[7][8] 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.

[12][13] 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.

[14] 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.

[19] 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.

[14] In early June 2009, using computational methods developed over the previous 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."

"[20] 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".

[21] In November 2009, a study was published in Virology Journal in which it was suggested that the virus may be the product of three strains from three continents that swapped genes in a lab or a vaccine-making plant, and subsequently "escaped".

[34] Research carried out at Imperial College London[35] has shown that, unlike seasonal flu, H1N1/09 can infect cells deep in the lungs.

)[citation needed] As of September 2009[update], most people infected by this flu suffered a mild illness, but the small minority hospitalized were often 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).

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.

[40][41] 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.

[43] 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.

[citation needed] 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.

Other studies concluded that the virus was likely well adapted to humans, had a clear biological advantage over seasonal flu strains and that reassortment was unlikely at that time due to its ease in replication and transmission.

[48] As of late July 2009, U.S. health officials said the swine flu wasn't yet mutating to become more dangerous, but they were closely tracking that as the virus continued to circle the globe.

[49] As of October 2009, research done by Taubenberger showed that the evolution of A (H1N1) is relatively slow since the structure of the 2009 H1N1 virus is similar to the strain of H1N1 implicated in the 1918 flu pandemic.

This may have played a role in individuals who had been infected with the 1918 strain and its early descendants in showing stronger specific immunity to the 2009 H1N1 virus.

[51] On November 20, 2013, the Norwegian Institute of Public Health released a statement saying they had discovered a potentially significant mutation in the H1N1 influenza strain that could be responsible for causing the severest symptoms among those infected.

Both clusters, detected in the UK (including Wales) and in North Carolina, occurred in a single ward and involved patients whose immune systems were severely compromised or suppressed.

[citation needed] As of December 2010[update], the WHO reported 314 samples of 2009 pandemic H1N1 flu tested worldwide have shown resistance to oseltamivir (Tamiflu).

The November 27, 2009 worldwide update by the U.N.'s World Health Organization (WHO) states that "more than 207 countries and overseas territories or communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including over 7,820 deaths".

[citation needed] 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".

[59] Virus experts were concerned that a more dangerous and easily transmitted strain could emerge if H1N1/09 combines again with avian flu, which is far more virulent but much less contagious to humans.

[5] A CDC investigative team arrived in Mexico City on April 25, 2009 to work with Mexican counterparts to study the virus.

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.

[98] Late on May 6, 2009, Canada's National Microbiology Laboratory first completed the sequencing of Mexican samples of the virus, publishing the result to GenBank as A/Mexico/InDRE4487/2009(H1N1).

[9] Samples from Mexico, Nova Scotia and Ontario had the same sequence, ruling out genetic explanations for the greater severity of the Mexican cases.