The virus is a novel strain of influenza. Existing vaccines against seasonal flu provide 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 new strain, adults aged 18 to 64 had 6-9%, and older adults 33%. It was also determined 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 on May 1 that the initial indications are that the virus was unlikely to cause severe symptoms for most people. 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 6 May.
On June 23, the New York Times reported that U.S. federal agriculture officials, “contrary to the popular assumption that the new swine flu pandemic arose on factory farms in Mexico,” now believe that it “most likely emerged in pigs in Asia, but then traveled to North America in a human.” They emphasized that there was no way to prove their theory, but stated that there is no evidence that this new virus, which combines Eurasian and North American genes, has ever circulated in North American pigs, “while there is tantalizing evidence that a closely related ‘sister virus’ has circulated in Asia.”
In early June 2009, using computational methods developed over the last ten years, an international team of researchers attempted to reconstruct the origins and timescale of the 2009 flu pandemic. Dr 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 that worked on this report also believe that 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 stated that this new pandemic “provides further evidence of the role of domestic pigs in the ecosystem of influenza A.” Some experts also suspect that a leading cause of the new virus outbreak is insufficient surveillance by the pork industry and the fact that “animal husbandry now more closely resembles the petrochemical industry than the happy family farm”
The virus is contagious and is believed to spread 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 touching a surface or the hand of a person contaminated with virus, and then touching one’s mouth or nose. H1N1/09 is more contagious than seasonal flu, and infected people are contagious for longer than had been thought. The US CDC had 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 days after that.
The contagiousness of the virus may change as it mutates.
The virulence of the virus may change as it mutates.
In mid-2009 the US Centers for Disease Control and Prevention (CDC) noted that most infections were mild, similar to seasonal flu, and that recovery tended to be fairly quick. The number of deaths as of September 2009[update] is a tiny fraction of the annual number of deaths from seasonal flu.
Research carried out at Imperial College London and reported in Nature Biotechnology  has shown that, unlike seasonal flu, H1N1/09 can infect cells deep in the lungs. Seasonal flu can only infect 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.)
As of September 2009[update] most people infected by this flu suffer a mild illness, but the small minority hospitalised are often severely ill. Arand Kumar, 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 hospitalised cases went to 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.
So far, in the US, 1,000 people have died of the H1N1 Novel virus, whereas 800 people per week die from the common flu. In fact, the death rate of people hospitalized with common influenza in the US is 18%, while the death rate of diagnosed H1N1 in the US is less than 8%. (It must be noted however that these mortality rates describe different things; the one relating to fatalities among those ill enough to warrant hospital treatment and the other relating to all cases of H1N1 flu, including mild cases. In other words, it would be incorrect to use them to conclude that normal influenza is three times as lethal.)
Existing vaccines against seasonal flu provide no protection. Vaccines were released in North America in late October. Production may be 3 billion doses per year rather than the earlier estimate of 5 billion.
 Evolution potential
On May 22, 2009, World Health Organization (WHO) Director-General Dr. Margaret Chan said that 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 New England Journal of Medicine note that historically, pandemic viruses have evolved between seasons, and the current strain may become more severe or transmissible in the coming months. They therefore stress 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.
Other experts are also concerned that the new virus strain could mutate over the coming months. Guan Yi, a leading virologist from the University of Hong Kong, for instance, described the new H1N1 influenza virus as “very unstable”, meaning it could mix and swap genetic material (reassortment)when exposed to other viruses. During an interview he said “Both H1N1 and H5N1 are unstable so the chances of them exchanging genetic material are higher, whereas a stable (seasonal flu) virus is less likely to take on genetic material.” The H5N1 virus is mostly limited to birds, but in rare cases when it infects humans it has a mortality rate of between 60% to 70%. Experts worry about the emergence of a hybrid of the more virulent Asian-lineage HPAI (highly pathogenic avian influenza) A/H5N1 strain (media labeled “bird flu”) with more human-transmissible Influenza A strains such as this novel 2009 swine-origin A/H1N1 strain (media labeled “swine flu”), especially since the H5N1 strain is and has been for years endemic in birds in countries like China, Indonesia, Vietnam and Egypt. (See the suite of H5N1 articles for details.)
Other studies conclude that the virus is likely well adapted to humans, has a clear biological advantage over seasonal flu strains and that reassortment is unlikely at this time due to its current ease in replication and transmission.
However, Federal health officials in the U.S. noted that the horrific 1918 flu epidemic, which killed hundreds of thousands in the United States alone, was preceded by a mild “herald” wave of cases in the spring, followed by devastating waves of illness in the autumn.
As of late July, U.S. health officials said that the swine flu isn’t yet mutating to become more dangerous, but they are closely tracking that as the virus continues to circle the globe.
 Species affected
Before being transmitted to humans, the viruses[which?] circulated in swine which has allowed for the undetected persistence and evolution of this potentially pandemic strain for many years. Pigs are known to have been infected by humans.
Humans have been affected since early 2009.
