Professor of epidemiology, Dr Mark Lipsitch, Harvard School of Public Health, presented his views last week at the conference, Options for Control of Influenza VIII.
His talk, entitled Transmissibility GOF Experiments with HPAI: Interesting Science but not worth the risk of an accidental pandemic, noted that these experiments will not (yet) produce results that are balanced by the risk of an accidental pandemic. An accident that is not beyond the realms of reality since such accidents have happened (FMDV in 2007, SARS in 2004 and possibly H1N1 in 1977) in high level biosecurity laboratories (BSL3/PC3). The required standards for these labs differ from country to country.
Further, Lipsitch noted, we don't need GOF studies for vaccine design when currently effective vaccines target haemagglutinin (HA) and not other influenza segments. Further our influenza surveillance is poor and our primary animal model for use in GOF studies for high-pathogenicity influenza virus, ferrets does not always "perform" as we expect it to.
So Lipsitch summarizes, there is much work still to be done to nail down influenza virus variability, impact of host genetic variation and whether before considering more GOF work. Any real benefit to offset the risk of GOF studies may simply be over-stated.
I enjoyed presentation this very much and it has greatly informed my understanding of the argument. Dr Lipsitch's views are clearly thought out and presented in a logical order intended to address some statements/justifications from the proponents of GOF influenza transmission studies.
Thanks to Avian Flu Diary for posting on this earlier.
Showing posts with label ferret. Show all posts
Showing posts with label ferret. Show all posts
Wednesday, September 11, 2013
Thursday, July 18, 2013
Latest article from CIDRAP: new H7N9 animal studies & comment from VDU EiC.
Shameless self-promotion - but very cool when someone asks for your opinion about something you are interested in.The CIDRAP article by Lisa Schnirring covers the newly released paper by Zhang and colleagues of the Prof Hualen Chen's uber-group at the Harbin Veterinary Research Institute, China.
To quote myself...to myself....
And just look at these numbers: 10,703 samples from 30.03.13-02.05.13, collected from poultry markets in all the key H7N9 provinces and municipalities. All (I said all!) were inoculated into eggs. 238 influenza viruses (136 Newcastle disease viruses as well) of which 52 were influenza A(H7N9) virus. They then sequenced the complete genome of 37. Phenomenal work.
While I am no expert on what each and every influenza mutation does (I'm thinking about making a table on the flu page), I was interested in how closely related all the genomes were (<4% nucleotide difference between them all) and that the major differences are at the level of amino acid changes. Also, there were no amino acid changes noted after animal inoculation or transmission. Does this mean the virus is already happy in its own skin?
Although highly similar, the most diverse genomes (those with <99.5% identity to the H7N9/Anhui/1 strain) came mostly from the Shanghai principality. Does that mean anything in terms of site of ground zero? The site of "youngest" viruses perhaps? PB1 seemed to be the most variable H7N9 segment in terms of nucleotide differences.
In the future it might be informative to look at genetic comparisons of complete H7N9 genomes from mild/asymptomatic cases and those from moderate/severe/fatal cases. As well as considering what other viruses and bacteria are in these two groups and whether virus:virus or virus:bacteria interactions may play a role in more severe outcomes.
And this study confirms that of Belser (see below) - if you're a mouse, don't get H7N9!
I haven't looked myself, but it would also be useful to know whether the recommended H7N9 PCR-based assay targets remain conserved in the latest genomes.
To quote myself...to myself....
The study reinforces that even 'lowly' or inefficient transmission-only 33% of ferrets, for example-is still transmission," Mackay said. "That proportion would lead to a lot of human cases in densely populated or frequented areas.
And just look at these numbers: 10,703 samples from 30.03.13-02.05.13, collected from poultry markets in all the key H7N9 provinces and municipalities. All (I said all!) were inoculated into eggs. 238 influenza viruses (136 Newcastle disease viruses as well) of which 52 were influenza A(H7N9) virus. They then sequenced the complete genome of 37. Phenomenal work.
While I am no expert on what each and every influenza mutation does (I'm thinking about making a table on the flu page), I was interested in how closely related all the genomes were (<4% nucleotide difference between them all) and that the major differences are at the level of amino acid changes. Also, there were no amino acid changes noted after animal inoculation or transmission. Does this mean the virus is already happy in its own skin?
Although highly similar, the most diverse genomes (those with <99.5% identity to the H7N9/Anhui/1 strain) came mostly from the Shanghai principality. Does that mean anything in terms of site of ground zero? The site of "youngest" viruses perhaps? PB1 seemed to be the most variable H7N9 segment in terms of nucleotide differences.
In the future it might be informative to look at genetic comparisons of complete H7N9 genomes from mild/asymptomatic cases and those from moderate/severe/fatal cases. As well as considering what other viruses and bacteria are in these two groups and whether virus:virus or virus:bacteria interactions may play a role in more severe outcomes.
And this study confirms that of Belser (see below) - if you're a mouse, don't get H7N9!
I haven't looked myself, but it would also be useful to know whether the recommended H7N9 PCR-based assay targets remain conserved in the latest genomes.
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