The influenza genome is segmented. Eight pieces of single-stranded RNA encode for 11 proteins: PB2, PB1, PB1-F2, PA, HA, NP, NA, M1, M2, NS1, and NS2. The segmentation allows influenza of different subtypes infecting the same host to trade segments like card players on a Friday night. Most of the resulting viruses will express phenotypes for the worse, but a small subset may be transformed into strains more infectious in their usual hosts or to a new host species.
This reassortment accounts in part for the origins of this year’s pandemic. Livestock pigs have long hosted their own version of seasonal H1N1, evolutionarily related to our own. From 1930-1998 the pig version evolved only slightly. But starting in 1998, the virus was subjected to a series of reassortment events. In North America, an aggressive swine H1N1 emerged with internal genes of a human H3N2 virus and an avian influenza. That virus subsequently spread across pig populations, with limited transfer to humans, usually to farm workers, who routinely offer the influenza virus human test subjects every step in its evolution.

In seeping through the world’s every nook and cranny, pandemics have a way of forcing themselves into our lives as a lurking presence. Even the most insular of functionaries, who typically makes his living solving problems by ignoring them, straightens up and takes notice.
Swine flu H1N1 appears at one and the same time moving full-boar and on its cloven heels. The World Health Organization