confirmed cases originated in the United States. Historian Alfred W. Crosby stated in 2003 that the flu originated in Kansas, and author John M. Barry described a January 1918 outbreak in Haskell County, Kansas, as the point of origin in his 2004 article.

A 2018 study of tissue slides and medical reports led by evolutionary biology professor Michael Worobey found evidence against the disease originating from Kansas, as those cases were milder and had fewer deaths compared to the infections in New York City in the same period. The study did find evidence through phylogenetic analyses that the virus likely had a North American origin, though it was not conclusive. In addition, the haemagglutinin glycoproteins of the virus suggest that it originated long before 1918, and other studies suggest that the reassortment of the H1N1 virus likely occurred in or around 1915.

Edvard Munch (1863-1944), Self-Portrait with the Spanish Flu (1919)

Egon Schiele (1880-1918), Die Familie, painted a few days before his death and just after the death of his wife Edith from the Spanish flu[177]

The major U.K. troop staging and hospital camp in Étaples in France has been theorized by virologist John Oxford as being at the center of the Spanish flu. His study found that in late 1916 the Étaples camp was hit by the onset of a new disease with high mortality that caused symptoms similar to the flu. According to Oxford, a similar outbreak occurred in March 1917 at army barracks in Aldershot, and military pathologists later recognized these early outbreaks as the same disease as the Spanish flu. The overcrowded camp and hospital at Étaples was an ideal environment for the spread of a respiratory virus.

The hospital treated thousands of victims of poison gas attacks, and other casualties of war, and 100,000 soldiers passed through the camp every day. It also was home to a piggery and poultry was regularly brought in from surrounding villages to feed the camp. Oxford and his team postulated that a precursor virus, harbored in birds, mutated and then migrated to pigs kept near the front.

A report published in 2016 in the Journal of the Chinese Medical Association found evidence that the 1918 virus had been circulating in the European armies for months and possibly years before the 1918 pandemic. Political scientist Andrew Price-Smith published data from the Austrian archives suggesting the influenza began in Austria in early 1917.

A 2009 study in Influenza and Other Respiratory Viruses found that Spanish flu mortality simultaneously peaked within the two-month period of October and November 1918 in all fourteen European countries analyzed, which is inconsistent with the pattern that researchers would expect if the virus had originated somewhere in Europe and then spread outwards.

In 1993, Claude Hannoun, the leading expert on the Spanish flu at the Pasteur Institute, asserted the precursor virus was likely to have come from China and then mutated in the United States near Boston and from there spread to Brest, France, Europe's battlefields, the rest of Europe, and the rest of the world, with Allied soldiers and sailors as the main disseminators. Hannoun considered several alternative hypotheses of origin, such as Spain, Kansas, and Brest, as being possible, but not likely.

In 2014, historian Mark Humphries argued that the mobilization of 96,000 Chinese laborers to work behind the British and French lines might have been the source of the pandemic. Humphries, of the Memorial University of Newfoundland in St. John's, based his conclusions on newly unearthed records. He found archival evidence that a respiratory illness that struck northern China (where the laborers came from) in November 1917 was identified a year later by Chinese health officials as identical to the Spanish flu. Unfortunately, no tissue samples have survived for modern comparison. Nevertheless, there were some reports of respiratory illness on parts of the path the laborers took to get to Europe, which also passed through North America.

China was one of the few regions of the world seemingly less affected by the Spanish flu pandemic, where several studies have documented a comparatively mild flu season in 1918. (Although this is disputed due to lack of data during the Warlord Period, see Around the globe.) This has led to speculation that the Spanish flu pandemic originated in China, as the lower rates of flu mortality may be explained by the Chinese population's previously acquired immunity to the flu virus. In the Guangdong Province it was reported that early outbreaks of influenza in 1918 disproportionately impacted young men. The June outbreak infected children and adolescents between 11 and 20 years of age, while the October outbreak was most common in those aged 11 to 15.

A report published in 2016 in the Journal of the Chinese Medical Association found no evidence that the 1918 virus was imported to Europe via Chinese and Southeast Asian soldiers and workers and instead found evidence of its circulation in Europe before the pandemic. The 2016 study found that the low flu mortality rate (an estimated one in a thousand) recorded among the Chinese and Southeast Asian workers in Europe suggests that the Asian units were not different from other Allied military units in France at the end of 1918 and, thus, were not a likely source of a new lethal virus. Further evidence against the disease being spread by Chinese workers was that workers entered Europe through other routes that did not result in a detectable spread, making them unlikely to have been the original hosts.

Epidemiology and pathology

Transmission and mutation

The basic reproduction number of the virus was between 2 and 3. The close quarters and massive troop movements of World War I hastened the pandemic, and probably both increased transmission and augmented mutation. The war may also have reduced people's resistance to the virus. Some speculate the soldiers' immune systems were weakened by malnourishment, as well as the stresses of combat and chemical attacks, increasing their susceptibility. A large factor in the worldwide occurrence of the flu was increased travel. Modern transportation systems made it easier for soldiers, sailors, and civilian travelers to spread the disease. Another was lies and denial by governments, leaving the population ill-prepared to handle the outbreaks.

The severity of the second wave has been attributed to the circumstances of the First World War. In civilian life, natural selection favors a mild strain. Those who get very ill stay home, and those mildly ill continue with their lives, preferentially spreading the mild strain. In the trenches, natural selection was reversed. Soldiers with a mild strain stayed where they were, while the severely ill were sent on crowded trains to crowded field hospitals, spreading the deadlier virus. The second wave began, and the flu quickly spread around the world again. Consequently, during modern pandemics, health officials look for deadlier strains of a virus when it reaches places with social upheaval. The fact that most of those who recovered from first-wave infections had become immune showed that it must have been the same strain of flu. This was most dramatically illustrated in Copenhagen, which escaped with a combined mortality rate of just 0.29% (0.02% in the first wave and 0.27% in the second wave) because of exposure to the less-lethal first wave. For the rest of the population, the second wave was far more deadly; the most vulnerable people were those like the soldiers in the trenches - adults who were young and fit.

After the lethal second wave struck in late 1918, new cases dropped abruptly. In Philadelphia, for example, 4,597 people died in the week ending 16 October, but by 11 November, influenza had almost disappeared from the city. One explanation for the rapid decline in the lethality of the disease is that doctors became more effective in the prevention and treatment of pneumonia that developed after the victims had contracted the virus. However, John Barry stated in his 2004 book The Great Influenza: The Epic Story of the Deadliest Plague In History that researchers have found no evidence to support this position. Another theory holds that the 1918 virus mutated extremely rapidly to a less lethal strain. Such evolution of influenza is a common occurrence: there is a tendency for pathogenic viruses to become less lethal with time, as the hosts of more dangerous strains tend to die out. Fatal cases did continue into 1919, however. One notable example was that of ice hockey player Joe Hall, who, while playing for the Montreal Canadiens, fell victim to the flu in April after an outbreak that resulted in the cancellation of the 1919 Stanley Cup Finals.

Signs and symptoms

The majority of the infected experienced only the typical flu symptoms of sore throat, headache, and fever, especially during the first wave. However, during the second wave, the disease was much more serious, often complicated by bacterial pneumonia, which was often the cause of death. This more serious type would cause heliotrope cyanosis to develop, whereby the skin would first develop two mahogany spots over the cheekbones which would then over a few hours spread to color the entire face blue, followed by black coloration first in the extremities and then further spreading to the limbs and the torso. After this, death would follow within hours or days due to the lungs being filled with fluids. Other signs and symptoms reported included spontaneous mouth and nosebleeds, miscarriages for pregnant women, a peculiar smell, teeth, and hair falling, delirium, dizziness, insomnia, loss of hearing or smell, and impaired vision. One observer wrote, "One of the most striking of the complications was hemorrhage from mucous membranes, especially from the nose, stomach, and intestine. Bleeding from the ears and petechial hemorrhages in the skin also occurred". The severity of the symptoms was believed to be caused by cytokine storms.

The majority of deaths were from bacterial pneumonia, a common secondary infection associated with influenza. This pneumonia was itself caused by common upper respiratory-tract bacteria, which were able to get into the lungs via the damaged bronchial tubes of the victims. The virus also killed people directly by causing massive hemorrhages and edema in the lungs. Modern analysis has shown the virus to be particularly deadly because it triggers a cytokine storm (overreaction of the body's immune system). One group of researchers recovered the virus from the bodies of frozen victims and transfected animals with it. The animals suffered rapidly progressive respiratory failure and death through a cytokine storm. The strong immune reactions of young adults were postulated to have ravaged the body, whereas the weaker immune reactions of children and middle-aged adults resulted in fewer deaths among those groups.

Misdiagnosis

Because the virus that caused the disease was too small to be seen under a microscope at the time, there were problems with correctly diagnosing it. The bacterium Haemophilus influenzae was instead mistakenly thought to be the cause, as it was big enough to be seen and was present in many, though not all, patients. For this reason, a vaccine that was used against that bacillus did not make an infection rarer but did decrease the death rate.

During the deadly second wave there were also fears that it was in fact plague, dengue fever, or cholera. Another common misdiagnosis was typhus, which was common in circumstances of social upheaval, and was therefore also affecting Russia in the aftermath of the October Revolution. In Chile, the view of the country's elite was that the nation was in severe decline, and therefore doctors assumed that the disease was typhus caused by poor hygiene, and not an infectious one, causing a mismanaged response which did not ban mass gatherings.

The role of climate conditions

Studies have shown that the immune system of Spanish flu victims was weakened by adverse climate conditions which were particularly unseasonably cold and wet for extended periods of time during the duration of the pandemic. This affected especially WWI troops exposed to incessant rains and lower-than-average temperatures for the duration of the conflict, and especially during the second wave of the pandemic. Ultra-high-resolution climate data combined with highly detailed mortality records analyzed at Harvard University and the Climate Change Institute at the University of Maine identified a severe climate anomaly that impacted Europe from 1914 to 1919, with several environmental indicators directly influencing the severity and spread of the Spanish flu pandemic. Specifically, a significant increase in precipitation affected all of Europe during the second wave of the pandemic, from September to December 1918. Mortality figures follow closely the concurrent increase in precipitation and decrease in temperatures. Several explanations have been proposed for this, including the fact that lower temperatures and increased precipitation provided ideal conditions for virus replication and transmission, while also negatively affecting the immune systems of soldiers and other people exposed to the inclement weather, a factor proven to increase likelihood of infection by both viruses and pneumococcal co-morbid infections documented to have affected a large percentage of pandemic victims (one fifth of them, with a 36% mortality rate). A six-year climate anomaly (1914-1919) brought cold, marine air to Europe, drastically changing its weather, as documented by eyewitness accounts and instrumental records, reaching as far as the Gallipoli campaign, in Turkey, where ANZAC troops suffered extremely cold temperatures despite the normally Mediterranean climate of the region. The climate anomaly likely influenced the migration of H1N1 avian vectors which contaminate bodies of water with their droppings, reaching 60% infection rates in autumn. The climate anomaly has been associated with an anthropogenic increase in atmospheric dust, due to the incessant bombardment; increased nucleation due to dust particles ( cloud condensation nuclei) contributed to increased precipitation.

Public health management

While systems for alerting public health authorities of infectious spread did exist in 1918, they did not generally include influenza, leading to a delayed response. Nevertheless, actions were taken. Maritime quarantines were declared on islands such as Iceland, Australia, and American Samoa, saving many lives. Social distancing measures were introduced, for example closing schools, theatres, and places of worship, limiting public transportation, and banning mass gatherings. Wearing face masks became common in some places, such as Japan, though there were debates over their efficacy. There was also some resistance to their use, as exemplified by the Anti-Mask League of San Francisco. Vaccines were also developed, but as these were based on bacteria and not the actual virus, they could only help with secondary infections. The actual enforcement of various restrictions varied. To a large extent, the New York City health commissioner ordered businesses to open and close on staggered shifts to avoid overcrowding on the subways.

A later study found that measures such as banning mass gatherings and requiring the wearing of face masks could cut the death rate up to 50 percent, but this was dependent on their being imposed early in the outbreak and not being lifted prematurely.

Medical treatment

As there were no antiviral drugs to treat the virus, and no antibiotics to treat the secondary bacterial infections, doctors would rely on a random assortment of medicines with varying degrees of effectiveness, such as aspirin, quinine, arsenics, digitalis, strychnine, epsom salts, castor oil, and iodine. Treatments of traditional medicine, such as bloodletting, ayurveda, and kampo were also applied.

Information dissemination

Due to World War I, many countries engaged in wartime censorship, and suppressed reporting of the pandemic. For example, the Italian newspaper Corriere della Sera was prohibited from reporting daily death tolls. The newspapers of the time were also generally paternalistic and worried about mass panic. Misinformation also spread along with the disease. In Ireland there was a belief that noxious gases were rising from the mass graves of Flanders Fields and being "blown all over the world by winds". There were also rumors that the Germans were behind it, for example by poisoning the aspirin manufactured by Bayer, or by releasing poison gas from U-boats.

Around the globe

Difference between the flu mortality age-distributions of the 1918 pandemic and normal epidemics - deaths per 100,000 persons in each age group, United States, for the interpandemic years 1911-1917 (dashed line) and the pandemic year 1918 (solid line)

Three pandemic waves: weekly combined flu and pneumonia mortality, United Kingdom, 1918-1919

The Spanish flu infected around 500 million people, about one-third of the world's population. Estimates as to how many infected people died vary greatly, but the flu is regardless considered to be one of the deadliest pandemics in history. An early estimate from 1927 put global mortality at 21.6 million. An estimate from 1991 states that the virus killed between 25 and 39 million people. A 2005 estimate put the death toll at 50 million (about 3% of the global population), and possibly as high as 100 million (more than 5%). However, a 2018 reassessment in the American Journal of Epidemiology estimated the total to be about 17 million, though this has been contested. With a world population of 1.8 to 1.9 billion, these estimates correspond to between 1 and 6 percent of the population.

A 2009 study in Influenza and Other Respiratory Viruses based on data from fourteen European countries estimated a total of 2.64 million excess deaths in Europe attributable to the Spanish flu during the major 1918-1919 phase of the pandemic, in line with the three prior studies from 1991, 2002, and 2006 that calculated a European death toll of between 2 million and 2.3 million. This represents a mortality rate of about 1.1% of the European population ( c. 250 million in 1918), considerably higher than the mortality rate in the U.S., which the authors hypothesize is likely due to the severe effects of the war in Europe. The excess mortality rate in the U.K. has been estimated at 0.28%-0.4%, far below this European average.

Some 12-17 million people died in India, about 5% of the population. The death toll in India's British-ruled districts was 13.88 million. Another estimate gives at least 12 million dead. The decade between 1911 and 1921 was the only census period in which India's population fell, mostly due to devastation of the Spanish flu pandemic. While India is generally described as the country most severely affected by the Spanish flu, at least one study argues that other factors may partially account for the very high excess mortality rates observed in 1918, citing unusually high 1917 mortality and wide regional variation (ranging from 0.47% to 6.66%). A 2006 study in also noted that Indian provinces had excess mortality rates ranging from 2.1% to 7.8%, stating: "Commentators at the time attributed this huge variation to differences in nutritional status and diurnal fluctuations in temperature."

In Finland, 20,000 died out of 210,000 infected. In Sweden, 34,000 died.

In Japan, the flu killed nearly 500,000 people over two waves between 1918 and 1920, with nearly 300,000 excess deaths between October 1918 and May 1919 and 182,000 between December 1919 and May 1920.

In the Dutch East Indies (now Indonesia), 1.5 million were assumed to have died among 30 million inhabitants. In Tahiti, 13% of the population died during one month. Similarly, in Western Samoa 22% of the population of 38,000 died within two months.

In Istanbul, capital of the Ottoman Empire, 6,403 to 10,000 died, giving the city a mortality rate of at least 0.56%.

In New Zealand, the flu killed an estimated 6,400 Pākehā (or "New Zealanders primarily of European descent") and 2,500 indigenous Māori in six weeks, with Māori dying at eight times the rate of Pākehā.

In Australia, the flu killed around 12,000 to 20,000 people. The country's death rate, 2.7 per 1,000 people, was one of the lowest recorded compared with other countries at the time; however, as much as 40 percent of the population were infected, and a mortality rate of 50 percent was recorded by some Aboriginal communities. New South Wales and Victoria saw the greatest relative mortality, with 3.19 and 2.40 deaths per 1,000 people respectively, while Western Australia, Queensland, Southern Australia, and Tasmania experienced rates of 1.70, 1.14, 1.13, and 1.09 per 1,000 respectively. In Queensland, at least one-third of deaths recorded were in the Aboriginal population.

