Tamiflu Resistance Development Gets Molecular Explanation
American biologists have come about with a molecular explanation for the development of Tamiflu resistance.
The study, which was led by David Baltimore, California Institute of Technology's Robert Andrews Millikan Professor of Biology and postdoctoral scholar, Jesse D. Bloom, appears in the journal Science.
Tamiflu and other antiviral drugs openly target viruses, not like vaccinations, which instead stimulate our body's immune system, so as to respond to the pathogens after an infection reaches its strongest level.
In a flu infection, viruses stick to sialic acid on the surface of a host cell that uses a protein that is called hemagglutinin, the H in H1N1.
The viruses then get into the cell and duplicate. When the newly bundled viruses exit the cell, they too stick to sialic acid.
The viruses then make use of a protein that is named neuraminidase, the N in H1N1, in order to cut the sialic acid, getting freed only to infect new cells.
This procedure, on the other hand, is blocked by Tamiflu, which helps in preventing neuraminidase from cutting the sialic acid.
Bloom said that it does this by binding in the active spot of the neuraminidase molecule, where neuraminidase usually cuts sialic acid.
Generally, for a virus to become resistant to Tamiflu, the neuraminidase protein has to be capable of telling the difference between sialic acid and Tamiflu.
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