Virus genomes constantly mutate and can easily swap genes with other viruses, sometimes endowing a pathogen with the power to infect different species or to trigger more serious disease in their hosts. The new swine flu virus appears to have done more swapping than usual, with genetic segments from four different sources: North American swine influenza viruses, North American avian influenza viruses, one gene segment from a human influenza virus, and two gene segments that are normally found in swine influenza viruses in Asia and in Europe.
“Parts of it are from the original 1918 virus, parts are similar to the current circulating H1N1 strain from seasonal flu,” says Sasisekharan. “We are still trying to understand what that means.” The 1918 Spanish flu triggered a pandemic that killed millions around the globe.
The new swine flu is of a subtype called H1N1, the class of influenza that is responsible for the majority of seasonal flu. (The 1918 virus was also an H1N1 strain.) But humans have no existing immunity to the novel swine flu virus. “We want to look and see how the [surface proteins] differ from current circulating H1N1 strains,” says Ian Wilson, a scientist at Scripps Research Institute, in La Jolla, CA.
One such protein, called hemagglutinin, sits on the outside of the influenza virus and determines which cells it can infiltrate. Preliminary analysis of the hemagglutinin gene for the new swine virus “has the telltale signatures for human receptor binding,” says Sasisekharan. “But until we make the protein and confirm whether it binds to receptors in human airways or deep lung,” we won’t know for sure. He adds that the gene for the hemagglutinin protein has close to 90 changes in the amino acids that make up the protein. “That’s significant from a vaccine-development point of view,” says Sasisekharan, since it suggests that existing seasonal flu vaccines will not be effective against it.