The pandemic H1N1/09 virus is a swine origin influenza A virus subtype H1N1 strain that was responsible for the 2009 swine flu pandemic. This strain is often called swine flu by the public media due to the prevailing belief that it originated in pigs. The virus is believed to have originated around September 2008 in central Mexico.
The H1N1 pandemic of 2009 was the first public health emergency of international concern designated by the World Health Organization. While H1N1/09 was the primary strain of flu seen that year, it was not unusually contagious or lethal.
Most cases were mild, although those who had to be hospitalized were often severely ill. In the fall of 2009, between 15 and 33% of those hospitalized with H1N1 in the Southern Hemisphere were taken to the ICU. One clinician remarked that the pandemic was "like two diseases" because of the stark difference between mild and severe cases, with few falling in between.
Viral characteristics The virus is a novel strain of the influenza virus, for which existing vaccines against seasonal flu provided no protection. A study at the U.S. Centers for Disease Control and Prevention (CDC) published in May 2009 found that children had no preexisting immunity to the new strain but that adults, particularly those over 60, had some degree of immunity. Children showed no cross-reactive antibody reaction to the then-new strain, while adults aged 18 to 64 had 6–9%, and older adults 34%. Much reporting of early analysis repeated that the strain contained genes from five different flu viruses: North American swine influenza, North American avian influenza, human influenza, and two swine influenza viruses typically found in Asia and Europe. Further analysis showed that several of the proteins of the virus are most similar to strains that cause mild symptoms in humans, leading virologist Wendy Barclay to suggest that the virus was unlikely to cause severe symptoms for most people. Other leading researchers indicated that all segments of the virus were in fact swine in origin, despite it being a multiple reassortment. The first complete genome sequence of the pandemic strain was deposited in public databases on April 27, 2009, by scientists from the U.S. Centers for Disease Control and Prevention in Atlanta. Scientists in Winnipeg later completed the full genetic sequencing of viruses from Mexico and Canada on May 6, 2009.
Viral origins
Analysis of the genetic divergence of the virus in samples from different cases indicated that the virus jumped to humans in 2008, probably after June, and not later than the end of November, likely around September 2008. A report by researchers at the Mount Sinai School of Medicine in 2016 found that the 2009 H1N1 virus likely originated from pigs in a very small region of central Mexico.
On April 17, 2009, the Centers for Disease Control and Prevention (CDC) determined that two cases of febrile respiratory illness occurring in children who resided in adjacent counties in Southern California were caused by infection with a swine influenza A (H1N1) virus. The viruses from the two cases were closely related genetically, resistant to amantadine and rimantadine, and contain a unique combination of gene segments that previously had not been reported among swine or human influenza viruses in the United States or elsewhere. After the emergence of the novel virus in the spring of 2009, it spread quickly across the United States, Mexico and the world.
In late April, the World Health Organization (WHO) declared its first ever "public health emergency of international concern", or PHEIC, and in June, the WHO and the U.S. CDC stopped counting cases and declared the outbreak a pandemic.
On June 23, 2009, The New York Times reported that U.S. federal agriculture officials believed that contrary to the popular assumption that the swine flu pandemic arose on factory farms in México, it most likely emerged in pigs in Asia and traveled to North America in a human." They emphasized that there was no way to prove this hypothesis but it seemed clear that the virus, which combined Eurasian and North American genes, had never circulated in North American pigs. However, there was evidence that a closely related 'sister virus' circulated in Asia. However, a subsequent report by researchers at the Mount Sinai School of Medicine in 2016 found that the 2009 H1N1 virus likely originated in central Mexico.
In early June 2009, using computational methods developed over ten years, an international team of researchers attempted to reconstruct the origins and timescale of the 2009 flu pandemic. Oliver Pybus of Oxford University's Department of Zoology, and part of the research team, claims "Our results show that this strain has been circulating among pigs, possibly among multiple continents, for many years prior to its transmission to humans." The research team who worked on this case also believed it was "derived from several viruses circulating in swine", and that the initial transmission to humans occurred several months before recognition of the outbreak. The team concluded that "despite widespread influenza surveillance in humans, the lack of systematic swine surveillance allowed for the undetected persistence and evolution of this potentially pandemic strain for many years."