In the U.S., about 28% of the population of 105 million became infected, and 500,000 to 850,000 died (0.48 to 0.81 percent of the population). Native American tribes were particularly hard hit. In the Four Corners area, there were 3,293 registered deaths among Native Americans. Entire Inuit and Alaskan Native village communities died in Alaska. In Canada, 50,000 died.

In Britain, as many as 250,000 died; in France, more than 400,000.

In Ghana, the influenza epidemic killed at least 100,000 people. Tafari Makonnen (the future Haile Selassie, Emperor of Ethiopia) was one of the first Ethiopians who contracted influenza but survived. Many of his subjects did not; estimates for fatalities in the capital city, Addis Ababa, range from 5,000 to 10,000, or higher.

The death toll in Russia has been estimated at 450,000, though the epidemiologists who suggested this number called it a "shot in the dark". If it is correct, Russia lost roughly 0.4% of its population, meaning it suffered the lowest influenza-related mortality in Europe. Another study considers this number unlikely, given that the country was in the grip of a civil war, and the infrastructure of daily life had broken down; the study suggests that Russia's death toll was closer to 2%, or 2.7 million people.

Devastated communities

Bristol Bay, a region of Alaska populated by indigenous people, suffered a death rate of 40 percent of the total population, with some villages entirely disappearing.

Several Pacific island territories were hit particularly hard. The pandemic reached them from New Zealand, which was too slow to implement measures to prevent ships, such as Talune, carrying the flu from leaving its ports. From New Zealand, the flu reached Tonga (killing 8% of the population), Nauru (16%), and Fiji (5%, 9,000 people). Worst affected was Western Samoa, formerly German Samoa, which had been occupied by New Zealand in 1914. 90% of the population was infected; 30% of adult men, 22% of adult women, and 10% of children died. By contrast, Governor John Martin Poyer prevented the flu from reaching neighboring American Samoa by imposing a blockade. The disease spread fastest through the higher social classes among the indigenous peoples, because of the custom of gathering oral tradition from chiefs on their deathbeds; many community elders were infected through this process.

In Iran, the mortality was very high: according to an estimate, between 902,400 and 2,431,000, or 8% to 22% of the total population died. The country was going through the Persian famine of 1917-1919 concurrently.

In Ireland, during the worst 12 months, the Spanish flu accounted for one-third of all deaths.

In South Africa it is estimated that about 300,000 people amounting to 6% of the population died within six weeks. Government actions in the early stages of the virus' arrival in the country in September 1918 are believed to have unintentionally accelerated its spread throughout the country. Almost a quarter of the working population of Kimberley, consisting of workers in the diamond mines, died. In British Somaliland, one official estimated that 7% of the native population died. This huge death toll resulted from an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms.

Less-affected areas

In the Pacific, American Samoa and the French colony of New Caledonia succeeded in preventing even a single death from influenza through effective quarantines. However, the outbreak was delayed into 1926 for American Samoa and 1921 for New Caledonia as the quarantine period ended. On American Samoa, at least 25% of the island residents were clinically attacked and 0.1% died, and on New Caledonia, there was widespread illness and 0.1% population died. Australia also managed to avoid the first two waves with a quarantine. Iceland protected a third of its population from exposure by blocking the main road of the island. By the end of the pandemic, the isolated island of Marajó, in Brazil's Amazon River Delta had not reported an outbreak. Saint Helena also reported no deaths.

Estimates for the death toll in China have varied widely, a range which reflects the lack of centralized collection of health data at the time due to the Warlord period. China may have experienced a relatively mild flu season in 1918 compared to other areas of the world. However, some reports from its interior suggest that mortality rates from influenza were perhaps higher in at least a few locations in China in 1918. At the very least, there is little evidence that China as a whole was seriously affected by the flu compared to other countries in the world.

The first estimate of the Chinese death toll was made in 1991 by Patterson and Pyle, which estimated a toll of between 5 and 9 million. However, this 1991 study was criticized by later studies due to flawed methodology, and newer studies have published estimates of a far lower mortality rate in China. For instance, Iijima in 1998 estimates the death toll in China to be between 1 and 1.28 million based on data available from Chinese port cities. The lower estimates of the Chinese death toll are based on the low mortality rates that were found in Chinese port cities (for example, Hong Kong) and on the assumption that poor communications prevented the flu from penetrating the interior of China. However, some contemporary newspaper and post office reports, as well as reports from missionary doctors, suggest that the flu did penetrate the Chinese interior and that influenza was severe in at least some locations in the countryside of China.

Although medical records from China's interior are lacking, extensive medical data were recorded in Chinese port cities, such as then British-controlled Hong Kong, Canton, Peking, Harbin and Shanghai. These data were collected by the Chinese Maritime Customs Service, which was largely staffed by non-Chinese foreigners, such as the British, French, and other European colonial officials in China. As a whole, data from China's port cities show low mortality rates compared to other cities in Asia. For example, the British authorities at Hong Kong and Canton reported a mortality rate from influenza at a rate of 0.25% and 0.32%, much lower than the reported mortality rate of other cities in Asia, such as Calcutta or Bombay, where influenza was much more devastating. Similarly, in the city of Shanghai - which had a population of over 2 million in 1918 - there were only 266 recorded deaths from influenza among the Chinese population in 1918. If extrapolated from the extensive data recorded from Chinese cities, the suggested mortality rate from influenza in China as a whole in 1918 was likely lower than 1% - much lower than the world average (which was around 3-5%). In contrast, Japan and Taiwan had reported a mortality rate from influenza around 0.45% and 0.69% respectively, higher than the mortality rate collected from data in Chinese port cities, such as Hong Kong (0.25%), Canton (0.32%), and Shanghai.

However, it is noted that the influenza mortality rate in Hong Kong and Canton are under-recorded, because only the deaths that occurred in colony hospitals were counted. Similarly, in Shanghai, these statistics are limited to that area of the city under the control of the health section of the Shanghai International Settlement, and the actual death toll in Shanghai was much higher. The medical records from China's interior indicate that, compared to cities, rural communities have substantially higher mortality rate. A published influenza survey in Houlu County, Hebei Province, found that the case fatality rate was 9.77% and 0.79% of county population died from influenza in October and November 1918.

Patterns of fatality

The pandemic mostly killed young adults. In 1918-1919, 99% of pandemic influenza deaths in the U.S. occurred in people under 65, and nearly half of deaths were in young adults 20 to 40 years old. In 1920, the mortality rate among people under 65 had decreased sixfold to half the mortality rate of people over 65, but 92% of deaths still occurred in people under 65. This is unusual since influenza is typically most deadly to weak individuals, such as infants under age two, adults over age 70, and the immunocompromised. In 1918, older adults may have had partial protection caused by exposure to the 1889-1890 flu pandemic, known as the "Russian flu". According to historian John M. Barry, the most vulnerable of all - "those most likely, of the most likely", to die - were pregnant women. He reported that in thirteen studies of hospitalized women in the pandemic, the death rate ranged from 23% to 71%. Of the pregnant women who survived childbirth, over one-quarter (26%) lost the child. Another oddity was that the outbreak was widespread in the summer and autumn (in the Northern Hemisphere); influenza is usually worse in winter.

There were also geographic patterns to the disease's fatality. Some parts of Asia had 30 times higher death rates than some parts of Europe, and generally, Africa and Asia had higher rates, while Europe and North America had lower ones. There was also great variation within continents, with three times higher mortality in Hungary and Spain compared to Denmark, two to three times higher chance of death in Sub-Saharan Africa compared to North Africa, and possibly up to ten times higher rates between the extremes of Asia. Cities were affected worse than rural areas. There were also differences between cities, which might have reflected exposure to the milder first wave giving immunity, as well as the introduction of social distancing measures.

Another major pattern was the differences between social classes. In Oslo, death rates were inversely correlated with apartment size, as the poorer people living in smaller apartments died at a higher rate. Social status was also reflected in the higher mortality among immigrant communities, with Italian Americans, a recently arrived group at the time, were nearly twice as likely to die compared to the average Americans. These disparities reflected worse diets, crowded living conditions, and problems accessing healthcare. Paradoxically, however, African Americans were relatively spared by the pandemic.

More men than women were killed by the flu, as they were more likely to go out and be exposed, while women would tend to stay at home. For the same reason men also were more likely to have pre-existing tuberculosis, which severely worsened the chances of recovery. However, in India the opposite was true, potentially because Indian women were neglected with poorer nutrition, and were expected to care for the sick.

A study conducted by He et al. (2011) used a mechanistic modeling approach to study the three waves of the 1918 influenza pandemic. They examined the factors that underlie variability in temporal patterns and their correlation to patterns of mortality and morbidity. Their analysis suggests that temporal variations in transmission rate provide the best explanation, and the variation in transmission required to generate these three waves is within biologically plausible values. Another study by He et al. (2013) used a simple epidemic model incorporating three factors to infer the cause of the three waves of the 1918 influenza pandemic. These factors were school opening and closing, temperature changes throughout the outbreak, and human behavioral changes in response to the outbreak. Their modeling results showed that all three factors are important, but human behavioral responses showed the most significant effects.

Academic Andrew Price-Smith has made the argument that the virus helped tip the balance of power in the latter days of the war towards the Allied cause. He provides data that the viral waves hit the Central Powers before the Allied powers and that both morbidity and mortality in Germany and Austria were considerably higher than in Britain and France. A 2006 Lancet study corroborates higher excess mortality rates in Germany (0.76%) and Austria (1.61%) compared to Britain (0.34%) and France (0.75%).

Many businesses in the entertainment and service industries suffered losses in revenue, while the healthcare industry reported profit gains. Historian Nancy Bristow has argued that the pandemic, when combined with the increasing number of women attending college, contributed to the success of women in the field of nursing. This was due in part to the failure of medical doctors, who were predominantly men, to contain and prevent the illness. Nursing staff, who were mainly women, celebrated the success of their patient care and did not associate the spread of the disease with their work.

A 2020 study found that U.S. cities that implemented early and extensive non-medical measures (quarantine, etc.) suffered no additional adverse economic effects due to implementing those measures. However, the validity of this study has been questioned because of the coincidence of WWI and other problems with data reliability.

Long-term effects

A 2006 study in the Journal of Political Economy found that "cohorts in utero during the pandemic displayed reduced educational attainment, increased rates of physical disability, lower income, lower socioeconomic status, and higher transfer payments received compared with other birth cohorts." A 2018 study found that the pandemic reduced educational attainment in populations. The flu has also been linked to the outbreak of encephalitis lethargica in the 1920s.

Survivors faced an elevated mortality risk. Some survivors did not fully recover from physiological conditions resulting from infection.

Despite the high morbidity and mortality rates that resulted from the epidemic, the Spanish flu began to fade from public awareness over the decades until the arrival of news about bird flu and other pandemics in the 1990s and 2000s. This has led some historians to label the Spanish flu a "forgotten pandemic". However, this label has been challenged by the historian Guy Beiner, who has charted a complex history of social and cultural forgetting, demonstrating how the pandemic was overshadowed by the commemoration of the First World War and mostly neglected in mainstream historiography, yet was remembered in private and local traditions across the globe.

There are various theories of why the Spanish flu was "forgotten". The rapid pace of the pandemic, which killed most of its victims in the United States within less than nine months, resulted in limited media coverage. The general population was familiar with patterns of pandemic disease in the late 19th and early 20th centuries: typhoid, yellow fever, diphtheria, and cholera all occurred near the same time. These outbreaks probably lessened the significance of the influenza pandemic for the public. In some areas, the flu was not reported on, the only mention being that of advertisements for medicines claiming to cure it.

Additionally, the outbreak coincided with the deaths and media focus on the First World War. Another explanation involves the age group affected by the disease. The majority of fatalities, from both the war and the epidemic, were among young adults. The high number of war-related deaths of young adults may have overshadowed the deaths caused by flu.

When people read the obituaries, they saw the war or postwar deaths and the deaths from the influenza side by side. Particularly in Europe, where the war's toll was high, the flu may not have had a tremendous psychological impact or may have seemed an extension of the war's tragedies. The duration of the pandemic and the war could have also played a role. The war, however, had initially been expected to end quickly but lasted for four years by the time the pandemic struck.

In literature and other media

Despite the toll of the pandemic, it was never a large theme in American literature. Alfred Crosby suspects that it may be due to the fact that it occurred after World War I, which was the most important event in that generation's lives. Katherine Anne Porter's 1939 novella Pale Horse, Pale Rider is one of the most well-known fictional accounts of the pandemic. The 2006 novel The Last Town on Earth focuses on a town which attempts to limit the spread of the flu by preventing people from entering or leaving. The Pull of the Stars is a 2020 novel by Emma Donoghue set in Dublin during the Spanish flu. Its final draft was submitted in March 2020, and publishers fast-tracked publication because of the then ongoing COVID-19 pandemic.

Comparison with other pandemics

The origin of the Spanish flu pandemic, and the relationship between the near-simultaneous outbreaks in humans and swine, have been controversial. One hypothesis is that the virus strain originated at Fort Riley, Kansas, in viruses in poultry and swine which the fort bred for food; the soldiers were then sent from Fort Riley around the world, where they spread the disease. Similarities between a reconstruction of the virus and avian viruses, combined with the human pandemic preceding the first reports of influenza in swine, led researchers to conclude the influenza virus jumped directly from birds to humans, and swine caught the disease from humans.

Others have disagreed, and more recent research has suggested the strain may have originated in a nonhuman, mammalian species. An estimated date for its appearance in mammalian hosts has been put at the period 1882-1913. This ancestor virus diverged about 1913-1915 into two clades (or biological groups each descended from a common ancestor), which gave rise to the classical swine and human H1N1 influenza lineages. The last common ancestor of human strains dates between February 1917 and April 1918. Because pigs are more readily infected with avian influenza viruses than are humans, they were suggested as the original recipients of the virus, passing the virus to humans sometime between 1913 and 1918.

An effort to recreate the Spanish flu strain (a subtype of avian strain H1N1) was a collaboration among the Armed Forces Institute of Pathology, the USDA ARS Southeast Poultry Research Laboratory, and Mount Sinai School of Medicine in New York City. The effort resulted in the announcement (on 5 October 2005) that the group had successfully determined the virus' genetic sequence, using historic tissue samples recovered by pathologist Johan Hultin from an Inuit female flu victim buried in the Alaskan permafrost and samples preserved from American soldiers Roscoe Vaughan and James Downs.

On 18 January 2007, Kobasa et al. (2007) reported that monkeys (Macaca fascicularis) infected with the recreated flu strain exhibited classic symptoms of the 1918 pandemic, and died from cytokine storms - an overreaction of the immune system. This may explain why the Spanish flu had its surprising effect on younger, healthier people, as a person with a stronger immune system would potentially have a stronger overreaction.

On 16 September 2008, the body of British politician and diplomat Sir Mark Sykes was exhumed to study the RNA of the flu virus in efforts to understand the genetic structure of modern H5N1 bird flu. Sykes had been buried in 1919 in a lead coffin which scientists hoped had helped preserve the virus. The coffin was found to be split and the cadaver badly decomposed; nonetheless, samples of lung and brain tissue were taken.

One of the few things known for certain about influenza in 1918 and for some years after was that it was, except in the laboratory, exclusively a disease of human beings.

In 2013, the AIR Worldwide Research and Modeling Group "characterized the historic 1918 pandemic and estimated the effects of a similar pandemic occurring today using the AIR Pandemic Flu Model". In the model, "a modern-day 'Spanish flu' event would result in additional life insurance losses of between US$15.3-27.8 billion in the United States alone", with 188,000-337,000 deaths in the United States.

In 2018, Michael Worobey, an evolutionary biology professor at the University of Arizona who is examining the history of the 1918 pandemic, revealed that he obtained tissue slides created by William Rolland, a physician who reported on a respiratory illness likely to be the virus while a pathologist in the British military during World War One. Rolland had authored an article in the during 1917 about a respiratory illness outbreak beginning in 1916 in Étaples, France. Worobey traced recent references to that article to family members who had retained slides that Rolland had prepared during that time. Worobey extracted tissue from the slides to potentially reveal more about the origin of the pathogen.

In 2021 an investigation used the virus sequence to obtain the Hemagglutinin (HA) antigen and observe the adaptive immunity in 32 survivors of the 1918 flu pandemic, all of them presented seroreactivity and 7 of 8 further tested presented memory B cells able to produce antibodies that bound to the HA antigen highlighting the ability of the immunological memory many decades after.

