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H1N1 virus shows genetic mutation, 'but not a worry'
Virology. Correlation between polymerase activity and pathogenicity in two duck H5N1 influenza viruses suggests that the polymerase contributes to pathogenicity.
My question is: Does increased efficiency of replication result in virulence changes or enhanced transmission?
I believe Niman's thoughts are that because this mutation allows for viral production in the upper airways of the human respiratory system, that it is more likely that the virus will be able to reproduce to higher numbers within a host and thus the host will incur a higher viral load. Thus the likelihood of a severe or fatal outcome increases.
Last edited by JetStuuby; March 16, 2010, 01:27 PM.
Reason: spelling
Re: H1N1 virus shows genetic mutation, 'but not a worry'
The article says:
The PB2 mutation has previously been associated with increased efficiency of replication and possible virulence changes in other influenza A viruses.
My question is: Does increased efficiency of replication result in virulence changes or enhanced transmission?
This was taken from the Influenza Research Database. It was from an Argentine sample, used just as an example of the mutations they are watching for. All on this sample had "no" execpt for the ones with "yes".
As you can see, there are a number of PB2 markers associated with enhanced transmission and increased virulence.
Re: H1N1 virus shows genetic mutation, 'but not a worry'
yes, but why the general strategy to keep things unclear,
not only in India ? Was it normal years/decades ago ?
why only comments from India-people, no good global cooperation
the Shanghai-virus with E627K was odd - signs of reassortment
or even recombination. Coincidence ?
H1N1 virus shows genetic mutation, 'but not a worry'
H1N1 virus shows genetic mutation, 'but not a worry'
Umesh Isalkar, TNN, Mar 16, 2010, 07.32am IST
PUNE: The swine flu virus isolated from the throat swab samples of three H1N1-infected patients at the National Institute of Virology (NIV) has shown a small genetic mutation in the polymerase 2 (PB2) gene, NIV director A C Mishra told TOI on Monday.
However, Mishra said there was no cause for worry as the virus was still not resistant to oseltamivir, which is an active ingredient in Tamiflu.
It may be noted that a small genetic mutation was earlier detected in the haemagglutinin (HA) region of the virus as well while testing the throat swab samples of two patients who eventually succumbed to the H1N1 infection.
The PB2 mutation has previously been associated with increased efficiency of replication and possible virulence changes in other influenza A viruses. ?However, we did not find such increased efficiency of replication or increased virulence in the isolates of the swine flu virus in which we have noticed mutation of the PB2 gene. The mutation is not very significant in that sense,? said Mishra.
Consulting microbiologist and immunologist Siddharth Dalvi said, ?The PB gene makes a protein that is responsible for viral replication. Since this enzymic protein is not directly involved in the immune responses, point mutations in this gene may not be of immediate clinical impact. However, it may, in theory, change the way the virus replicates.?
Most RNA viruses (including influenza virus) replicate their genome by using the viral enzyme to make copies from the parent RNA. ?This enzyme has a weak proof-reading activity, that is, checking if the right nucleotides have been incorporated in the genome. Hence, over time, point mutations are bound to happen in the genome of these viruses. In fact, we would be surprised if they don?t. The majority of these mutations may not have any significance, either for the virus, or for the host,? said Dalvi.
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