Back in 2007, I wrote about an outbreak of swine influenza from an Ohio county fair. The peer-reviewed paper analyzing the swine influenza isolated from that outbreak has just recently come out. From the abstract:
The swine isolate, A/SW/OH/511445/2007 (OH07), was evaluated in an experimental challenge and transmission study reported here. Our results indicate that the OH07 virus was pathogenic in pigs, was transmissible among pigs, and failed to cross-react with many swine H1 anti-sera. Naturally exposed pigs shed virus as early as 3 days and as long as 7 days after contact with experimentally infected pigs. This suggests there was opportunity for exposure of people handling the pigs at the fair. The molecular analysis of the OH07 isolates demonstrated that the eight gene segments were similar to those of currently circulating triple reassortant swine influenza viruses. However, numerous nucleotide changes leading to amino acid changes were demonstrated in the HA gene and throughout the genome as compared to contemporary swine viruses in the same genetic cluster. It remains unknown if any of the amino acid changes were related to the ability of this virus to infect people. The characteristics of the OH07 virus in our pig experimental model as well as the documented human transmission warrant close monitoring of the spread of this virus in pig and human populations.
Meanwhile, I mentioned yesterday that gene sequences from the new H1N1 virus had been released. Sandy has taken a look at some of these, and compared them with H1N1 and H1N2 viruses from humans and pigs.
Yes, there is a point to the juxtaposition of these two points, and it’s big–after the jump…
According to her analyses, the Ohio pig isolates are the most closely related to the new Texas and California human isolates. [Note: see comments in Sandy’s post regarding methods and other sequences also; expecting an update later today on her methods etc.]
Does this mean the virus came from these Ohio pigs? *Well, no, not necessarily*. First, we’re missing a lot of data. The sequences from any patients from Mexico still aren’t up (as of this posting), and we don’t have sequence information from Mexican pigs. Ideally, it would be very helpful to have not only data from pigs in the outbreak areas of Mexico, but multiple sequences over time, to see if this isolate was circulating there, had been recently introduced, had showed up in people, etc. However, that’s a lot of wishful thinking–more on this tomorrow. For now, this is a pretty big find.
I also assume this is where the human-avian-swine reassortant claim came from. The authors note that:
The H1N1 viruses contain the HA and NA from the classical swine virus and the internal genes from the triple reassortant H3N2 viruses (rH1N1); the H1N2 viruses contain the HA from the classical swine virus and the NA and internal genes from the triple reassortant H3N2 viruses (Karasin et al., 2002; Webby et al., 2004). Contemporary triple reassortant viruses were demonstrated to have acquired a PB1 gene of human virus origin; PA and PB2 genes of avian virus origin; and the remaining internal genes, M, NS, and NP, of swine virus origin, thus giving rise to the triple reassortant designation (Zhou et al., 1999).
So what it looks like to me is that this isn’t a *new* reassortant virus, but is closely related to one that had already been identified in swine–and that had already caused an outbreak in humans right here in the US.
I’ll have more about this tomorrow…this is pretty huge and I’m still digesting it all and looking for additional analyses…
[Update: additional analysis didn’t find what Sandy did using a different method, here…still developing…]