Secondary Mutations M36I and A71V in the Human Immunodeficiency Virus Type 1 Protease Can Provide an Advantage for the Emergence of the Primary Mutation D30N

Abstract excerpt

Development of resistance mutations in enzymatic targets of human immunodeficiency virus 1 (HIV-1) hampers the ability to provide adequate therapy. Of special interest is the effect mutations outside the active site of HIV-1 protease have on inhibitor binding and virus viability. We engineered protease mutants containing the active site mutation D30N alone and with the nonactive site polymorphisms M36I and/or...

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