A crystal ball for predicting the future of flu

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This blog has opened several doors for me. It has been a gateway to writing opportunities, speaking engagements and new friendships, and none of these benefits were apparent when I started. Everyone has similar stories of innocuous events that led to greater and unanticipated things. And such stories abound in the narrative of life.

Take the H1N1 flu virus. The drug Tamiflu was generally effective against last year’s H1N1 swine flu pandemic, but it doesn’t work against the seasonal strains that naturally circulate among humans. Ever since 2007, these seasonal strains have evolved to resist the drug thanks to a mutation called H274Y. This genetic tweak prevents Tamiflu from sticking to the virus’s surface, masking the virus from the drug.

The first viruses with this mutation were discovered in 1999. While they shrugged off Tamiflu, they proved to be otherwise feeble versions of their normal kin. This is a common theme – mutations that bestow resistance to drugs often hobble viruses in some other way. As a result, scientists dismissed the upstart mutation. But they were wrong – flu viruses bearing H274Y soon spread around the world.

Last year, Jesse Bloom from the California Institute of Technology discovered why. He showed that H274Y rose to power thanks to two other “gateway mutations” called V234M and R222Q. These changes did little by themselves, but they helped to compensate for the crippling effects of H274Y. They made it easier for the flu virus to develop resistance to Tamiflu. It’s like giving someone a monitor one year, and then a computer the year later. Both presents are useless on their own, and the value of the first only becomes apparent when you have the second.