# 4620
A fascinating press release today from Caltech, in advance of publication tomorrow in Science, of a paper that the authors say shows how seasonal H1N1 managed to pick up Tamiflu resistance back in 2008 and still spread efficiently from person to person.
While Tamiflu resistance was certainly known to occur, prior to 2008 it was believed that the mutation (H274Y) that caused resistance also hindered its ongoing transmission.
But all of that changed in 2008 when resistant viruses suddenly exploded around the world. In less than a year, reports of resistant H1N1 went from the single digits to nearly 100%.
Caltech scientists have identified two other mutations that, in concert with H274Y, allowed the virus to develop resistance and still transmit efficiently. These two "pre-adaptive mutations” paved the way for the H274Y strains to spread.
Follow the link to read the release in its entirety.
Caltech biologists provide molecular explanation for the evolution of Tamiflu resistance
PASADENA, Calif.—Biologists at the California Institute of Technology (Caltech) have pinpointed molecular changes that helped allow the global spread of resistance to the antiviral medication Tamiflu (oseltamivir) among strains of the seasonal H1N1 flu virus.
The study—led by David Baltimore, Caltech's Robert Andrews Millikan Professor of Biology and recipient of the 1975 Nobel Prize in Physiology or Medicine, and postdoctoral scholar Jesse D. Bloom—appears in the June 4 issue of the journal Science.
Tamiflu and other antiviral drugs directly target viruses, unlike vaccines, which instead stimulate our body's immune system to respond to the pathogens after an infection is established.
In a flu infection, viruses bind to sialic acid on the surface of a host cell using a protein called hemagglutinin (the "H" in H1N1). The viruses then enter the cell and replicate. When the newly minted viruses exit the cell, they too bind to sialic acid. The viruses then use a protein called neuraminidase (the "N" in H1N1) to cut the sialic acid, freeing themselves to infect new cells.
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