Sex differences in mortality

The high mortality rate of the influenza pandemic is one aspect that sets the pandemic apart from other disease outbreaks. Another factor is the higher mortality rate of men compared with women. Men with an underlying condition were at significantly more risk. Tuberculosis was one of the deadliest diseases in the 1900s, and killed more men than women. But with the spread of influenza disease, the cases of tuberculosis cases in men decreased. Many scholars have noted that tuberculosis increased the mortality rate of influenza in males, decreasing their life expectancy. During the 1900s tuberculosis was more common in males than females, but studies show that when influenza spread the tuberculosis mortality rate among females changed. The death rate of tuberculosis in females increased significantly and would continue to decline until post-pandemic.

Island of Newfoundland

Influenza pandemic among Canadian soldiers

References

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Spanish flu Disease Influenza Virus strain Strains of A/H1N1 Location Worldwide First outbreak Unknown Date February 1918 - April 1920[1] Suspected cases‡ 500 million (estimated) 25-50 million (generally accepted), other estimates range from 17 to 100 million[3] [4] [5] ‡ Suspected cases have not been confirmed by laboratory tests as being due to this strain, although some other strains may have been ruled out.

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The 1957-58 influenza pandemic, also known as Asian flu, was a global pandemic of influenza A virus subtype H2N2 which originated in Guizhou, China and killed at least 1 million people worldwide.

The strain of virus that caused the pandemic, influenza A virus subtype H2N2, was a recombination of avian influenza (probably from geese) and human influenza viruses. As it was a novel strain of the virus, there was minimal immunity in the population.

The first cases were reported in Guizhou in late 1956 or February 1957, and were reported in the neighboring province of Yunnan before the end of February. On 17 April, reported that "an influenza epidemic has affected thousands of Hong Kong residents". The same month, Singapore also experienced an outbreak of the new flu. In Taiwan, 100,000 were affected by mid-May and India suffered a million cases by June. In late June, the pandemic reached the United Kingdom.

By June 1957 it reached the United States, where it initially caused few infections. Some of the first affected were United States Navy personnel at destroyers docked at Newport Naval Station, as well as new military recruits elsewhere. The first wave peaked in October (among children who returned to school) and the second wave, in January and February 1958 among elderly people, which was more fatal. Microbiologist Maurice Hilleman was alarmed by pictures of those affected by the virus in Hong Kong published in The New York Times. He obtained samples of the virus from a United States Navy doctor in Japan. The Public Health Service released the virus cultures to vaccine manufacturers on 12 May 1957, and a vaccine entered trials at Fort Ord on 26 July and Lowry Air Force Base on 29 July. The vaccine was available from October 1957 in the United Kingdom. Although it was only available initially in limited quantities, its rapid deployment helped contain the pandemic.

H2N2 influenza virus continued to circulate until 1968, when it transformed via antigenic shift into influenza A virus subtype H3N2, the cause of the 1968 influenza pandemic.

The disease was estimated to have a 3% rate of complications and 0.3% mortality in the United Kingdom; it could cause pneumonia by itself, without the presence of secondary bacterial infection. It may have infected as many or more people than the 1918 Spanish flu pandemic, but the vaccine, improved health care, and the invention of antibiotics contributed to a lower mortality rate. Overall, the pandemic caused 1 to 2 million deaths worldwide or 2 to 4 million. The CDC estimates 1.1 million deaths worldwide. According to a study in the Journal of Infectious Diseases, the highest excess mortality occurred in Latin America. About 70,000 to 116,000 people died in the United States. In early 1958, it was estimated that 14,000 people had already died of the flu in the United Kingdom of the 9 million who became sick. It caused many infections in children, spreading in schools and leading to many school closures, but was rarely fatal in children. The virus was most deadly in pregnant women, the elderly, and those with pre-existing heart and lung disease. According to research by Barbara Sands, some of the excess mortality attributed to the Great Leap Forward in Maoist China may have actually been caused by the 1957 flu.

The Dow Jones Industrial Average lost 15% of its value in the second half of 1957. In the United Kingdom, the government paid out £10 000 000 in sickness benefit and some factories and mines had to close. Many schools had to close in Ireland, including 17 in Dublin.

Chowell, Gerardo; Simonsen, Lone; Fuentes, Rodrigo; Flores, Jose; Miller, Mark A.; Viboud, Cécile (May 2017). "Severe mortality impact of the 1957 influenza pandemic in Chile". Influenza and Other Respiratory Viruses. 11 (3): 230-239. doi:10.1111/irv.12439.

Cobos, April J.; Nelson, Clinton G.; Jehn, Megan; Viboud, Cécile; Chowell, Gerardo (2016). "Mortality and transmissibility patterns of the 1957 influenza pandemic in Maricopa County, Arizona". BMC Infectious Diseases. 16 (1): 405. doi:10.1186/s12879-016-1716-7. ISSN 1471-2334.

# data[].attributes.attachment_link.description
The 1957-58 influenza pandemic, also known as Asian flu, was a global pandemic of influenza A virus subtype H2N2 which originated in Guizhou, China and killed at least 1 million people worldwide. The strain of virus that caused the pandemic, influenza A virus subtype H2N2, was a recombination of avian influenza (probably from geese) and human influenza viruses.

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The seventh cholera pandemic was the seventh major outbreak of cholera and occurred principally from the years 1961 to 1975; the strain involved persists to the present. This pandemic, based on the strain called El Tor, started in Indonesia in 1961 and spread to Bangladesh by 1963. Then it went to India in 1964, followed by the Soviet Union by 1966. In July 1970 there was an outbreak in Odessa and in 1972 there were reports of outbreaks in Baku, but the Soviet Union suppressed this information. It reached Italy in 1973 from North Africa. Japan and the South Pacific saw a few outbreaks by the late 1970s.

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The seventh cholera pandemic was the seventh major outbreak of cholera and occurred principally from the years 1961 to 1975; the strain involved persists to the present. This pandemic, based on the strain called El Tor, started in Indonesia in 1961 and spread to Bangladesh by 1963. Then it went to India in 1964, followed by the Soviet Union by 1966. In July 1970 there was an outbreak in Odessa and in 1972 there were reports of outbreaks in Baku, but the Soviet Union suppressed this information. It reached Italy in 1973 from North Africa. Japan and the South Pacific saw a few outbreaks by the late 1970s. In 1971, the number of cases reported worldwide was 155,000. In 1991, it reached 570,000. The spread of the disease was helped by modern transportation and mass migrations. Mortality rates, however, dropped markedly as governments began modern curative and preventive measures. The usual mortality rate of 50% dropped to 10% by the 1980s and less than 3% by the 1990s.

In 1991, the strain made a comeback in Latin America. It began in Peru, where it killed roughly 10,000 people. Research has traced the origin of the strain to the seventh cholera pandemic. It was suspected the strain came to Latin America through Asia from contaminated water, but samples from Latin America and samples from Africa were found to be identical.

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The seventh cholera pandemic was the seventh major outbreak of cholera and occurred principally from the years 1961 to 1975; the strain involved persists to the present. This pandemic, based on the strain called El Tor, started in Indonesia in 1961 and spread to Bangladesh by 1963.

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My mother had Hong Kong Flu

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The Hong Kong flu, also known as the 1968 flu pandemic, was a flu pandemic whose outbreak in 1968 and 1969 killed between one and four million people globally. It is among the deadliest pandemics in history, and was caused by an H3N2 strain of the influenza A virus. The virus was descended from H2N2 (which caused the Asian flu pandemic in 1957-1958) through antigenic shift, a genetic process in which genes from multiple subtypes are reassorted to form a new virus.

The first recorded instance of the outbreak appeared on 13 July 1968 in British Hong Kong. It has been speculated that the outbreak began in mainland China before it spread to Hong Kong; On 11 July, before the outbreak in the colony was first noted, the Hong Kong newspaper reported an outbreak of respiratory illness in Guangdong Province, and the next day, issued a similar report of an epidemic in southeastern China. Later reporting suggested that the flu had spread from the central provinces of Sichuan, Gansu, Shaanxi, and Shanxi, which had experienced epidemics in the spring. However, due to a lack of etiological information on the outbreak and a strained relationship between Chinese health authorities and those in other countries at the time, it cannot be ascertained whether the Hong Kong virus was to blame.

The outbreak in Hong Kong, where the population density was greater than 6,000 people per square kilometre (20,000 per sq. mi.), [clarify ] reached its maximum intensity in two weeks. The outbreak lasted around six weeks, affecting about 15% of the population (some 500,000 people infected), but the mortality rate was low and the clinical symptoms were mild.

There were two waves of the flu in mainland China, one between July-September in 1968 and the other between June-December in 1970. The reported data were very limited due to the Cultural Revolution, but retrospective analysis of flu activity between 1968 and 1992 shows that flu infection was the most serious in 1968, implying that most areas in China were affected at the time.

Despite the lethality of the 1957-1958 pandemic in China, little improvement had been made regarding the handling of such epidemics.

By 13 August, it was clear to virologists that strains isolated from the outbreak in Hong Kong differed markedly from previous strains of influenza. However, they were not at the time considered to be an entirely new subtype of influenza A, only a variant of older strains. Nevertheless, the World Health Organization warned of potential worldwide spread of the virus on 16 August. An outbreak of influenza-like illness in Singapore during the second week of August was the first indication of spread outside of Hong Kong. Around the same time, an outbreak became apparent in the Philippines and Malaysia, and, before the end of the month, an epidemic was underway in the Republic of Vietnam.

In September 1968, the flu reached India, northern Australia, Thailand, and Europe. The same month, the virus entered the United States and was carried by troops returning from the Vietnam War, but it did not become widespread in the country until December 1968.

During the second week of September, nearly 2000 participants from 92 countries, including some in southeast Asia where the flu was epidemic, met in Tehran for the Eighth International Congresses on Tropical Medicine and Malaria. An outbreak of influenza soon erupted among the participants, afflicting at least a third of them. The convention was the apparent origin of a broader outbreak within the capital city, which thereafter spread rapidly throughout Iran.

The development of the pandemic at first resembled that of the 1957 pandemic, which had spread unencumbered throughout the spring and summer and had become truly worldwide by October, by which point nearly all countries were experiencing their first or even second wave. However, the two experiences eventually diverged within a couple of months after their initial outbreaks. In 1968, many countries (e.g., the UK, Japan) did not immediately see outbreaks despite repeated introductions of the virus throughout August and September. Additionally, after September, there was little evidence of continued spread in new areas, despite similar importations of the virus into those areas. Epidemics did eventually develop during the winter months, but these were often mild (especially when compared to the US experience). In some countries (such as the UK and Japan), it was not until the following winter of 1969-1970 that truly severe epidemics developed.

At the time of the outbreak, the Hong Kong flu was also known as the "Mao flu" or " Mao Tse-tung flu". The name "Hong Kong flu" was not used within the colony, where the press dubbed it the "killer flu" after the first several deaths. Before the end of July, the South China Morning Post predicted that "Fingers of scorn" would be directed at Hong Kong in the coming weeks and stated that the colony had "acted, unwillingly, in our old role as an entrepot for a sneeze". (An outbreak of influenza in Hong Kong had been the first one to occur outside of mainland China during the 1957-1958 pandemic and had been what alerted the rest of the world to the developing situation, when international press began to report on it.)

A city councillor[who? ] later decried the widespread adoption of the name "Hong Kong flu", claiming that it was "giving Hong Kong a bad name". He asked why foreign press and health authorities did not refer to it by its "proper name-China flu". China certainly did not escape associations with the new virus, however, as the name "Mao flu" suggests. It was speculated even at the time that the virus had originated from "Red China". These differing names for the flu resulted in some confusion: In January 1969, a British member of parliament asked David Ennals, the Secretary of State for Social Services, "in what way the characteristics of Mao flu can be distinguished from those of Hong Kong flu". In addition to these names, the virus was also often referred to as "Asian flu" or "Asiatic flu", as it was not yet considered an entirely different subtype from the previously circulating influenza A.

Worldwide deaths from the virus peaked in December 1968 and January 1969, when public health warnings and virus descriptions had been widely issued in the scientific and medical journals. Isolated countries like Albania reported the first cases of the flu in December 1969, reaching a peak in infections in the first months of the year 1970. In Berlin, the excessive number of deaths led to corpses being stored in subway tunnels, and in West Germany, garbage collectors had to bury the dead because of a lack of undertakers. In total, East and West Germany registered 60,000 estimated deaths. In some areas of France, half of the workforce was bedridden, and manufacturing suffered large disruptions because of absenteeism. The UK postal and rail services were also severely disrupted.

United States

After a major epidemic of H2N2 during the 1967-1968 flu season that resulted in outbreaks in all but four states, the Communicable Disease Center (today the Centers for Disease Control and Prevention) in June 1968 forecasted little or no activity in 1968-1969. The vaccines for the upcoming season would incorporate the then-circulating seasonal flu strains, and the CDC's recommendations for their use extended mainly to individuals in older age groups (over the age of 45) and the chronically ill.

Following the outbreak in Hong Kong and the recognition that it had been caused by a new variant of influenza, the CDC on 4 September revised its prediction for the 1968-1969 season. An extensive outbreak across the country was now more likely. It repeated more strongly its recommendation that existing vaccines go only to those at highest risk and recommended vaccinating or revaccinating this group once the monovalent vaccine specific to the new variant became available.

The first cases of the virus were reported in Atlanta on 2 September. The first was a Marine Corps major returning from Vietnam, who fell ill four days after arriving back in the US. Two days later, his wife, who had not left the country, fell ill as well. The first outbreak occurred in a Marine Corps school in San Diego that same week. Before the end of the week, influenza surveillance was heightened all across the country, and summaries of the data were thereafter reported regularly by the CDC each week in its Morbidity and Mortality Weekly Report. Further outbreaks among military personnel with connections to southeast Asia were soon to follow during the middle of September.

Isolated cases, mostly in those recently returning from the Far East, seeded the virus across the country throughout September. The first outbreaks in the civilian population occurred in late September and in October, and activity increased markedly throughout November, affecting 21 states by Thanksgiving.

The epidemic became widespread in December, involving all 50 states before the end of the year. Outbreaks occurred in colleges and hospitals, in some places the disease attacking upwards of 40% of their populations. Reports of absenteeism among students and nurses grew. Schools in Los Angeles, for example, reported rates ranging from 10 to 25%, compared to a typical 5 or 6%. The Greater New York Hospital Association reported absenteeism of 15 to 20% among staff and urged its members to impose visitor restrictions to safeguard patients.

Institutions in many states dismissed their students early for the holidays. In New York and many other areas, holiday sales suffered mid-December, which affected retailers blamed on the flu epidemic (though inflation could have contributed to this as well). Economic activity was also hampered by high levels of industrial absenteeism.

On 18 December, it was reported that President Johnson had been hospitalized at Bethesda Naval Hospital with flu-like symptoms, but whether the new variant was the cause of his illness was not made clear. He returned to the White House on 22 December. Vice President Humphrey was also reported to be ailing from the flu on the day Johnson's condition was revealed. Flu-like illness kept other senior governmental officials from their posts around this time, such as National Security Advisor Walt Rostow, Deputy White House Press Secretary Tom Johnson, and chairman of the Joint Chiefs of Staff General Earle Wheeler. On 23 December, it was reported that President-elect Nixon had been ill with the flu at his daughter's wedding the day before. Nixon later claimed that "the wedding cured the flu."

Peak influenza activity for most states most likely occurred in the latter half of December or early January, but the exact week was impossible to determine due to the holiday season. Activity declined throughout January. Excess pneumonia-influenza mortality passed the epidemic threshold during the first week of December and increased rapidly over the next month, peaking in the first half of January. It took until late March for mortality to return to normal levels. There was no second wave during this season.

Following the epidemic of influenza A, outbreaks of influenza B began in late January and continued until late March. Mostly elementary-school children were affected. This influenza B activity fit within the pattern of epidemics every three to six years, but the 1968-1969 flu season became the first documented instance of two major influenza A epidemics to occur in successive seasons.

Given the widespread epidemic levels of influenza A activity in 1968-1969, the CDC in June 1969 predicted little more than "sporadic cases" of influenza A in the 1969-1970 season. Influenza activity was indeed less than the preceding season, but there was "considerably more" than expected. The flu affected 48 states the following season but was widespread in only six, compared to 44 out of the 50 states in which activity was reported in 1968-1969.

