Influenza virus is a
pretty fascinating virus, primarily because of its tremendous ability to
change. The versatility of the virus is described as "the chameleon-like
power to mutate keeps them ahead of the game". These creepy RNA viruses,
as we know, enjoy negotiating with their hosts. They are not like DNA viruses
or bacteria that can cause diseases with high mortality. Instead, they stay
with the hosts while performing their amazingly high-speed evolution, by both
antigenic shift and antigenic drift.
Antigenic drift refers to
mutations in surface glycoproteins of the viruses (hemagglutinin and
neuraminidase). The high rate of mutation (an error rate between 1×10−3 and8×10−3 substitutions
per site per year) is due to the lack of proofreading mechanism of viral RNA
polymerase. The mutations that happen in the receptor binding site of the
antigens will result in the failure of host immunity recognition and the
subsequent immunity evasion.
Another mechanism that
keeps influenza virus changing is antigenic shift, which is known as
reassortment of genome segments from different strains. The most telling
example of antigenic shift, the swine-origin H1N2 in 2009, is the result of
triple reassortment. The virus contains four segments from classic American
swine influenza virus, two segments from human influenza virus and two from
avian lineage. The reassortment of the virus causes new host adaptation
and pandemic formation, posing great threat to public health.
Here is a review article
that depics the evolution of influenza A viruses
References
wikipedia.org
http://pathogenposse.tumblr.com
http://www.ncbi.nlm.nih.gov/pubmed/20542248
wikipedia.org
http://pathogenposse.tumblr.com
http://www.ncbi.nlm.nih.gov/pubmed/20542248
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