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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