It became apparent once the extent of antigenic variation in the virus was recognized that a new vaccine would be needed to protect against it. However, production of the previously recommended vaccines in the US had concluded by July 1968, and supply of fertilized chicken eggs, in which flu vaccines are grown, was limited. The first cultures of the virus were provided to manufacturers in August by the Division of Biologics of the National Institutes of Health for preliminary study. A strain isolated in Japan was sent to the US and, after showing greater potential for vaccine production, was given to manufacturers on 9 September.

In 1968, American microbiologist Maurice Hilleman was head of the virus and vaccination research programs at the pharmaceutical firm Merck & Co., one of the licensed vaccine manufacturers in the US. Hilleman, as the director of the Department of Respiratory Diseases at the Army Medical School (now the Walter Reed Army Institute of Research), had foreseen the 1957 pandemic and kickstarted vaccine production then. He was similarly instrumental in the development of the 1968 pandemic vaccine and, with the use of the Japanese strain, helped initiate early production. Merck would go on to produce over 9 million of the nearly 21 million doses of vaccine produced. The other half was produced together by Eli Lilly & Co., Lederle Laboratories, Parke Davis & Co., the National Drug Company, and Wyeth Laboratories. All of these except Wyeth had been involved in the production of the 1957 vaccine.

On 15 November, 66 days after the production strain became available, the first batch of 110,000 doses of vaccine was released, most of which went to the Armed Forces. This represented a quicker turnaround than the release of the first doses of the 1957 vaccine, which took three months after its production strain became available. At this time, the flu was spreading fast around the country. There was much interest within the press and among public figures in the vaccine. On 18 November, the Pharmaceutical Manufacturers Association announced that 17.5 million doses would be available for civilian use but said that "substantial quantities" would only come after the New Year. By the end of the year, over 10 million doses had been released. At this point, influenza was widespread in the country.

Notably, the crew of Apollo 8 received the vaccine on 3 December prior to their mission later in the month. President Johnson received "two types" of vaccine prior to his bout of flu in December, but it is not clear if one of these was the pandemic vaccine. Johnson, 60 at the time, was in poor health and had been hospitalized several times during his presidency. He thus would have been prioritized for vaccine given the CDC recommendations, even outside of being the president.

Lots of vaccine continued to be released throughout January 1969, with nearly 21 million doses available by the end of the month. By this point, however, influenza activity and subsequent mortality had already peaked. Demand for the vaccine diminished and a considerable surplus remained. Given the time it took to build up antibodies, it is unlikely a significant number of people were effectively immunized to alter the course of the epidemic. Hilleman himself would later acknowledge that the vaccine was "too little and too late" for most of the country. However, it was estimated that a "considerably higher" proportion of the recommended priority group of older and chronically ill persons received the pandemic vaccine than in 1957. Nevertheless, even after the debacle that was the vaccination effort in 1957, US health officials by 1968 still had "no meaningful information regarding [influenza vaccine's] actual distribution", such as "to what extent it actually reaches persons at highest risk."

Following the epidemic in the US, leftover vaccine was made available for the southern hemisphere and parts of Europe where the main outbreak had not yet happened. The Japanese strain of the new variant was incorporated into the bivalent vaccines recommended for the 1969-1970 flu season in the US.

Outside the US, vaccination efforts were undertaken in many countries in anticipation of an epidemic. In contrast to US policy, Japan had, since 1963, carried out mass vaccination campaigns against influenza every year regardless of whether an epidemic was expected. This began with the immunization of all children in kindergartens and primary and secondary schools followed by the vaccination of those working in crowded conditions. Enough vaccine was produced each year to vaccinate about 24 million people (nearly a quarter of Japan's population at this time), and this became the goal in 1968, targeting the same priority groups as in a typical flu season.

The same Japanese strain used for vaccine production in the US was immediately sent out to the seven manufacturing firms in Japan. It was soon decided a bivalent vaccine consisting of two parts the new variant and one part influenza B would be produced, in contrast to the US's use of monovalent vaccine. The objective was also set that enough vaccine to immunize about 12 million people would be produced by the end of October, with the hope of at least vaccinating children to guard against an epidemic developing out of schools. After some delay, the mass vaccination campaign was nearly completed before the end of the year.

In Denmark, the influenza department at the governmental Statens Serum Institut produced about 200,000 doses of pandemic vaccine during the winter of 1968-1969, incorporating a strain isolated in Stockholm. There were no particular difficulties in production, but yield was poor.

By January 1969, vaccine production in Australia was underway at the Commonwealth Serum Laboratories (CSL), then a department of the federal government. The trivalent pandemic vaccine, composed of two influenza A strains and a B strain, was anticipated for release in early March ahead of the winter flu season. The inoculation consisted of a two-dose series, each given four weeks apart.

CSL was aggressive in its promotion of the vaccine, at least to doctors. A spokesman for the laboratories described the new virus as "the worst flu we have had" and called an epidemic that year "almost certain". In light of the situation, the Australian Pensioners Federation in early January wrote to Minister for Health Jim Forbes "demanding" that the vaccine be given free of charge to pensioners. In contrast to CSL's bolder predictions, Forbes described an outbreak that winter as "possible" but did not think it would "necessarily be serious or extensive". While the Department of Health reviewed the question of pandemic vaccine allocation in Australia, the government exported 1 million doses of its vaccine to Britain, already at the peak of its epidemic.

In early February, the epidemiology committee of Australia's National Health and Medical Research Council met in Melbourne to discuss the influenza threat and the best use of vaccine the coming winter. A "serious epidemic" was considered the "strongest possibility", and it was recommended to Forbes that older people, children, and pregnant women receive free immunization against the flu. However, the council advised against a mass vaccination campaign, citing the findings of its study which showed the unreliable protection against infection of the present vaccines, and considered it unwise to vaccinate healthy people while the limited supply could be better used to mitigate severe outcomes in at-risk groups.

On the last day of February, the Pharmaceutical Benefits Advisory Committee met to consider the question of making the pandemic vaccine a pharmaceutical benefit for pensioners. Before the end of the week, Forbes announced that shots would be given for free to all pensioners and their dependents, representing about two-thirds of the three groups recommended for priority immunization. The policy would go into effect starting 1 April.

Vaccination against the flu was recommended beginning 1 March, but issues surrounding availability of vaccine soon became apparent throughout the month. In response to Representative Gordon Scholes of Victoria, who had heard complaints from chemists unable to acquire vaccine, Forbes clarified that bulk orders from larger establishments would be met first. He relayed the expectation of the director of CSL that the present situation would be met once quantities of single doses became available in early April.

In the middle of March, Forbes assured that all medical practitioners would be able to acquire the vaccine by the middle of April. He described the new type of flu as milder than that which Australia had typically seen each year.

Representative Charles Jones of Newcastle later in the month questioned Forbes why his home city's order had not been filled. Forbes revealed the export of 1 million doses to Britain earlier in the year but assured that the order "did not delay, or in any way hinder, [the Commonwealth Serum Laboratories'] capacity to fill Australian orders" and that there would be enough supply to meet expected demand. By this time, 1,755,000 doses had been released, and production continued its pace of 200,000 doses per week.

Despite these assurances from Forbes, the Director General of the Department of Health William Refshauge sent a letter on 9 April to all doctors in the country asking them not to vaccinate healthy people until at-risk groups in the community have been inoculated. Forbes reported meeting with the Commonwealth Serum Laboratories commission to discuss how to speed up distribution of vaccine. Two days later, the director of CSL, W. R. Lane, dismissed criticism of the supply situation from the New South Wales branch of the Australian Medical Association as "a lot of nonsense". Contradicting the laboratories' more forceful marketing earlier in the year, he downplayed the likelihood of a serious epidemic but shared the expectation of 4 million doses distributed by the end of May, eight times as much as the average annual total distribution of 500,000 vaccine doses.

On 22 April, Forbes testified in the House of Representatives regarding the vaccine situation. He reported 2.5 million doses had been produced by this time since February. When asked by Representative Theo Nicholls of South Australia to consider importing vaccine to alleviate the present shortage, Forbes noted that the country had already imported the 150,000 doses available. He lamented CSL's recent subjection to a "good deal of abuse" regarding the "temporary shortages" around the country, repeating the comparison between the present production effort and the country's average annual distribution of only 500,000 doses. That same day, N. F. Keith, president of the Victorian branch of the Pharmacy Guild, called on CSL to explain the situation surrounding vaccine supply to the public, which was putting pressure on chemists due to the lack of vaccines.

On 25 April, it was reported that the Department of Health had reimported the remaining vaccine from the order of 1 million that the government had exported to Britain in January. After being sent to Britain, packaged there, and then sent back to Australia, it was sold to doctors at a markup of nearly 50 percent. Doctors criticized the Department and CSL's poor planning with respect to vaccine supply and the decision to export vaccine to Britain when it had already reached the peak of its flu season. They also blamed the shortage on an overreaction by the public, a response which they considered largely due to public statements made by CSL and health officials. The Department later attributed the decision to reimport the vaccine to a desire to ensure a reliable supply for pensioners. It also denied any involvement in the commercial sales of vaccine, in response to reporting on price markups on the reimported vaccine, saying that all it did was authorize the reimportation and list the product as a pharmaceutical benefit. The government itself was paying the same for the reimported vaccine as it was for that being distributed by CSL.

By the end of April, 2.8 million doses of vaccine had been produced and distributed, with no signs of production slowing down. 250,000 doses were now being produced each week, and nearly half a million more were anticipated for 2 May.

The H3N2 virus displaced the previously circulating H2N2 virus, which first emerged in 1957, and returned during the following 1969-70 flu season, which resulted in a second, deadlier wave of deaths in Europe, Japan, and Australia.

Following the season of intense activity in many countries in the Southern Hemisphere, there was relatively low incidence of flu the subsequent two global flu seasons, from October 1970 to September 1971. Influenza B was predominant in the north, causing extensive outbreaks in the United States, but minimal in the south. The Hong Kong virus, on the other hand, was responsible for some large outbreaks in the Southern Hemisphere, some most likely occurring in populations that had still not been exposed to the virus.

It was during this period that the city of Coonoor, in India, experienced a "fairly extensive" outbreak, in July 1971. Samples of the virus responsible were collected but their significance was not immediately recognized. The virus did not immediately spread to other countries, or at least did not immediately cause outbreaks, but it was amid an epidemic in England in early 1972, fueled by more original strains, that a variant showing considerable antigenic drift was identified in one isolate tested out of over 700. It ultimately came to be designated A/England/42/72. It was soon recognized, by comparison with the strains isolated then, that this virus had been the one responsible for the epidemic in India.

The novel variant did not immediately spread after that outbreak, and circulating strains largely continued to resemble quite closely the original Hong Kong virus through April 1972. In May, however, at the onset of the flu season in the Southern Hemisphere, epidemics caused by the variant struck Malaysia, Singapore, and Australia, though South Africa and South America were unaffected. The die seemingly cast, the novel variant went on to cause widespread outbreaks in the Northern Hemisphere, by which point US press had dubbed the bug " London flu". It completely replaced the previous strains still resembling the original pandemic virus. In places such as the US and England and Wales, the 1972-1973 flu season was the deadliest since their respective deadliest waves of the pandemic between 1968 and 1970.

Influenza A/H3N2 remains in circulation today as a strain of seasonal flu.

Flu symptoms typically lasted four to five days, but some cases persisted for up to two weeks.

The influenza viruses that caused the Hong Kong flu (magnified approximately 100,000 times)

The Hong Kong flu was the first known outbreak of the H3N2 strain, but there is serologic evidence of H3N1 infections in the late 19th century. The virus was isolated in Queen Mary Hospital.

Soon after the initial outbreak in Hong Kong, the virus responsible was recognized to be antigenically distinct from the current influenza A strain in circulation (which at the time was called "A2") but was generally not considered an entirely new subtype. Analysis using the conventional techniques at the time revealed that it was indeed very different from older A2 viruses but also, at the same time, seemingly related to them, depending on one's reading of the data. Experiments involving newer methods of analysis soon identified another surface antigen, neuraminidase, in addition to hemagglutinin, which had already been recognized. It thus became clear that it was the hemagglutinin that had changed compared to older strains while the neuraminidase was identical. These findings, in part, prompted the World Health Organization in 1971 to revise its system of nomenclature for influenza viruses, taking into consideration both antigens. The novel virus was thereafter designated H3N2, indicating its partial similarity to H2N2 but also its antigenic distinction.

The H3N2 pandemic flu strain contained genes from a low- pathogenicity avian influenza virus. Specifically, it had acquired a new hemagglutinin gene and a new PB1 gene, while it preserved the neuraminidase and five other genes from the preexisting human H2N2 strain. The new hemagglutinin helped H3N2 evade preexisting immunity in humans. It is possible that the new PB1 facilitated viral replication and human-to-human transmission.

The new subtype arose in pigs coinfected with avian and human viruses and was soon transferred to humans. Swine were considered the original "intermediate host" for influenza because they supported reassortment of divergent subtypes. However, other hosts appear capable of similar coinfection (such as many poultry species), and direct transmission of avian viruses to humans is possible. H1N1, associated with the 1918 flu pandemic, may have been transmitted directly from birds to humans.

Accumulated antibodies to the neuraminidase or internal proteins may have resulted in many fewer casualties than most other pandemics. However, cross-immunity within and between subtypes of influenza is poorly understood.[citation needed ]

The estimates of the total death toll due to Hong Kong flu (from its beginning in July 1968 until the outbreak faded during the winter of 1969-70) vary:

However, the death rate from the Hong Kong flu was lower than most other 20th-century pandemics. The World Health Organization estimated the case fatality rate of Hong Kong flu to be lower than 0.2%. The disease was allowed to spread through the population without restrictions on economic activity, and a vaccine created by American microbiologist Maurice Hilleman and his team became available four months after it had started. Fewer people died during this pandemic than in previous pandemics for several reasons:

1. Some immunity against the N2 flu virus may have been retained in populations struck by the Asian Flu strains that had been circulating since 1957.

2. The pandemic did not gain momentum until near the winter school holidays in the Northern Hemisphere, thus limiting the infection's spread.

3. Improved medical care gave vital support to the very ill.

4. The availability of antibiotics that were more effective against secondary bacterial infections.

For this pandemic, there were two geographically distinct mortality patterns. In North America (the United States and Canada), the first pandemic season (1968-69) was more severe than the second (1969-70). In the "smoldering" pattern seen in Europe and Asia (United Kingdom, France, Japan, and Australia), the second pandemic season was two to five times more severe than the first. The United States health authorities estimated that about 34,000 to 100,000 people died in the US; most excess deaths were in those aged 65 and older.

1. ^ Paul, William E. (2008). Fundamental Immunology. Lippincott Williams & Wilkins. p. 1273. ISBN 9780781765190. Archived from the original on 2 July 2014.

2. ^ "World health group issues alert Mexican president tries to isolate those with swine flu". Associated Press. 25 April 2009. Archived from the original on 27 April 2009.

3. ^ Mandel, Michael (26 April 2009). "No need to panic... yet Ontario officials are worried swine flu could be pandemic, killing thousands". Toronto Sun. Archived from the original on 27 April 2009.

4. ^ Chang, W. K. (1969). "National Influenza Experience in Hong Kong, 1968" (PDF). Bulletin of the World Health Organization. WHO. 41 (3): 349-351. PMC . PMID 5309438.

5. ^ Murray, Roderick (1969). "Production and testing in the USA of influenza virus vaccine made from the Hong Kong variant in 1968-69". Bulletin of the World Health Organization. 41: 493-496. hdl:10665/262478 - via IRIS.

6. ^ Coleman, Marion T.; Dowdle, Walter R.; Pereira, Helio G.; Schild, Geoffrey C.; Chang, W. K. (1968), "The Hong Kong/68 Influenza A2 Variant", , 292 (7583): 1384-1386, doi:10.1016/S0140-6736(68)92683-4, PMID 4177941

7. ^ "Si u prek Shqipëria nga gripi spanjoll në 1918 dhe ai kinez në 1970! Dokumentet e panjohura|DOSJA E". .

8. ^ World Health Organization; Candau, Marcolino Gomes (April 1969). "The work of WHO, 1968: annual report of the Director-General to the World Health Assembly and to the United Nations". Official Records of the World Health Organization. hdl:10665/85812. ISBN 9789241601726 - via IRIS.

9. "Vaccine for Hong Kong Influenza Pandemic". History of Vaccines. Archived from the original on 17 April 2021.

