Gag mutations strongly contribute to HIV-1 resistance to protease inhibitors in highly drug-experienced patients besides compensating for fitness loss.

Human immunodeficiency virus type 1 (HIV-1) resistance to protease inhibitors (PI) results from mutations in the viral protease (PR) that gotrax handlebar reduce PI binding but also decrease viral replicative capacity (RC).Additional mutations compensating for the RC loss subsequently accumulate within PR and in Gag substrate cleavage sites.We exam

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