Neuron Culture


While I’m at it, here are a few other recent posts about modulating our thinking about the swine flu outbreak that is a) so far less horrid than our worst fears and b) still working its way around the globe, as it may well be doing for some time to come.

Greg Laden notes that nothing has changed.

The Avian Flu Diary first considers, in the wonderfully titled post, “Before We Ride Down and Shoot the Survivors,” the editorializing about “panic” ; and then ponders what might change as/if this flu works its work in the southern hemisphere over the coming months.

Peter Palese writes on why H1N1 isn’t so scary but is still sorta scary. As it’s behind paywall, I’ll pass on the bullet version gathered at the Virology Blog:

First, Palese reviews the concerns about the new H1N1 viruses:

1. The swine virus belongs to the same H1N1 group as did the 1918 pandemic virus.

2. The swine virus is readily transmitted from human to human. At this point, swine virus isolates have been reported on four continents. The avian H5N1 virus (another virus with pandemic potential) was never proven to readily transmit from person to person; rather, humans were probably infected directly from chickens and these infections required large quantities of virus.

3. The swine virus shows an unusual robustness in emerging outside the normal seasonal period for the virus. Influenza viruses are rarely isolated at the end of April in the northern hemisphere, and winter hasn’t yet started in New Zealand, where several isolates have already been reported.

4. Mutations and/or acquisition of genes derived from other human or animal influenza viruses could make the swine virus into something much more virulent than it is now. Mutations and acquisition of genes are natural processes for influenza viruses against which there are no man-made interventions.

Furthermore, these processes (and the extent to which they could enhance virulence) cannot be predicted.

Next, he argues why we should be optimistic:

1. In 1976 there was a an outbreak of an H1N1 swine virus in Fort Dix, New Jersey, which showed human to human transmission but did not go on to become a highly virulent pandemic strain.

2. The presently circulating swine virus is most likely not more virulent than the other seasonal strains we have experienced over the last several years.

3. The current swine virus lacks an important molecular signature (the protein PB1-F2) which was present in the 1918 virus and in the highly lethal H5N1 chicken viruses. If this virulence marker is necessary for an influenza virus to become highly pathogenic in humans or in chickens, then the current swine virus doesn’t have what it takes to become a major killer.

4. Since people have been exposed to H1N1 viruses over many decades, we likely have some cross-reactive immunity against the swine H1N1 virus. While it may not be sufficient to prevent becoming ill, it may very well dampen the impact of the virus on mortality. I would postulate that by virtue of this “herd immunity” even a 1918-like H1N1 virus could never have the horrific effect it had in the past. The most likely outcome is that the current swine virus will become another (fourth) strain of regular seasonal influenza.

5. The landscape of vaccines and anti-influenza drugs has dramatically improved over what it was just a few years ago. Based on what we know of the structure and sequence of the swine virus, these FDA-approved drugs and FDA-licensed vaccines (modified to include the swine strain) would be highly effective against this new virus. Also, present technologies as well as manufacturing capacities will allow us to make sufficient quantities of a swine virus vaccine for the winter 2009-10 season in this country.