Mexico hasn’t had a new swine flu case in a week and is lowering its threat level. Oh boy, now we can forget about that cocktail of pig, bird and human genes and concentrate on Ms. California’s homophobic boobs.  But, few of us lived through the 1918 pandemic where millions died in the second wave of the Spanish Flu virus.  See, it comes on during the first flu season and then subsides, only to come back again the next year with full throttled vengeance. The history and issues, after the jump.

Flu’s genetic material is made up of just eight strands and only about 30 genes. Flu RNA is sub microscopic and much smaller than DNA or bacteria.  It’s kind of like a half-step between a mere chemical compound (not alive?) and the 25000 genes in each of our cells (alive?).  These flu genes invade the much larger cell and contain the instructions for making the virus’s simple components, including the capsule and surface markers, which our cells copy.  The surface markers are what give the influenza its labels. The subtype for swine flu is H1N1.  H stands for Haemagglutinin and N for Neuraminidase.  This is the same subtype as the deadly Spanish flu of 1918.

Things worked more slowly in the early 20th century.  It took about 15 years for researchers to understand what exactly had killed millions in 1918.  The influenza A virus was first isolated in 1931 from swine and in 1933 from humans.  The close relationship between the 1918 flu and today’s virus was reconfirmed recently by the Armed Forces Institute of Pathology (AFIP) in Maryland, from two sources: first, from stored specimens of 70 human autopsy cases of the 1918 flu pandemic and secondly, from a preserved bird from the 1915-1918 era stored at the Smithsonian.  However, because the Smithsonian’s 1918 bird virus was genetically different than the 1930’s human and pig viruses, the AFIP believes that the 1918 virus was probably circulated among swine and/or humans for some period, undergoing genetic “drift”, before leading to widespread illness in 1918’s second seasonal disease wave. 1918 virus is likely to have reassorted, or mixed genetically for years in an intermediate host.

The same “mixing” for a decade is likely to have occurred with the current swine flu.  Pigs have receptors for both human and bird flu viruses, which makes them ideal “mixing vessels” for new viral combinations. Bird flu is easily transmitted to pigs via their droppings. If a pig catches two kinds of flu at once, a new hybrid can emerge with genes from both viruses.