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.