10. "Govt unlikely to give mass flu 'shots'". The Canberra Times. 13 February 1969. p. 3.

11. ^ Belshe, R. B. (2005). "The origins of pandemic influenza - lessons from the 1918 virus". New England Journal of Medicine. 353 (21): 2209-2211. doi:10.1056/NEJMp058281. PMID 16306515. Cited in Harder, Timm C.; Werner, Ortrud. Kamps, Bernd Sebastain; Hoffmann, Christian; Preiser, Wolfgang (eds.). "Influenza Report". Archived from the original on 10 May 2016.

12. ^ Biggerstaff, M.; Cauchemez, S.; Reed, C.; et al. (2014). "Estimates of the reproduction number for seasonal, pandemic, and zoonotic influenza: a systematic review of the literature". BMC Infectious Diseases. 14 (480): 480. doi:10.1186/1471-2334-14-480. PMC . PMID 25186370.

13. ^ "Pandemics and Pandemic Threats since 1900". U.S. Department of Health and Human Services. Archived from the original on 31 March 2009.

14. ^ Shiel, William. "Medical Definition of Hong Kong flu". MedicineNet. Archived from the original on 28 October 2020.

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The Hong Kong flu, also known as the 1968 flu pandemic, was a flu pandemic whose outbreak in 1968 and 1969 killed between one and four million people globally. It is among the deadliest pandemics in history, and was caused by an H3N2 strain of the influenza A virus.

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AIDS was first clinically reported on June 5, 1981, with five cases in the United States.

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HIV/AIDS

Other names

HIV disease, HIV infection[1][2]

The red ribbon is a symbol for solidarity with HIV-positive people and those living with AIDS.[3]

Specialty
Infectious disease

Symptoms

Early: Flu-like illness[4]
Later: Large lymph nodes, fever, weight loss[4]

Complications

Opportunistic infections, tumors[4]

Duration

Lifelong[4]

Causes

Human immunodeficiency virus (HIV)[4]

Risk factors

Exposure to blood, breast milk, sex[4]

Diagnostic method

Blood tests[4]

Prevention

Safe sex, needle exchange, male circumcision, pre-exposure prophylaxis, post-exposure prophylaxis[4]

Treatment
Antiretroviral therapy[4]

Prognosis

Near normal life expectancy with treatment[5][6]
11 years life expectancy without treatment[7]

Frequency

1.7 million new cases (2018)[8]
37.9 million living with HIV (2018)[8]

Deaths

770,000 (2018)[8]

Human immunodeficiency virus infection and acquired immune deficiency syndrome ( HIV/AIDS) is a spectrum of conditions caused by infection with the human immunodeficiency virus (HIV). Following initial infection a person may not notice any symptoms, or may experience a brief period of influenza-like illness. Typically, this is followed by a prolonged period with no symptoms. If the infection progresses, it interferes more with the immune system, increasing the risk of developing common infections such as tuberculosis, as well as other opportunistic infections, and tumors which are otherwise rare in people who have normal immune function. These late symptoms of infection are referred to as acquired immunodeficiency syndrome (AIDS). This stage is often also associated with unintended weight loss.

HIV is spread primarily by unprotected sex (including anal and oral sex), contaminated blood transfusions, hypodermic needles, and from mother to child during pregnancy, delivery, or breastfeeding. Some bodily fluids, such as saliva, sweat and tears, do not transmit the virus. HIV is a member of the group of viruses known as retroviruses.

Methods of prevention include safe sex, needle exchange programs, treating those who are infected, pre- and post-exposure prophylaxis, and male circumcision. Disease in a baby can often be prevented by giving both the mother and child antiretroviral medication. There is no cure or vaccine; however, antiretroviral treatment can slow the course of the disease and may lead to a near-normal life expectancy. Treatment is recommended as soon as the diagnosis is made. Without treatment, the average survival time after infection is 11 years.

In 2018 about 37.9 million people were living with HIV and it resulted in 770,000 deaths. An estimated 20.6 million of these live in eastern and southern Africa. Between the time that AIDS was identified (in the early 1980s) and 2018, the disease caused an estimated 32 million deaths worldwide. HIV/AIDS is considered a pandemic-a disease outbreak which is present over a large area and is actively spreading. HIV made the jump from other primates to humans in west-central Africa in the early-to-mid 20th century. AIDS was first recognized by the United States Centers for Disease Control and Prevention (CDC) in 1981 and its cause-HIV infection-was identified in the early part of the decade.

HIV/AIDS has had a large impact on society, both as an illness and as a source of discrimination. The disease also has large economic impacts. There are many misconceptions about HIV/AIDS, such as the belief that it can be transmitted by casual non-sexual contact. The disease has become subject to many controversies involving religion, including the Catholic Church's position not to support condom use as prevention. It has attracted international medical and political attention as well as large-scale funding since it was identified in the 1980s.

Signs and symptoms

There are three main stages of HIV infection: acute infection, clinical latency, and AIDS.

Acute infection

The initial period following the contraction of HIV is called acute HIV, primary HIV or acute retroviral syndrome. Many individuals develop an influenza-like illness or a mononucleosis-like illness 2-4 weeks after exposure while others have no significant symptoms. Symptoms occur in 40-90% of cases and most commonly include fever, large tender lymph nodes, throat inflammation, a rash, headache, tiredness, and/or sores of the mouth and genitals. The rash, which occurs in 20-50% of cases, presents itself on the trunk and is maculopapular, classically. Some people also develop opportunistic infections at this stage. Gastrointestinal symptoms, such as vomiting or diarrhea may occur. Neurological symptoms of peripheral neuropathy or Guillain-Barré syndrome also occurs. The duration of the symptoms varies, but is usually one or two weeks.

Owing to their nonspecific character, these symptoms are not often recognized as signs of HIV infection. Even cases that do get seen by a family doctor or a hospital are often misdiagnosed as one of the many common infectious diseases with overlapping symptoms. Thus, it is recommended that HIV be considered in people presenting with an unexplained fever who may have risk factors for the infection.

Clinical latency

The initial symptoms are followed by a stage called clinical latency, asymptomatic HIV, or chronic HIV. Without treatment, this second stage of the natural history of HIV infection can last from about three years to over 20 years (on average, about eight years). While typically there are few or no symptoms at first, near the end of this stage many people experience fever, weight loss, gastrointestinal problems and muscle pains. Between 50% and 70% of people also develop persistent generalized lymphadenopathy, characterized by unexplained, non-painful enlargement of more than one group of lymph nodes (other than in the groin) for over three to six months.

Although most HIV-1 infected individuals have a detectable viral load and in the absence of treatment will eventually progress to AIDS, a small proportion (about 5%) retain high levels of CD4⁺ T cells ( T helper cells) without antiretroviral therapy for more than five years. These individuals are classified as "HIV controllers" or long-term nonprogressors (LTNP). Another group consists of those who maintain a low or undetectable viral load without anti-retroviral treatment, known as "elite controllers" or "elite suppressors". They represent approximately 1 in 300 infected persons.

Acquired immunodeficiency syndrome

Acquired immunodeficiency syndrome (AIDS) is defined as an HIV infection with either a CD4⁺ T cell count below 200 cells per µL or the occurrence of specific diseases associated with HIV infection. In the absence of specific treatment, around half of people infected with HIV develop AIDS within ten years. The most common initial conditions that alert to the presence of AIDS are pneumocystis pneumonia (40%), cachexia in the form of HIV wasting syndrome (20%), and esophageal candidiasis. Other common signs include recurrent respiratory tract infections.

Opportunistic infections may be caused by bacteria, viruses, fungi, and parasites that are normally controlled by the immune system. Which infections occur depends partly on what organisms are common in the person's environment. These infections may affect nearly every organ system.

People with AIDS have an increased risk of developing various viral-induced cancers, including Kaposi's sarcoma, Burkitt's lymphoma, primary central nervous system lymphoma, and cervical cancer. Kaposi's sarcoma is the most common cancer, occurring in 10% to 20% of people with HIV. The second-most common cancer is lymphoma, which is the cause of death of nearly 16% of people with AIDS and is the initial sign of AIDS in 3% to 4%. Both these cancers are associated with human herpesvirus 8 (HHV-8). Cervical cancer occurs more frequently in those with AIDS because of its association with human papillomavirus (HPV). Conjunctival cancer (of the layer that lines the inner part of eyelids and the white part of the eye) is also more common in those with HIV.

Additionally, people with AIDS frequently have systemic symptoms such as prolonged fevers, sweats (particularly at night), swollen lymph nodes, chills, weakness, and unintended weight loss. Diarrhea is another common symptom, present in about 90% of people with AIDS. They can also be affected by diverse psychiatric and neurological symptoms independent of opportunistic infections and cancers.

Transmission

HIV is spread by three main routes: sexual contact, significant exposure to infected body fluids or tissues, and from mother to child during pregnancy, delivery, or breastfeeding (known as vertical transmission). There is no risk of acquiring HIV if exposed to feces, nasal secretions, saliva, sputum, sweat, tears, urine, or vomit unless these are contaminated with blood. It is also possible to be co-infected by more than one strain of HIV-a condition known as HIV superinfection.

The most frequent mode of transmission of HIV is through sexual contact with an infected person. However, an HIV-positive person who has an undetectable viral load as a result of long-term treatment has effectively no risk of transmitting HIV sexually. Globally, the most common mode of HIV transmission is via sexual contacts between people of the opposite sex; however, the pattern of transmission varies among countries. As of 2017, most HIV transmission in the United States occurred among men who had sex with men (82% of new HIV diagnoses among males aged 13 and older and 70% of total new diagnoses). In the US, gay and bisexual men aged 13 to 24 accounted for an estimated 92% of new HIV diagnoses among all men in their age group and 27% of new diagnoses among all gay and bisexual men. About 15% of gay and bisexual men have HIV, while 28% of transgender women test positive in the US.

With regard to unprotected heterosexual contacts, estimates of the risk of HIV transmission per sexual act appear to be four to ten times higher in low-income countries than in high-income countries. In low-income countries, the risk of female-to-male transmission is estimated as 0.38% per act, and of male-to-female transmission as 0.30% per act; the equivalent estimates for high-income countries are 0.04% per act for female-to-male transmission, and 0.08% per act for male-to-female transmission. The risk of transmission from anal intercourse is especially high, estimated as 1.4-1.7% per act in both heterosexual and homosexual contacts. While the risk of transmission from oral sex is relatively low, it is still present. The risk from receiving oral sex has been described as "nearly nil"; however, a few cases have been reported. The per-act risk is estimated at 0-0.04% for receptive oral intercourse. In settings involving prostitution in low-income countries, risk of female-to-male transmission has been estimated as 2.4% per act, and of male-to-female transmission as 0.05% per act.

Risk of transmission increases in the presence of many sexually transmitted infections and genital ulcers. Genital ulcers appear to increase the risk approximately fivefold. Other sexually transmitted infections, such as gonorrhea, chlamydia, trichomoniasis, and bacterial vaginosis, are associated with somewhat smaller increases in risk of transmission.

The viral load of an infected person is an important risk factor in both sexual and mother-to-child transmission. During the first 2.5 months of an HIV infection a person's infectiousness is twelve times higher due to the high viral load associated with acute HIV. If the person is in the late stages of infection, rates of transmission are approximately eightfold greater.

Commercial sex workers (including those in pornography) have an increased likelihood of contracting HIV. Rough sex can be a factor associated with an increased risk of transmission. Sexual assault is also believed to carry an increased risk of HIV transmission as condoms are rarely worn, physical trauma to the vagina or rectum is likely, and there may be a greater risk of concurrent sexually transmitted infections.

Body fluids

The second-most frequent mode of HIV transmission is via blood and blood products. Blood-borne transmission can be through needle-sharing during intravenous drug use, needle-stick injury, transfusion of contaminated blood or blood product, or medical injections with unsterilized equipment. The risk from sharing a needle during drug injection is between 0.63% and 2.4% per act, with an average of 0.8%. The risk of acquiring HIV from a needle stick from an HIV-infected person is estimated as 0.3% (about 1 in 333) per act and the risk following mucous membrane exposure to infected blood as 0.09% (about 1 in 1000) per act. This risk may, however, be up to 5% if the introduced blood was from a person with a high viral load and the cut was deep. In the United States intravenous drug users made up 12% of all new cases of HIV in 2009, and in some areas more than 80% of people who inject drugs are HIV-positive.

HIV is transmitted in about 93% of blood transfusions using infected blood. In developed countries the risk of acquiring HIV from a blood transfusion is extremely low (less than one in half a million) where improved donor selection and HIV screening is performed; for example, in the UK the risk is reported at one in five million and in the United States it was one in 1.5 million in 2008. In low-income countries, only half of transfusions may be appropriately screened (as of 2008), and it is estimated that up to 15% of HIV infections in these areas come from transfusion of infected blood and blood products, representing between 5% and 10% of global infections. It is possible to acquire HIV from organ and tissue transplantation, although this is rare because of screening.

Unsafe medical injections play a role in HIV spread in sub-Saharan Africa. In 2007, between 12% and 17% of infections in this region were attributed to medical syringe use. The World Health Organization estimates the risk of transmission as a result of a medical injection in Africa at 1.2%. Risks are also associated with invasive procedures, assisted delivery, and dental care in this area of the world.

People giving or receiving tattoos, piercings, and scarification are theoretically at risk of infection but no confirmed cases have been documented. It is not possible for mosquitoes or other insects to transmit HIV.

Mother-to-child

HIV can be transmitted from mother to child during pregnancy, during delivery, or through breast milk, resulting in the baby also contracting HIV. As of 2008, vertical transmission accounted for about 90% of cases of HIV in children. In the absence of treatment, the risk of transmission before or during birth is around 20%, and in those who also breastfeed 35%. Treatment decreases this risk to less than 5%.

Antiretrovirals when taken by either the mother or the baby decrease the risk of transmission in those who do breastfeed. If blood contaminates food during pre-chewing it may pose a risk of transmission. If a woman is untreated, two years of breastfeeding results in an HIV/AIDS risk in her baby of about 17%. Due to the increased risk of death without breastfeeding in many areas in the developing world, the World Health Organization recommends either exclusive breastfeeding or the provision of safe formula. All women known to be HIV-positive should be taking lifelong antiretroviral therapy.

HIV is the cause of the spectrum of disease known as HIV/AIDS. HIV is a retrovirus that primarily infects components of the human immune system such as CD4⁺ T cells, macrophages and dendritic cells. It directly and indirectly destroys CD4⁺ T cells.

HIV is a member of the genus Lentivirus, part of the family Retroviridae. Lentiviruses share many morphological and biological characteristics. Many species of mammals are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. Lentiviruses are transmitted as single-stranded, positive- sense, enveloped RNA viruses. Upon entry into the target cell, the viral RNA genome is converted (reverse transcribed) into double-stranded DNA by a virally encoded reverse transcriptase that is transported along with the viral genome in the virus particle. The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded integrase and host co-factors. Once integrated, the virus may become latent, allowing the virus and its host cell to avoid detection by the immune system. Alternatively, the virus may be transcribed, producing new RNA genomes and viral proteins that are packaged and released from the cell as new virus particles that begin the replication cycle anew.

HIV is now known to spread between CD4⁺ T cells by two parallel routes: cell-free spread and cell-to-cell spread, i.e. it employs hybrid spreading mechanisms. In the cell-free spread, virus particles bud from an infected T cell, enter the blood/extracellular fluid and then infect another T cell following a chance encounter. HIV can also disseminate by direct transmission from one cell to another by a process of cell-to-cell spread. The hybrid spreading mechanisms of HIV contribute to the virus's ongoing replication against antiretroviral therapies.

Two types of HIV have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was originally discovered (and initially referred to also as LAV or HTLV-III). It is more virulent, more infective, and is the cause of the majority of HIV infections globally. The lower infectivity of HIV-2 as compared with HIV-1 implies that fewer people exposed to HIV-2 will be infected per exposure. Because of its relatively poor capacity for transmission, HIV-2 is largely confined to West Africa.

Pathophysiology

After the virus enters the body there is a period of rapid viral replication, leading to an abundance of virus in the peripheral blood. During primary infection, the level of HIV may reach several million virus particles per milliliter of blood. This response is accompanied by a marked drop in the number of circulating . The acute viremia is almost invariably associated with activation of , which kill HIV-infected cells, and subsequently with antibody production, or seroconversion. The CD8⁺ T cell response is thought to be important in controlling virus levels, which peak and then decline, as the CD4⁺ T cell counts recover. A good CD8⁺ T cell response has been linked to slower disease progression and a better prognosis, though it does not eliminate the virus.