In late August 2009 the government of Chile discovered that the human H1N1/09 virus had jumped, unmutated, to birds, “opening a new chapter in the global epidemic.” Top flu and animal-health experts with WHO and the CDC were monitoring the situation closely. They said the infected turkeys have suffered only mild effects, easing concern about a potentially dangerous development. Chile’s turkey meat remains safe to eat, they said, and so far there have been no signs of a potentially dangerous mutation. Virus experts are concerned that a more dangerous and easily transmitted strain could emerge if H1N1/09 combines again with avian flu, which at present is far more virulent but much less contagious to humans. By October another outbreak at a turkey breeder was identified in Ontario, Canada.
In October 2009, a ferret exhibiting flu symptoms was confirmed to have contracted the H1N1 virus from its owner in Oregon.
The initial outbreak was called the “H1N1 influenza.” In July 2009 WHO experts changed the name to “pandemic H1N1/09 virus” to distinguish it from the current “seasonal H1N1 virus”, as H1N1 is the medical term used for the most common form of influenza. In August 2009 the CDC began referring to it as the “novel H1N1 virus”.
Some authorities object to calling the flu outbreak “swine flu”. U.S. Agriculture Secretary Tom Vilsack expressed concerns that this would lead to the misconception that pork is unsafe for consumption. The CDC began referring to it as “Novel influenza A (H1N1)”; “A/H1N1” is sometimes used.[not in citation given] In the Netherlands it was originally called “pig flu” but is now called “Mexican flu” by the national health institute and in the media. South Korea and Israel briefly considered calling it the “Mexican virus”. Later the South Korean press used “SI”, short for “swine influenza”. Taiwan suggested the names “H1N1 flu” or “new flu”, which most local media adopted. The World Organization for Animal Health proposed the name “North American influenza”. The European Commission adopted the term “novel flu virus”.
|Genetic origins of the 2009 swine flu virus|
|HA||Hemagglutinin||swine (H1)||North America|
|PA||RNA polymerase subunit PA||avian||North America|
|PB1||RNA polymerase subunit PB1||human||1993 H3N2 strain|
|PB2||RNA polymerase subunit PB2||avian||North America|
|M||Matrix protein M1, M2||swine||Eurasia|
|NS/NEP||Non-structural proteins NS1,
NEP (Nuclear Export Protein)
On April 24, the U.S. Centers for Disease Control and Prevention (CDC) determined that seven samples from suspected cases in Mexico matched the strain that had infected patients in Texas and California with no known linkages to animals or one another; the strain appeared to be spreading from human to human. The CDC determined that the strain contained genes from four different flu viruses – North American swine influenza, North American avian influenza, human influenza, and swine influenza virus typically found in Asia and Europe – “an unusually mongrelised mix of genetic sequences.” A CDC investigative team arrived in Mexico City on April 25 to work with Mexican counterparts to study the virus.
Pigs are susceptible to influenza viruses that can also infect both humans and birds, so they may act as a “mixing vessel” in which reassortment can occur between flu viruses of several species. Reassortment is a process that happens if two different types of influenza virus infect a single cell and it can produce a new strain of influenza. This is because the virus genome is split between eight independent pieces of RNA, which allows pieces of RNA from different viruses to mix together and form a novel type of virus as new virus particles are being assembled. This new strain appears to be a result of the reassortment of two swine influenza viruses, one from North America and one from Europe. But the North American pig strain was itself the product of previous reassortments, and has carried an avian PB2 gene for at least ten years and a human PB1 gene since 1993. These genes were passed on to the new virus.
Gene sequences for every viral gene were made available through the Global Initiative on Sharing Avian Influenza Data (GISAID). A preliminary analysis found that the hemagglutinin (HA) gene was similar to that of swine flu viruses present in U.S. pigs since 1999, but the neuraminidase (NA) and matrix protein (M) genes resembled versions present in European swine flu isolates. While viruses with this genetic makeup had not previously been found to be circulating in humans or pigs, there is no formal national surveillance system to determine what viruses are circulating in pigs in the U.S. So far, little is known about the spread of the virus in any pig population. A preliminary analysis has also shown that several of the proteins involved in the pathophysiology of the virus are most similar to strains that cause mild symptoms in humans. This suggests that the virus is unlikely to cause severe infections similar to those caused by the 1918 pandemic flu virus or the H5N1 avian influenza.
Late on May 6, Canada’s National Microbiology Laboratory first completed the sequencing of the virus, publishing the result to GenBank. Samples from Mexico, Nova Scotia and Ontario had the same sequence, ruling out genetic explanations for the greater severity of the Mexican cases.
The genetic divergence of the virus in samples from different cases has been analysed by Mike Worobey at the University of Arizona at Tucson, USA, who found that the virus jumped to humans in 2008 probably after June, and not later than the end of November. Worobey’s research also indicated the virus had been latent in pigs for several months prior to the outbreak, suggesting a need to increase agricultural surveillance to prevent future outbreaks.  Presentation of Worobey’s Research
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- H1N1 issue