The highly pathogenic H7N3 avian influenza strain from July 2012 in Mexico acquired an extended cleavage site through recombination with host 28S rRNA

A characteristic difference between highly and non-highly pathogenic avian influenza strains is the presence of an extended, often multibasic, cleavage motif insertion in the hemagglutinin protein.

Conclusions

This highly pathogenic H7N3 avian influenza strain acquired a novel extended cleavage site which likely originated from recombination with 28S rRNA from the avian host. Notably, this new virus can infect humans but currently lacks critical host receptor adaptations that would facilitate human to human transmission.

Ed Rybicki‘s insight:

This is rather sinister! Not only can influenza viruses mutate, for antigenic drift, and reassort with one aother for antigenic shift – they can now recombine with HOST sequences to increase pathogenicity!

See on www.virologyj.com

This entry was posted on 3 May, 2013 at 12:43 and is filed under Uncategorized. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.

One Response to “The highly pathogenic H7N3 avian influenza strain from July 2012 in Mexico acquired an extended cleavage site through recombination with host 28S rRNA”

gsgs Says:
7 August, 2014 at 17:59 | Reply
such recombination is rare and I’ve only seen it at the HA-cleavage site.. There was one event in Chile, where it recombined with NP
segment 5, to achieve a high path. (=longer) cleavage site.
These occasional insertions and deletions –
are they always some sort of recombination ?

ViroBlogy