Ultimately, HIV causes AIDS by depleting CD4⁺ T cells. This weakens the immune system and allows opportunistic infections. T cells are essential to the immune response and without them, the body cannot fight infections or kill cancerous cells. The mechanism of CD4⁺ T cell depletion differs in the acute and chronic phases. During the acute phase, HIV-induced cell lysis and killing of infected cells by CD8⁺ T cells accounts for CD4⁺ T cell depletion, although apoptosis may also be a factor. During the chronic phase, the consequences of generalized immune activation coupled with the gradual loss of the ability of the immune system to generate new T cells appear to account for the slow decline in CD4⁺ T cell numbers.

Although the symptoms of immune deficiency characteristic of AIDS do not appear for years after a person is infected, the bulk of CD4⁺ T cell loss occurs during the first weeks of infection, especially in the intestinal mucosa, which harbors the majority of the lymphocytes found in the body. The reason for the preferential loss of mucosal CD4⁺ T cells is that the majority of mucosal CD4⁺ T cells express the CCR5 protein which HIV uses as a co-receptor to gain access to the cells, whereas only a small fraction of CD4⁺ T cells in the bloodstream do so. A specific genetic change that alters the CCR5 protein when present in both chromosomes very effectively prevents HIV-1 infection.

HIV seeks out and destroys CCR5 expressing CD4⁺ T cells during acute infection. A vigorous immune response eventually controls the infection and initiates the clinically latent phase. CD4⁺ T cells in mucosal tissues remain particularly affected. Continuous HIV replication causes a state of generalized immune activation persisting throughout the chronic phase. Immune activation, which is reflected by the increased activation state of immune cells and release of pro-inflammatory cytokines, results from the activity of several HIV gene products and the immune response to ongoing HIV replication. It is also linked to the breakdown of the immune surveillance system of the gastrointestinal mucosal barrier caused by the depletion of mucosal CD4⁺ T cells during the acute phase of disease.

HIV/AIDS is diagnosed via laboratory testing and then staged based on the presence of certain signs or symptoms. HIV screening is recommended by the United States Preventive Services Task Force for all people 15 years to 65 years of age, including all pregnant women. Additionally, testing is recommended for those at high risk, which includes anyone diagnosed with a sexually transmitted illness. In many areas of the world, a third of HIV carriers only discover they are infected at an advanced stage of the disease when AIDS or severe immunodeficiency has become apparent.

HIV testing

Most people infected with HIV develop specific antibodies (i.e. seroconvert) within three to twelve weeks after the initial infection. Diagnosis of primary HIV before seroconversion is done by measuring HIV- RNA or p24 antigen. Positive results obtained by antibody or PCR testing are confirmed either by a different antibody or by PCR.

Antibody tests in children younger than 18 months are typically inaccurate, due to the continued presence of maternal antibodies. Thus HIV infection can only be diagnosed by PCR testing for HIV RNA or DNA, or via testing for the p24 antigen. Much of the world lacks access to reliable PCR testing, and people in many places simply wait until either symptoms develop or the child is old enough for accurate antibody testing. In sub-Saharan Africa between 2007 and 2009, between 30% and 70% of the population were aware of their HIV status. In 2009, between 3.6% and 42% of men and women in sub-Saharan countries were tested; this represented a significant increase compared to previous years.

Classifications

Two main clinical staging systems are used to classify HIV and HIV-related disease for surveillance purposes: the WHO disease staging system for HIV infection and disease, and the CDC classification system for HIV infection. The CDC's classification system is more frequently adopted in developed countries. Since the WHO's staging system does not require laboratory tests, it is suited to the resource-restricted conditions encountered in developing countries, where it can also be used to help guide clinical management. Despite their differences, the two systems allow comparison for statistical purposes.

The World Health Organization first proposed a definition for AIDS in 1986. Since then, the WHO classification has been updated and expanded several times, with the most recent version being published in 2007. The WHO system uses the following categories:

Primary HIV infection: May be either asymptomatic or associated with acute retroviral syndrome

Stage I: HIV infection is asymptomatic with a CD4⁺ T cell count (also known as CD4 count) greater than 500 per microlitre (µl or cubic mm) of blood. May include generalized lymph node enlargement.

Stage II: Mild symptoms, which may include minor mucocutaneous manifestations and recurrent upper respiratory tract infections. A CD4 count of less than 500/µl

Stage III: Advanced symptoms, which may include unexplained chronic diarrhea for longer than a month, severe bacterial infections including tuberculosis of the lung, and a CD4 count of less than 350/µl

Stage IV or AIDS: severe symptoms, which include toxoplasmosis of the brain, candidiasis of the esophagus, trachea, bronchi, or lungs, and Kaposi's sarcoma. A CD4 count of less than 200/µl

The United States Center for Disease Control and Prevention also created a classification system for HIV, and updated it in 2008 and 2014. This system classifies HIV infections based on CD4 count and clinical symptoms, and describes the infection in five groups. In those greater than six years of age it is:

Stage 0: the time between a negative or indeterminate HIV test followed less than 180 days by a positive test.

Stage 1: CD4 count ≥ 500 cells/µl and no AIDS-defining conditions.

Stage 2: CD4 count 200 to 500 cells/µl and no AIDS-defining conditions.

Stage 3: CD4 count ≤ 200 cells/µl or AIDS-defining conditions.

Unknown: if insufficient information is available to make any of the above classifications.

For surveillance purposes, the AIDS diagnosis still stands even if, after treatment, the CD4⁺ T cell count rises to above 200 per µL of blood or other AIDS-defining illnesses are cured.

Prevention

Sexual contact

Consistent condom use reduces the risk of HIV transmission by approximately 80% over the long term. When condoms are used consistently by a couple in which one person is infected, the rate of HIV infection is less than 1% per year. There is some evidence to suggest that female condoms may provide an equivalent level of protection. Application of a vaginal gel containing tenofovir (a reverse transcriptase inhibitor) immediately before sex seems to reduce infection rates by approximately 40% among African women. By contrast, use of the spermicide nonoxynol-9 may increase the risk of transmission due to its tendency to cause vaginal and rectal irritation.

Circumcision in Sub-Saharan Africa "reduces the acquisition of HIV by heterosexual men by between 38% and 66% over 24 months". Owing to these studies, both the World Health Organization and UNAIDS recommended male circumcision in 2007 as a method of preventing female-to-male HIV transmission in areas with high rates of HIV. However, whether it protects against male-to-female transmission is disputed, and whether it is of benefit in developed countries and among men who have sex with men is undetermined. The International Antiviral Society, however, does recommend it for all sexually active heterosexual males and that it be discussed as an option with men who have sex with men. Some experts fear that a lower perception of vulnerability among circumcised men may cause more sexual risk-taking behavior, thus negating its preventive effects.

Programs encouraging sexual abstinence do not appear to affect subsequent HIV risk. Evidence of any benefit from peer education is equally poor. Comprehensive sexual education provided at school may decrease high-risk behavior. A substantial minority of young people continues to engage in high-risk practices despite knowing about HIV/AIDS, underestimating their own risk of becoming infected with HIV. Voluntary counseling and testing people for HIV does not affect risky behavior in those who test negative but does increase condom use in those who test positive. Enhanced family planning services appear to increase the likelihood of women with HIV using contraception, compared to basic services. It is not known whether treating other sexually transmitted infections is effective in preventing HIV.

Pre-exposure

Antiretroviral treatment among people with HIV whose CD4 count ≤ 550 cells/µL is a very effective way to prevent HIV infection of their partner (a strategy known as treatment as prevention, or TASP). TASP is associated with a 10- to 20-fold reduction in transmission risk. Pre-exposure prophylaxis (PrEP) with a daily dose of the medications tenofovir, with or without emtricitabine, is effective in people at high risk including men who have sex with men, couples where one is HIV-positive, and young heterosexuals in Africa. It may also be effective in intravenous drug users, with a study finding a decrease in risk of 0.7 to 0.4 per 100 person years. The USPSTF, in 2019, recommended PrEP in those who are at high risk.

Universal precautions within the health care environment are believed to be effective in decreasing the risk of HIV. Intravenous drug use is an important risk factor, and harm reduction strategies such as needle-exchange programs and opioid substitution therapy appear effective in decreasing this risk.

Post-exposure

A course of antiretrovirals administered within 48 to 72 hours after exposure to HIV-positive blood or genital secretions is referred to as post-exposure prophylaxis (PEP). The use of the single agent zidovudine reduces the risk of a HIV infection five-fold following a needle-stick injury. As of 2013, the prevention regimen recommended in the United States consists of three medications- tenofovir, emtricitabine and raltegravir -as this may reduce the risk further.

PEP treatment is recommended after a sexual assault when the perpetrator is known to be HIV-positive, but is controversial when their HIV status is unknown. The duration of treatment is usually four weeks and is frequently associated with adverse effects-where zidovudine is used, about 70% of cases result in adverse effects such as nausea (24%), fatigue (22%), emotional distress (13%) and headaches (9%).

Mother-to-child

Programs to prevent the vertical transmission of HIV (from mothers to children) can reduce rates of transmission by 92-99%. This primarily involves the use of a combination of antiviral medications during pregnancy and after birth in the infant, and potentially includes bottle feeding rather than breastfeeding. If replacement feeding is acceptable, feasible, affordable, sustainable and safe, mothers should avoid breastfeeding their infants; however, exclusive breastfeeding is recommended during the first months of life if this is not the case. If exclusive breastfeeding is carried out, the provision of extended antiretroviral prophylaxis to the infant decreases the risk of transmission. In 2015, Cuba became the first country in the world to eradicate mother-to-child transmission of HIV.

Vaccination

Currently there is no licensed vaccine for HIV or AIDS. The most effective vaccine trial to date, RV 144, was published in 2009; it found a partial reduction in the risk of transmission of roughly 30%, stimulating some hope in the research community of developing a truly effective vaccine. Further trials of the RV 144 vaccine are ongoing.

There is currently no cure, nor an effective HIV vaccine. Treatment consists of highly active antiretroviral therapy (HAART) which slows progression of the disease. As of 2010 more than 6.6 million people were receiving this in low- and middle-income countries. Treatment also includes preventive and active treatment of opportunistic infections. As of March 2020, two persons have been successfully cleared of HIV.

Antiviral therapy

Current HAART options are combinations (or "cocktails") consisting of at least three medications belonging to at least two types, or "classes", of antiretroviral agents. Initially, treatment is typically a non-nucleoside reverse transcriptase inhibitor (NNRTI) plus two nucleoside analog reverse transcriptase inhibitors (NRTIs). Typical NRTIs include: zidovudine (AZT) or tenofovir (TDF) and lamivudine (3TC) or emtricitabine (FTC). As of 2019, dolutegravir/lamivudine/tenofovir is listed by the World Health Organization as the first-line treatment for adults, with tenofovir/lamivudine/efavirenz as an alternative. Combinations of agents that include protease inhibitors (PI) are used if the above regimen loses effectiveness.

The World Health Organization and the United States recommend antiretrovirals in people of all ages (including pregnant women) as soon as the diagnosis is made, regardless of CD4 count. Once treatment is begun, it is recommended that it is continued without breaks or "holidays". Many people are diagnosed only after treatment ideally should have begun. The desired outcome of treatment is a long-term plasma HIV-RNA count below 50 copies/mL. Levels to determine if treatment is effective are initially recommended after four weeks and once levels fall below 50 copies/mL checks every three to six months are typically adequate. Inadequate control is deemed to be greater than 400 copies/mL. Based on these criteria treatment is effective in more than 95% of people during the first year.

Benefits of treatment include a decreased risk of progression to AIDS and a decreased risk of death. In the developing world, treatment also improves physical and mental health. With treatment, there is a 70% reduced risk of acquiring tuberculosis. Additional benefits include a decreased risk of transmission of the disease to sexual partners and a decrease in mother-to-child transmission. The effectiveness of treatment depends to a large part on compliance. Reasons for non-adherence to treatment include poor access to medical care, inadequate social supports, mental illness and drug abuse. The complexity of treatment regimens (due to pill numbers and dosing frequency) and adverse effects may reduce adherence. Even though cost is an important issue with some medications, 47% of those who needed them were taking them in low- and middle-income countries as of 2010, and the rate of adherence is similar in low-income and high-income countries.

Specific adverse events are related to the antiretroviral agent taken. Some relatively common adverse events include: lipodystrophy syndrome, dyslipidemia, and diabetes mellitus, especially with protease inhibitors. Other common symptoms include diarrhea, and an increased risk of cardiovascular disease. Newer recommended treatments are associated with fewer adverse effects. Certain medications may be associated with birth defects and therefore may be unsuitable for women hoping to have children.

Treatment recommendations for children are somewhat different from those for adults. The World Health Organization recommends treating all children less than 5 years of age; children above 5 are treated like adults. The United States guidelines recommend treating all children less than 12 months of age and all those with HIV RNA counts greater than 100,000 copies/mL between one year and five years of age.

Opportunistic infections

Measures to prevent opportunistic infections are effective in many people with HIV/AIDS. In addition to improving current disease, treatment with antiretrovirals reduces the risk of developing additional opportunistic infections. Adults and adolescents who are living with HIV (even on anti-retroviral therapy) with no evidence of active tuberculosis in settings with high tuberculosis burden should receive isoniazid preventive therapy (IPT); the tuberculin skin test can be used to help decide if IPT is needed. Vaccination against hepatitis A and B is advised for all people at risk of HIV before they become infected; however, it may also be given after infection. Trimethoprim/sulfamethoxazole prophylaxis between four and six weeks of age, and ceasing breastfeeding of infants born to HIV-positive mothers, is recommended in resource-limited settings. It is also recommended to prevent PCP when a person's CD4 count is below 200 cells/uL and in those who have or have previously had PCP. People with substantial immunosuppression are also advised to receive prophylactic therapy for toxoplasmosis and MAC. Appropriate preventive measures reduced the rate of these infections by 50% between 1992 and 1997. Influenza vaccination and pneumococcal polysaccharide vaccine are often recommended in people with HIV/AIDS with some evidence of benefit.

The World Health Organization (WHO) has issued recommendations regarding nutrient requirements in HIV/AIDS. A generally healthy diet is promoted. Dietary intake of micronutrients at RDA levels by HIV-infected adults is recommended by the WHO; higher intake of vitamin A, zinc, and iron can produce adverse effects in HIV-positive adults, and is not recommended unless there is documented deficiency. Dietary supplementation for people who are infected with HIV and who have inadequate nutrition or dietary deficiencies may strengthen their immune systems or help them recover from infections; however, evidence indicating an overall benefit in morbidity or reduction in mortality is not consistent.

Evidence for supplementation with selenium is mixed with some tentative evidence of benefit. For pregnant and lactating women with HIV, multivitamin supplement improves outcomes for both mothers and children. If the pregnant or lactating mother has been advised to take anti-retroviral medication to prevent mother-to-child HIV transmission, multivitamin supplements should not replace these treatments. There is some evidence that vitamin A supplementation in children with an HIV infection reduces mortality and improves growth.

Alternative medicine

In the US, approximately 60% of people with HIV use various forms of complementary or alternative medicine, whose effectiveness has not been established. There is not enough evidence to support the use of herbal medicines. There is insufficient evidence to recommend or support the use of medical cannabis to try to increase appetite or weight gain.

HIV/AIDS has become a chronic rather than an acutely fatal disease in many areas of the world. Prognosis varies between people, and both the CD4 count and viral load are useful for predicted outcomes. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype. After the diagnosis of AIDS, if treatment is not available, survival ranges between 6 and 19 months. HAART and appropriate prevention of opportunistic infections reduces the death rate by 80%, and raises the life expectancy for a newly diagnosed young adult to 20-50 years. This is between two thirds and nearly that of the general population. If treatment is started late in the infection, prognosis is not as good: for example, if treatment is begun following the diagnosis of AIDS, life expectancy is ~10-40 years. Half of infants born with HIV die before two years of age without treatment.

The primary causes of death from HIV/AIDS are opportunistic infections and cancer, both of which are frequently the result of the progressive failure of the immune system. Risk of cancer appears to increase once the CD4 count is below 500/μL. The rate of clinical disease progression varies widely between individuals and has been shown to be affected by a number of factors such as a person's susceptibility and immune function; their access to health care, the presence of co-infections; and the particular strain (or strains) of the virus involved.

