Get Started for FREE
Sign up with Facebook Sign up with X
I don't have a Facebook or a X account
 Your new post is loading...
Your new post is loading...
Scoop.it!
I just love it when long standing mysteries in virology are suddenly solved, typically by the use of new technologies. In this story, the long standing mystery was why poxvirus mRNAs have a stretch of poly(A) in their 5′-noncoding regions. The answer is that it allows the ribosome to preferentially translate these viral mRNAs over those of the host 
No comment yet.
Sign up to comment
|
Scoop.it!
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.
Avian influenza virus graphic courtesy of Russell Kightley Media
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!
|
