|
Flu Wiki Forum
Welcome to the conversation Forum of Flu Wiki
This is an international website intended to remain accessible to as many people as possible. The opinions expressed here are those of the individual posters who remain solely responsible for the content of their messages.
The use of good judgement during the discussion of controversial issues would be greatly appreciated.
|
Sat May 02, 2009 at 08:44:46 AM EDT
|
"What we have found by looking very carefully at the sequences of the new H1N1 virus is that we do not see the markers for virulence that we're seeing in the 1918 virus."
Dr Nancy Cox, Director, CDC Influenza Division, May 1 2009 press briefing |
| SusanC :: Swine Flu Strain not as Deadly? |
| Thus far, the CDC has done an exemplary job in keeping the public informed by detailed daily press briefings. Yesterday, Dr Nancy Cox, director of CDC's Influenza Division and world-class expert on seasonal and pandemic flu, took part in the briefing and answered journalists questions. The full transcript is available here and is well worth reading. The comment quoted above, has prompted journalists to report that the swine flu virus may not be as deadly as feared.
Here's what came out in the Chicago Tribune today:
Swine flu: Strain not as deadly as suspected
Health officials downshift response as first cases confirmed in Illinois
On a day when federal health officials confirmed the first cases of swine flu in Illinois, it also seemed clearer to health officials Friday that this strain of flu wasn't becoming the killer once feared, and the state's reaction to the outbreak downshifted in response.
The flu chief for the Centers for Disease Control and Prevention, Dr. Nancy Cox, said Friday the latest swine flu virus lacked traits that made the 1918 pandemic strain so deadly.
Local emergency room staffs were told to employ a new swine flu testing policy: Don't do it so much. Doctors had new guidelines for prescribing anti-viral drugs: Save them for people with underlying medical conditions, and use them within 48 hours of symptoms, when they would do the most good.
More http://www.chicagotribune.com/...
While it may be true that the current virus does not have the same mutations as the 1918 one, the devil, as always, is in the details. Here are 2 reasons to be cautious about thinking this virus is not so virulent.
- Our knowledge about the characteristics of the 1918 virus is based on samples taken from the fall of 1918, ie the 'second wave' of that pandemic. (For the full story of how scientists found and re-constructed the genetic code of the 1918 virus, read Searching for the 1918 Killer) Because the first wave was mild, very few people died, and far fewer autopsy samples are available. Which means that we actually do not know whether the 1918 virus already had those 'virulence markers' that they found in the second wave, or whether these mutations only happened afterwards and were responsible for the change in severity.
Comparing the current virus to the second wave virus of 1918, actually does not tell us much about whether it will become more virulent later.
- The second question is, how predictive are these known 'virulence markers'? Do all viruses, or even do all H1N1 viruses, use the same mutations to adapt to a new host and cause disease? To answer this question, scientists at Jeffery Taubenberger's lab at the NIAID recently completed a very interesting study. Different evolutionary trajectories of European avian-like and classical swine H1N1 influenza A viruses
To understand what they did, and found, here's a bit of background. In the fall of 1918, the H1N1 virus that was causing such deadly infections in humans, started to infect pigs. It became established in pigs, and had since circulated among pigs all over the world. This swine H1N1 is called 'classical swine flu'.
In 1979, an avian H1N1 virus, that had so far only circulated in birds, started infecting pigs in Europe. The virus was transmitted among pigs, and started another lineage of swine flu in Europe, called the Eurasian swine H1N1.
So these are 2 different swine H1N1s, both came from birds (although the classical one had a human intermediate host), and both switched host species without reassortment. This creates the perfect opportunity, to observe what happens to avian viruses when they switch to a mammalian host. We know that they would mutate to adapt, but would they use the same mutations? Here's what they found:
ABSTRACT:
In 1979 a lineage of avian-like H1N1 influenza A virus emerged in European swine populations independently from the 'classical' swine H1N1 virus lineage that had circulated in pigs since the 'Spanish' influenza pandemic of 1918. To determine whether these two distinct lineages of swine-adapted A/H1N1 viruses have evolved in similar ways, as might be expected given their common host species and origin from avian-like A/H1N1 ancestors, we compared patterns of nucleotide and amino acid change in whole genome sequences of both groups. An analysis of nucleotide compositional bias across all 8 genomic segments for the two swine lineages showed a clear lineage-specific bias, although a segment-specific effect was also apparent. As such, there only appears to be a relatively weak host-specific selection pressure. Strikingly, despite each lineage evolving in the same species host for decades, amino acid analysis revealed little evidence for either parallel or convergent changes. These findings suggest that although adaptation due to evolutionary lineages can be distinguished, there are functional and structural constraints on all gene segments, and that the evolutionary trajectory of each lineage of swine A/H1N1 virus has a strong historical contingency. Thus, in the context of emergence of an influenza A virus strain via a host-switch event, it is difficult to predict what specific polygenic changes are needed for mammalian adaptation.
So there you have it. "it is difficult to predict what specific polygenic changes are needed for mammalian adaptation."
|
|
|