Tuberculosis co-infection is one of the leading causes of sickness and death in those with HIV/AIDS being present in a third of all HIV-infected people and causing 25% of HIV-related deaths. HIV is also one of the most important risk factors for tuberculosis. Hepatitis C is another very common co-infection where each disease increases the progression of the other. The two most common cancers associated with HIV/AIDS are Kaposi's sarcoma and AIDS-related non-Hodgkin's lymphoma. Other cancers that are more frequent include anal cancer, Burkitt's lymphoma, primary central nervous system lymphoma, and cervical cancer.

Even with anti-retroviral treatment, over the long term HIV-infected people may experience neurocognitive disorders, osteoporosis, neuropathy, cancers, nephropathy, and cardiovascular disease. Some conditions, such as lipodystrophy, may be caused both by HIV and its treatment.

Epidemiology

HIV/AIDS is a global pandemic. As of 2016 approximately 36.7 million people worldwide have HIV, the number of new infections that year being about 1.8 million. This is down from 3.1 million new infections in 2001. Slightly over half the infected population are women and 2.1 million are children. It resulted in about 1 million deaths in 2016, down from a peak of 1.9 million in 2005.

Sub-Saharan Africa is the region most affected. In 2010, an estimated 68% (22.9 million) of all HIV cases and 66% of all deaths (1.2 million) occurred in this region. This means that about 5% of the adult population is infected and it is believed to be the cause of 10% of all deaths in children. Here, in contrast to other regions, women comprise nearly 60% of cases. South Africa has the largest population of people with HIV of any country in the world at 5.9 million. Life expectancy has fallen in the worst-affected countries due to HIV/AIDS; for example, in 2006 it was estimated that it had dropped from 65 to 35 years in Botswana. Mother-to-child transmission in Botswana and South Africa, as of 2013, has decreased to less than 5%, with improvement in many other African nations due to improved access to antiretroviral therapy.

South & South East Asia is the second most affected; in 2010 this region contained an estimated 4 million cases or 12% of all people living with HIV resulting in approximately 250,000 deaths. Approximately 2.4 million of these cases are in India.

During 2008 in the United States approximately 1.2 million people were living with HIV, resulting in about 17,500 deaths. The US Centers for Disease Control and Prevention estimated that in that year, 20% of infected Americans were unaware of their infection. As of 2016 about 675,000 people have died of HIV/AIDS in the US since the beginning of the HIV epidemic. In the United Kingdom as of 2015, there were approximately 101,200 cases which resulted in 594 deaths. In Canada as of 2008, there were about 65,000 cases causing 53 deaths. Between the first recognition of AIDS (in 1981) and 2009, it has led to nearly 30 million deaths. Rates of HIV are lowest in North Africa and the Middle East (0.1% or less), East Asia (0.1%), and Western and Central Europe (0.2%). The worst-affected European countries, in 2009 and 2012 estimates, are Russia, Ukraine, Latvia, Moldova, Portugal and Belarus, in decreasing order of prevalence.

AIDS was first clinically reported on June 5, 1981, with five cases in the United States. The initial cases were a cluster of injecting drug users and homosexual men with no known cause of impaired immunity who showed symptoms of Pneumocystis carinii pneumonia (PCP), a rare opportunistic infection that was known to occur in people with very compromised immune systems. Soon thereafter, an unexpected number of homosexual men developed a previously rare skin cancer called Kaposi's sarcoma (KS). Many more cases of PCP and KS emerged, alerting U.S. Centers for Disease Control and Prevention (CDC) and a CDC task force was formed to monitor the outbreak.

In the early days, the CDC did not have an official name for the disease, often referring to it by way of the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus. They also used Kaposi's sarcoma and opportunistic infections, the name by which a task force had been set up in 1981. At one point the CDC coined the phrase "the 4H disease", for the syndrome seemed to affect heroin users, homosexuals, hemophiliacs, and Haitians. In the general press the term GRID, which stood for gay-related immune deficiency, had been coined. However, after determining that AIDS was not isolated to the gay community, it was realized that the term GRID was misleading, and the term AIDS was introduced at a meeting in July 1982. By September 1982 the CDC started referring to the disease as AIDS.

In 1983, two separate research groups led by Robert Gallo and Luc Montagnier declared that a novel retrovirus may have been infecting people with AIDS, and published their findings in the same issue of the journal . Gallo claimed a virus which his group had isolated from a person with AIDS was strikingly similar in shape to other human T-lymphotropic viruses (HTLVs) that his group had been the first to isolate. Gallo's group called their newly isolated virus HTLV-III. At the same time, Montagnier's group isolated a virus from a person presenting with swelling of the lymph nodes of the neck and physical weakness, two characteristic symptoms of AIDS. Contradicting the report from Gallo's group, Montagnier and his colleagues showed that core proteins of this virus were immunologically different from those of HTLV-I. Montagnier's group named their isolated virus lymphadenopathy-associated virus (LAV). As these two viruses turned out to be the same, in 1986, LAV and HTLV-III were renamed HIV.

Both HIV-1 and HIV-2 are believed to have originated in non-human primates in West-central Africa and were transferred to humans in the early 20th century. HIV-1 appears to have originated in southern Cameroon through the evolution of SIV(cpz), a simian immunodeficiency virus (SIV) that infects wild chimpanzees (HIV-1 descends from the SIVcpz endemic in the chimpanzee subspecies Pan troglodytes troglodytes). The closest relative of HIV-2 is SIV(smm), a virus of the sooty mangabey ( Cercocebus atys atys), an Old World monkey living in coastal West Africa (from southern Senegal to western Ivory Coast). New World monkeys such as the owl monkey are resistant to HIV-1 infection, possibly because of a genomic fusion of two viral resistance genes. HIV-1 is thought to have jumped the species barrier on at least three separate occasions, giving rise to the three groups of the virus, M, N, and O.

There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV. However, SIV is a weak virus which is typically suppressed by the human immune system within weeks of infection. It is thought that several transmissions of the virus from individual to individual in quick succession are necessary to allow it enough time to mutate into HIV. Furthermore, due to its relatively low person-to-person transmission rate, SIV can only spread throughout the population in the presence of one or more high-risk transmission channels, which are thought to have been absent in Africa before the 20th century.

Specific proposed high-risk transmission channels, allowing the virus to adapt to humans and spread throughout the society, depend on the proposed timing of the animal-to-human crossing. Genetic studies of the virus suggest that the most recent common ancestor of the HIV-1 M group dates back to c. 1910. Proponents of this dating link the HIV epidemic with the emergence of colonialism and growth of large colonial African cities, leading to social changes, including a higher degree of sexual promiscuity, the spread of prostitution, and the accompanying high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities. While transmission rates of HIV during vaginal intercourse are low under regular circumstances, they are increased manyfold if one of the partners suffers from a sexually transmitted infection causing genital ulcers. Early 1900s colonial cities were notable for their high prevalence of prostitution and genital ulcers, to the degree that, as of 1928, as many as 45% of female residents of eastern Kinshasa were thought to have been prostitutes, and, as of 1933, around 15% of all residents of the same city had syphilis.

An alternative view holds that unsafe medical practices in Africa after World War II, such as unsterile reuse of single-use syringes during mass vaccination, antibiotic and anti-malaria treatment campaigns, were the initial vector that allowed the virus to adapt to humans and spread.

The earliest well-documented case of HIV in a human dates back to 1959 in the Congo. The earliest retrospectively described case of AIDS is believed to have been in Norway beginning in 1966. In July 1960, in the wake of Congo's independence, the United Nations recruited Francophone experts and technicians from all over the world to assist in filling administrative gaps left by Belgium, who did not leave behind an African elite to run the country. By 1962, Haitians made up the second-largest group of well-educated experts (out of the 48 national groups recruited), that totaled around 4500 in the country. Dr. Jacques Pépin, a Quebecer author of The Origins of AIDS, stipulates that Haiti was one of HIV's entry points to the United States and that one of them may have carried HIV back across the Atlantic in the 1960s. Although the virus may have been present in the United States as early as 1966, the vast majority of infections occurring outside sub-Saharan Africa (including the U.S.) can be traced back to a single unknown individual who became infected with HIV in Haiti and then brought the infection to the United States at some time around 1969. The epidemic then rapidly spread among high-risk groups (initially, sexually promiscuous men who have sex with men). By 1978, the prevalence of HIV-1 among homosexual male residents of New York City and San Francisco was estimated at 5%, suggesting that several thousand individuals in the country had been infected.

Society and culture

AIDS stigma exists around the world in a variety of ways, including ostracism, rejection, discrimination and avoidance of HIV-infected people; compulsory HIV testing without prior consent or protection of confidentiality; violence against HIV-infected individuals or people who are perceived to be infected with HIV; and the quarantine of HIV-infected individuals. Stigma-related violence or the fear of violence prevents many people from seeking HIV testing, returning for their results, or securing treatment, possibly turning what could be a manageable chronic illness into a death sentence and perpetuating the spread of HIV.

AIDS stigma has been further divided into the following three categories:

Instrumental AIDS stigma-a reflection of the fear and apprehension that are likely to be associated with any deadly and transmissible illness.

Symbolic AIDS stigma-the use of HIV/AIDS to express attitudes toward the social groups or lifestyles perceived to be associated with the disease.

Courtesy AIDS stigma-stigmatization of people connected to the issue of HIV/AIDS or HIV-positive people.

Often, AIDS stigma is expressed in conjunction with one or more other stigmas, particularly those associated with homosexuality, bisexuality, promiscuity, prostitution, and intravenous drug use.

In many developed countries, there is an association between AIDS and homosexuality or bisexuality, and this association is correlated with higher levels of sexual prejudice, such as anti-homosexual or anti-bisexual attitudes. There is also a perceived association between AIDS and all male-male sexual behavior, including sex between uninfected men. However, the dominant mode of spread worldwide for HIV remains heterosexual transmission.

In 2003, as part of an overall reform of marriage and population legislation, it became legal for people with AIDS to marry in China.

In 2013, the U.S. National Library of Medicine developed a traveling exhibition titled Surviving and Thriving: AIDS, Politics, and Culture; this covered medical research, the U.S. government's response, and personal stories from people with AIDS, caregivers, and activists.

Economic impact

HIV/AIDS affects the economics of both individuals and countries. The gross domestic product of the most affected countries has decreased due to the lack of human capital. Without proper nutrition, health care and medicine, large numbers of people die from AIDS-related complications. Before death they will not only be unable to work, but will also require significant medical care. It is estimated that as of 2007 there were 12 million AIDS orphans. Many are cared for by elderly grandparents.

Returning to work after beginning treatment for HIV/AIDS is difficult, and affected people often work less than the average worker. Unemployment in people with HIV/AIDS also is associated with suicidal ideation, memory problems, and social isolation. Employment increases self-esteem, sense of dignity, confidence, and quality of life for people with HIV/AIDS. Anti-retroviral treatment may help people with HIV/AIDS work more, and may increase the chance that a person with HIV/AIDS will be employed (low-quality evidence).

By affecting mainly young adults, AIDS reduces the taxable population, in turn reducing the resources available for public expenditures such as education and health services not related to AIDS, resulting in increasing pressure on the state's finances and slower growth of the economy. This causes a slower growth of the tax base, an effect that is reinforced if there are growing expenditures on treating the sick, training (to replace sick workers), sick pay and caring for AIDS orphans. This is especially true if the sharp increase in adult mortality shifts the responsibility from the family to the government in caring for these orphans.

At the household level, AIDS causes both loss of income and increased spending on healthcare. A study in Côte d'Ivoire showed that households having a person with HIV/AIDS spent twice as much on medical expenses as other households. This additional expenditure also leaves less income to spend on education and other personal or family investment.

Religion and AIDS

The topic of religion and AIDS has become highly controversial, primarily because some religious authorities have publicly declared their opposition to the use of condoms. The religious approach to prevent the spread of AIDS, according to a report by American health expert Matthew Hanley titled The Catholic Church and the Global AIDS Crisis, argues that cultural changes are needed, including a re-emphasis on fidelity within marriage and sexual abstinence outside of it.

Some religious organizations have claimed that prayer can cure HIV/AIDS. In 2011, the BBC reported that some churches in London were claiming that prayer would cure AIDS, and the Hackney-based Centre for the Study of Sexual Health and HIV reported that several people stopped taking their medication, sometimes on the direct advice of their pastor, leading to a number of deaths. The Synagogue Church Of All Nations advertised an "anointing water" to promote God's healing, although the group denies advising people to stop taking medication.

Media portrayal

One of the first high-profile cases of AIDS was the American Rock Hudson, a gay actor who had been married and divorced earlier in life, who died on October 2, 1985, having announced that he was suffering from the virus on July 25 that year. He had been diagnosed during 1984. A notable British casualty of AIDS that year was Nicholas Eden, a gay politician and son of the late prime minister Anthony Eden. On November 24, 1991, the virus claimed the life of British rock star Freddie Mercury, lead singer of the band Queen, who died from an AIDS-related illness having only revealed the diagnosis on the previous day. However, he had been diagnosed as HIV-positive in 1987. One of the first high-profile heterosexual cases of the virus was American tennis player Arthur Ashe. He was diagnosed as HIV-positive on August 31, 1988, having contracted the virus from blood transfusions during heart surgery earlier in the 1980s. Further tests within 24 hours of the initial diagnosis revealed that Ashe had AIDS, but he did not tell the public about his diagnosis until April 1992. He died as a result on February 6, 1993, aged 49.

Therese Frare's photograph of gay activist David Kirby, as he lay dying from AIDS while surrounded by family, was taken in April 1990. magazine said the photo became the one image "most powerfully identified with the HIV/AIDS epidemic." The photo was displayed in Life, was the winner of the World Press Photo, and acquired worldwide notoriety after being used in a United Colors of Benetton advertising campaign in 1992.

Criminal transmission

Criminal transmission of HIV is the intentional or reckless infection of a person with the human immunodeficiency virus (HIV). Some countries or jurisdictions, including some areas of the United States, have laws that criminalize HIV transmission or exposure. Others may charge the accused under laws enacted before the HIV pandemic.

In 1996, Ugandan-born Canadian Johnson Aziga was diagnosed with HIV; he subsequently had unprotected sex with 11 women without disclosing his diagnosis. By 2003, seven had contracted HIV; two died from complications related to AIDS. Aziga was convicted of first-degree murder and sentenced to life imprisonment.

Misconceptions

There are many misconceptions about HIV and AIDS. Three of the most common are that AIDS can spread through casual contact, that sexual intercourse with a virgin will cure AIDS, and that HIV can infect only gay men and drug users. In 2014, some among the British public wrongly thought one could get HIV from kissing (16%), sharing a glass (5%), spitting (16%), a public toilet seat (4%), and coughing or sneezing (5%). Other misconceptions are that any act of anal intercourse between two uninfected gay men can lead to HIV infection, and that open discussion of HIV and homosexuality in schools will lead to increased rates of AIDS.

A small group of individuals continue to dispute the connection between HIV and AIDS, the existence of HIV itself, or the validity of HIV testing and treatment methods. These claims, known as AIDS denialism, have been examined and rejected by the scientific community. However, they have had a significant political impact, particularly in South Africa, where the government's official embrace of AIDS denialism (1999-2005) was responsible for its ineffective response to that country's AIDS epidemic, and has been blamed for hundreds of thousands of avoidable deaths and HIV infections.

Several discredited conspiracy theories have held that HIV was created by scientists, either inadvertently or deliberately. Operation INFEKTION was a worldwide Soviet active measures operation to spread the claim that the United States had created HIV/AIDS. Surveys show that a significant number of people believed-and continue to believe-in such claims.

HIV/AIDS research includes all medical research which attempts to prevent, treat, or cure HIV/AIDS, along with fundamental research about the nature of HIV as an infectious agent, and about AIDS as the disease caused by HIV.

Many governments and research institutions participate in HIV/AIDS research. This research includes behavioral health interventions such as sex education, and drug development, such as research into microbicides for sexually transmitted diseases, HIV vaccines, and antiretroviral drugs. Other medical research areas include the topics of pre-exposure prophylaxis, post-exposure prophylaxis, and circumcision and HIV. Public health officials, researchers, and programs can gain a more comprehensive picture of the barriers they face, and the efficacy of current approaches to HIV treatment and prevention, by tracking standard HIV indicators. Use of common indicators is an increasing focus of development organizations and researchers.

