Published this week on-line in PLoS Biology, Sara Sawyer, Michael Emerman, and Harmit Malik investigate the genetic roots of the battle for evolutionary advantage between HIV-type viruses and the hosts they infect. What they find is surprising.
Antiviral editing enzymes like Apobec3G have been involved in an ancient genome defense strategy in primates
The gene, APOBEC3G, belongs to a family of primate genes that produce enzymes (in this case, APOBEC3G) that "edit" DNA and RNA, by slipping into viral particles and inducing mutations that replace one base (cytosine) with another (uracil) as the virus undergoes reverse transcription in the host cells cytoplasm. The edited virus fails to replicate. HIV, in turn, generates a protein called Vif that binds to the APOBEC3G enzyme and targets it for degradation, thereby eliminating its antiviral activity.
Since the protein-binding regions that govern these interactions have a direct effect on the fitness of both virus and host, one would expect to see the proteins angling for advantage, with Vif maximizing its ability to recognize APOBEC3G and APOBEC3G doing its best to evade Vif. Such battles are thought to result in frequent mutations that alter the amino acids involved in the interaction; the perpetuation of such advantageous mutations is called positive selection.
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