H1N1 influenza adopted novel strategy to move from birds to humans

BERKELEY — The 2009 H1N1 influenza virus used a new strategy to cross from birds into humans, a warning that it has more than one trick up its sleeve to jump the species barrier and become virulent. The sequence of the three subunits of the influenza virus polymerase (center) determines whether or not the enzyme works efficiently in birds, pigs or humans. A mutation in the PB2 subunit allows the bird virus to function in humans, as does switching out the bird PA subunit for a human PA subunit. Two mutations in the PB2 subunit of 2009 H1N1 allow the pig virus to work in humans. The background is a false-color electron micrograph image of influenza virions. (Andrew Mehle/UC Berkeley) In a report in this week's early online edition of the journal Proceedings of the National Academy of Sciences , University of California, Berkeley, researchers show that the H1N1, or swine flu, virus adopted a new mutation in one of its genes distinct from the mutations found in previous flu viruses, including those responsible for the Spanish influenza pandemic of 1918, the "Asian" flu pandemic in 1957 and the "Hong Kong" pandemic of 1968. Previous influenza strains that crossed from birds into people had a specific point mutation in the bird virus's polymerase gene that allowed the protein to operate efficiently inside humans as well.