References

External links

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HIV/AIDS Other names HIV disease, HIV infection[1] [2] The red ribbon is a symbol for solidarity with HIV-positive people and those living with AIDS.[3] Specialty Infectious disease Symptoms Early: Flu-like illness[4] Later: Large lymph nodes, fever, weight loss[4] Complications Opportunistic infections, tumors [4] Duration Lifelong[4] Causes Human immunodeficiency virus (HIV)[4]

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Severe acute respiratory syndrome
(SARS)

Electron micrograph of SARS coronavirus virion

Pronunciation

Specialty
Infectious disease

Symptoms

Fever, dry cough, headache, muscle aches and difficulty breathing

Complications

Acute Respiratory Distress Syndrome (ARDS) with other comorbidities that eventually leads to death

Prevention

Hand washing, cough etiquette, avoiding close contact with affected people, avoiding travel to affected areas[1]

Prognosis

9.5% chance of death (all countries)

Frequency

8,098 cases

Deaths

774

Severe acute respiratory syndrome ( SARS) is a viral respiratory disease of zoonotic origin that surfaced in the early 2000s caused by severe acute respiratory syndrome coronavirus (SARS-CoV or SARS-CoV-1), the first-identified strain of the SARS coronavirus species severe acute respiratory syndrome-related coronavirus (SARSr-CoV). The syndrome caused the 2002-2004 SARS outbreak. In late 2017, Chinese scientists traced the virus through the intermediary of civets to cave-dwelling horseshoe bats in Yunnan province. No cases of the first SARS-CoV have been reported worldwide since 2004.

Symptoms are flu-like symptoms and may include fever, muscle pain, lethargy, cough, sore throat, and other nonspecific symptoms. The only symptom common to all patients appears to be a fever above 38 °C (100 °F). SARS may eventually lead to shortness of breath and pneumonia; either direct viral pneumonia or secondary bacterial pneumonia.[citation needed ]

The average incubation period for SARS is 4-6 days, although rarely it could be as short as 1 day or as long as 14 days.

The primary route of transmission for SARS-CoV is contact of the mucous membranes with respiratory droplets or fomites. While diarrhea is common in people with SARS, the fecal-oral route does not appear to be a common mode of transmission. The basic reproduction number of SARS-CoV, R ₀, ranges from 2 to 4 depending on different analyses. Control measures introduced in April 2003 reduced the R to 0.4.

SARS-CoV may be suspected in a patient who has:

Any of the symptoms, including a fever of 38 °C (100 °F) or higher, and

Either a history of:

Contact (sexual or casual) with someone with a diagnosis of SARS within the last 10 days or

Travel to any of the regions identified by the World Health Organization (WHO) as areas with recent local transmission of SARS.

For a case to be considered probable, a chest X-ray must be positive for atypical pneumonia or respiratory distress syndrome.

The appearance of SARS-CoV in chest X-rays is not always uniform but generally appears as an abnormality with patchy infiltrates.

There is no vaccine for SARS, although doctor Anthony Fauci mentioned that the CDC developed one and placed it in the US national stockpile. Clinical isolation and quarantine remain the most effective means to prevent the spread of SARS. Other preventive measures include:

Hand-washing with soap and water, or use of alcohol-based hand sanitizer

Disinfection of surfaces of fomites to remove viruses

Avoiding contact with bodily fluids

Washing the personal items of someone with SARS in hot, soapy water (eating utensils, dishes, bedding, etc.)

Keeping children with symptoms home from school

Simple hygiene measures

Isolating oneself as much as possible to minimize the chances of transmission of the virus

Many public health interventions were made to try to control the spread of the disease, which is mainly spread through respiratory droplets in the air. These interventions included earlier detection of the disease; isolation of people who are infected; droplet and contact precautions; and the use of personal protective equipment (PPE), including masks and isolation gowns. Studies done during the outbreak found that for medical professionals, wearing any type of mask compared to none could reduce the chances of getting sick by about 80%. A screening process was also put in place at airports to monitor air travel to and from affected countries.

SARS-CoV is most infectious in severely ill patients, which usually occurs during the second week of illness. This delayed infectious period meant that quarantine was highly effective; people who were isolated before day five of their illness rarely transmitted the disease to others.

Although no cases have been identified since 2004, the CDC was still working to make federal and local rapid response guidelines and recommendations in the event of a reappearance of the virus as of 2017.

As SARS is a viral disease, antibiotics do not have direct effect but may be used against bacterial secondary infection. Treatment of SARS is mainly supportive with antipyretics, supplemental oxygen and mechanical ventilation as needed. Antiviral medications are used as well as high doses of steroids to reduce swelling in the lungs.[citation needed ]

People with SARS-CoV must be isolated, preferably in negative-pressure rooms, with complete barrier nursing precautions taken for any necessary contact with these patients, to limit the chances of medical personnel getting infected with SARS.[citation needed ] In certain cases, natural ventilation by opening doors and windows are documented to help decreasing indoor concentration of virus particles.

Some of the more serious damage caused by SARS may be due to the body's own immune system reacting in what is known as cytokine storm.

As of 2020, there is no cure or protective vaccine for SARS that has been shown to be both safe and effective in humans. According to research papers published in 2005 and 2006, the identification and development of novel vaccines and medicines to treat SARS is a priority for governments and public health agencies around the world. In early 2004, an early clinical trial on volunteers was planned.

Several consequent reports from China on some recovered SARS patients showed severe long-time sequelae. The most typical diseases include, among other things, pulmonary fibrosis, osteoporosis, and femoral necrosis, which have led in some cases to the complete loss of working ability or even self-care ability of people who have recovered from SARS. As a result of quarantine procedures, some of the post-SARS patients have been documented as suffering from post-traumatic stress disorder (PTSD) and major depressive disorder.

SARS was a relatively rare disease; at the end of the epidemic in June 2003, the incidence was 8,422 cases with a case fatality rate (CFR) of 11%.

The case fatality rate (CFR) ranges from 0% to 50% depending on the age group of the patient. Patients under 24 were least likely to die (less than 1%); those 65 and older were most likely to die (over 55%).

As with MERS and COVID-19, SARS resulted in significantly more deaths of males than females.

The viral outbreak can be genetically traced to a colony of cave-dwelling horseshoe bats in China's Yunnan province.

The outbreak first appeared on 27 November 2002, when Canada's Global Public Health Intelligence Network (GPHIN), an electronic warning system that is part of the World Health Organization's Global Outbreak Alert and Response Network (GOARN), picked up reports of a "flu outbreak" in China through Internet media monitoring and analysis and sent them to the WHO. While GPHIN's capability had recently been upgraded to enable Arabic, Chinese, English, French, Russian, and Spanish translation, the system was limited to English or French in presenting this information. Thus, while the first reports of an unusual outbreak were in Chinese, an English report was not generated until 21 January 2003. The first super-spreader was admitted to the Sun Yat-sen Memorial Hospital in Guangzhou on 31 January, which soon spread the disease to nearby hospitals.

Subsequent to this, the WHO requested information from Chinese authorities on 5 and 11 December. Despite the successes of the network in previous outbreaks of diseases, it did not receive intelligence until the media reports from China several months after the outbreak of SARS. Along with the second alert, WHO released the name, definition, as well as an activation of a coordinated global outbreak response network that brought sensitive attention and containment procedures. By the time the WHO took action, over 500 deaths and an additional 2,000 cases had already occurred worldwide.

In early April 2003, after Jiang Yanyong pushed to report the danger to China, there appeared to be a change in official policy when SARS began to receive a much greater prominence in the official media. Some have directly attributed this to the death of American James Earl Salisbury. It was around this same time that Jiang Yanyong made accusations regarding the undercounting of cases in Beijing military hospitals. After intense pressure, Chinese officials allowed international officials to investigate the situation there. This revealed problems plaguing the aging mainland Chinese healthcare system, including increasing decentralization, red tape, and inadequate communication.

Many healthcare workers in the affected nations risked and lost their lives by treating patients, and trying to contain the infection before ways to prevent infection were known.

The severity of the symptoms and the infection among hospital staff alarmed global health authorities, who were fearful of another emergent pneumonia epidemic. On 12 March 2003, the WHO issued a global alert, followed by a health alert by the United States Centers for Disease Control and Prevention (CDC). Local transmission of SARS took place in Toronto, Ottawa, San Francisco, Ulaanbaatar, Manila, Singapore, Taiwan, Hanoi and Hong Kong whereas within China it spread to Guangdong, Jilin, Hebei, Hubei, Shaanxi, Jiangsu, Shanxi, Tianjin, and Inner Mongolia.[citation needed ]

The disease spread in Hong Kong from Liu Jianlun, a Guangdong doctor who was treating patients at Sun Yat-Sen Memorial Hospital. He arrived in February and stayed on the ninth floor of the Metropole Hotel in Kowloon, infecting 16 of the hotel visitors. Those visitors traveled to Canada, Singapore, Taiwan, and Vietnam, spreading SARS to those locations.

Another larger cluster of cases in Hong Kong centred on the Amoy Gardens housing estate. Its spread is suspected to have been facilitated by defects in its bathroom drainage system that allowed sewer gases including virus particles to vent into the room. Bathroom fans exhausted the gases and wind carried the contagion to adjacent downwind complexes. Concerned citizens in Hong Kong worried that information was not reaching people quickly enough and created a website called sosick.org, which eventually forced the Hong Kong government to provide information related to SARS in a timely manner. The first cohort of affected people were discharged from hospital on 29 March 2003.

The first case of SARS in Toronto was identified on 23 February 2003. Beginning with an elderly woman, Kwan Sui-Chu, returning from a trip to Hong Kong, the virus killed her on 5 March and eventually infected 257 individuals in the province of Ontario. The trajectory of this outbreak is typically divided into two phases, the first centring around her son Tse Chi Kwai, who infected other patients at the Scarborough Grace Hospital and died on 13 March. The second major wave of cases was clustered around accidental exposure among patients, visitors, and staff within the North York General Hospital. The WHO officially removed Toronto from its list of infected areas by the end of June 2003.

The official response by the Ontario provincial government and Canadian federal government has been widely criticized in the years following the outbreak. Brian Schwartz, vice-chair of Ontario's SARS Scientific Advisory Committee, described public health officials' preparedness and emergency response at the time of the outbreak as "very, very basic and minimal at best". Critics of the response often cite poorly outlined and enforced protocol for protecting healthcare workers and identifying infected patients as a major contributing factor to the continued spread of the virus. The atmosphere of fear and uncertainty surrounding the outbreak resulted in staffing issues in area hospitals when healthcare workers elected to resign rather than risk exposure to SARS.[citation needed ]

In late February 2003, Italian doctor Carlo Urbani was called into The French Hospital of Hanoi to look at Johnny Chen, an American businessman who had fallen ill with what doctors thought was a bad case of influenza. Urbani realized that Chen's ailment was probably a new and highly contagious disease. He immediately notified the WHO. He also persuaded the Vietnamese Health Ministry to begin isolating patients and screening travelers, thus slowing the early pace of the epidemic. He subsequently contracted the disease himself, and died in March 2003.

The CDC and Canada's National Microbiology Laboratory identified the SARS genome in April 2003. Scientists at Erasmus University in Rotterdam, the Netherlands demonstrated that the SARS coronavirus fulfilled Koch's postulates thereby confirming it as the causative agent. In the experiments, macaques infected with the virus developed the same symptoms as human SARS victims.

In late May 2003, studies were conducted using samples of wild animals sold as food in the local market in Guangdong, China. The results found that the SARS coronavirus could be isolated from masked palm civets ( Paguma sp.), even if the animals did not show clinical signs of the virus. The preliminary conclusion was the SARS virus crossed the xenographic barrier from asian palm civet to humans, and more than 10,000 masked palm civets were killed in Guangdong Province. The virus was also later found in raccoon dogs ( Nyctereuteus sp.), ferret badgers ( Melogale spp.), and domestic cats. In 2005, two studies identified a number of SARS-like coronaviruses in Chinese bats.

Phylogenetic analysis of these viruses indicated a high probability that SARS coronavirus originated in bats and spread to humans either directly or through animals held in Chinese markets. The bats did not show any visible signs of disease but are the likely natural reservoirs of SARS-like coronaviruses. In late 2006, scientists from the Chinese Centre for Disease Control and Prevention of Hong Kong University and the Guangzhou Centre for Disease Control and Prevention established a genetic link between the SARS coronavirus appearing in civets and humans, bearing out claims that the disease had jumped across species.

In December 2017, "after years of searching across China, where the disease first emerged, researchers reported ... that they had found a remote cave in Yunnan province, which is home to horseshoe bats that carry a strain of a particular virus known as a coronavirus. This strain has all the genetic building blocks of the type that triggered the global outbreak of SARS in 2002." The research was performed by Shi Zheng-Li, Cui Jie and coworkers at the Wuhan Institute of Virology, China, and published in PLOS Pathogens. The authors are quoted as stating that "another deadly outbreak of SARS could emerge at any time. As they point out, the cave where they discovered their strain is only a kilometre from the nearest village."

The World Health Organization declared severe acute respiratory syndrome contained on 5 July 2003. In the following years, four SARS cases were reported in China between December 2003 and January 2004. There were also three separate laboratory accidents that resulted in infection. In one of these cases, an ill lab worker spread the virus to several other people. Study of live SARS specimens requires a biosafety level 3 (BSL-3) facility; some studies of inactivated SARS specimens can be done at biosafety level 2 facilities.

A small number of cats and dogs tested positive for the virus during the outbreak. However, these animals did not transmit the virus to other animals of the same species or to humans.

Fear of contracting the virus from consuming infected wild animals resulted in public bans and reduced business for meat markets in southern China and Hong Kong.

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Severe acute respiratory syndrome(SARS) Electron micrograph of SARS coronavirus virion Pronunciation Specialty Infectious disease Symptoms Fever, dry cough, headache, muscle aches and difficulty breathing Complications Acute Respiratory Distress Syndrome (ARDS) with other comorbidities that eventually leads to death Prevention Hand washing, cough etiquette, avoiding close contact with affected people, avoiding

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Australian Government Department of Health

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The situation changes often. Stay up to date with the latest information about the spread of COVID-19 and the steps being taken to slow the spread.

Local outbreak information

Read the latest advice from ATAGI about the use of the AstraZeneca vaccine in the context of an outbreak of the COVID-19 delta strain.

Support for people and businesses affected by COVID-19 hotspots and restrictions

Visit the Services Australia website to find out more about about payments and support for people and businesses affected by COVID-19 hotspots and restrictions.

Check your local state and territory website for directives, hotspot information and travel restrictions:

Symptoms

If you have serious symptoms such as difficulty breathing, call 000 for urgent medical help.

Symptoms include:

If you are sick and think you might have COVID-19, check your symptoms using healthdirect's Coronavirus (COVID-19) Symptom Checker.

Protect others and stop the spread

We can all help slow the spread of COVID-19 in Australia.

To protect others you must:

If you have a confirmed case, you must isolate yourself to stop the virus spreading to other people.

If you're concerned

You can call the National Coronavirus Helpline for information and advice about COVID-19.

How to seek medical help for COVID-19

If you have used the symptom checker and it advises you should seek help or get tested, see how to seek medical help for COVID-19.

If you are having a medical emergency call 000.

GP respiratory clinics

The Australian Government is establishing GP respiratory clinics around the country to assess people with fever, cough, a sore throat, or shortness of breath.

These are being rolled out gradually. If there is not one in your area yet visit your state or territory health department website for more information on fever clinics and other services.

Find out if there is a clinic near you and how to register for an appointment:

If there is not yet one in your area, visit healthdirect or your state or territory health department website for more information on fever clinics and other available services.

Vaccines and treatments

Everyone in Australia will be offered a safe and effective COVID-19 vaccine.

Australia now has 3 COVID-19 vaccines approved for use - AstraZeneca, Pfizer and Moderna.

Learn more about:

Advice for people most at risk

See more information and advice for people most at risk, including:

General public advice

Health and aged care sector advice

Government response

How we are managing the outbreak

The Prime Minister has activated the Emergency Response Plan for Novel Coronavirus (COVID-19).

To find out how the Australian Government is managing COVID-19, go to Government response to the outbreak.

Resources

Check our collections of resources and translated resources for more information about COVID-19.

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Find out how we are monitoring and responding to the COVID-19 pandemic, how you can help stop the spread of the virus in Australia and what to do if you have symptoms. We also report the latest case numbers, official medical advice and information on treatment.

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Sick With Something That Isn't COVID-19 or the Flu? Here's What It Might Be

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If you're sick but testing negative for COVID-19 and the flu, you may be sick with another respiratory virus, like human metapneumovirus.