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, 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). This was later shown to be nearly identical to A/California/07/2009 (H1N1), the strain from California sequenced and published by the CDC on 27 April. 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.