According to the researchers, movement of live pigs between Eurasia and North America "seems to have facilitated the mixing of diverse swine influenza viruses, leading to the multiple reassortment events associated with the genesis of the (new H1N1) strain". They also said this new pandemic "provides further evidence of the role of domestic pigs in the ecosystem of influenza A"."New flu has been around for years in pigs—study" Reuters, June 11, 2009
In November 2009, a study was published in Virology Journal in which it was suggested that the virus was the product of three strains from three continents that swapped genes in a lab or a vaccine-making plant, and subsequently "escaped". The study followed debate among researchers in May 2009, when the authors asked the World Health Organization (WHO) to consider the hypothesis. After reviewing the initial paper, WHO and other organizations concluded the pandemic strain was a naturally occurring virus and not laboratory-derived.
Contagiousness
The virus is contagious with an R0 of 1.4 to 1.6 and spreads from human to human in much the same way as seasonal flu. The most common mechanisms by which it spreads are by droplets from coughs and sneezes of infected people, and also potentially touching a surface or the hand of a person contaminated with the virus and then touching one's eyes, nose or mouth. In 2009, the WHO reported that H1N1/09 seemed to be more contagious than seasonal flu. However, a New England Journal of Medicine report said the transmissibility of the 2009 H1N1 influenza virus in households was lower than that seen in past pandemics. The U.S. CDC recommended that people should wait at least a day after their fever subsides (usually 3–4 days after the onset of symptoms) before resuming normal activities, but it has been found that they can continue to shed virus for several more days.
Virulence
The virulence of swine flu virus is mild and the mortality rates are very low.
In mid-2009, the U.S. CDC noted that most infections were mild, similar to seasonal flu, and that recovery tended to be fairly quick. The number of deaths was said to be a tiny fraction of the annual number of deaths from seasonal flu. However, comparisons of human fatality figures with seasonal influenza are prone to underestimate impact of the pandemic, and the pandemic H1N1/09 virus was in fact the dominant strain of influenza causing illness in the 2009/10 flu season.For example,
Research carried out at Imperial College London has shown that, unlike seasonal flu, H1N1/09 can infect cells deep in the lungs. Seasonal flu can infect only cells with receptor type a2-6 which are typically located in the nose and throat but H1N1/09 can also infect cells with receptor type a2-3. This may explain why some patients experience severe respiratory symptoms. (The H5N1 virus is also able to infect cells deep in the lungs with receptor type a2-3 but cannot infect cells with receptor type a2-6 making it less contagious than H1N1/09.)
, most people infected by this flu suffered a mild illness, but a small minority were hospitalized and severely ill. Arand Kumar, an intensive care expert at the University of Manitoba, Winnipeg, Canada, said "this pandemic is like two diseases; either you're off work for a few days or you go to hospital, often to the intensive-care unit (ICU). There's no middle ground." In the southern hemisphere 15 to 33% of hospitalized cases went to the ICU in July and August 2009. Unlike H5N1 avian flu and SARS which provoke a runaway body-wide immune response, H1N1/09 destroys the lungs' alveoli, often causing acute respiratory distress syndrome, which kills in half of all cases. Preliminary research suggests that severity is linked to a genetic variation in immune systems.
From April 2009 to November 2009, 3,900 people died of the H1N1 pandemic virus in the U.S. This is sometimes compared to the 36,000 people per year who die from the "common flu", mostly in winter, although this number is an estimate. The death rate of H1N1 in the U.S. was calculated as less than 0.02% from November 2009 figures from the CDC, and has been explicitly calculated as 0.026% in England.
Vaccine
A study at the U.S. Centers for Disease Control and Prevention published in May 2009 found that children had no preexisting immunity to the new strain but that adults, particularly those older than 60, had some degree of immunity. Children showed no cross-reactive antibody reaction to the new strain, adults aged 18 to 60 had 6–9%, and older adults 33%. While it has been thought that these findings suggest the partial immunity in older adults may be due to previous exposure to similar seasonal influenza viruses, a November 2009 study of a rural unvaccinated population in China found only a 0.3% cross-reactive antibody reaction to the H1N1 strain, suggesting that previous vaccinations for seasonal flu and not exposure may have resulted in the immunity found in the older U.S. population. Production may be three billion doses per year rather than the earlier estimate of five billion.
Evolutionary potential
On May 22, 2009, World Health Organization (WHO) Director-General Margaret Chan said the virus must be closely monitored in the southern hemisphere, as it could mix with ordinary seasonal influenza and change in unpredictable ways. Experts writing in the July issue of The New England Journal of Medicine noted that historically, pandemic viruses have evolved between seasons, and the current strain may become more severe or transmissible in the coming months. They therefore stressed the importance of international cooperation to engage in proper surveillance to help monitor changes in the virus's behavior, which will aid in both "vaccine targeting" and interpreting illness patterns in the fall of 2009.