Background: Mutations in the genome of HIV conferring drug resistance are a major reason for the failure of antiretroviral therapy, but they often compromise viral fitness. Protease (PR) cleavage site (CS) mutations could compensate for impaired replication capacity of drug-resistant viruses.
Patients And Methods: We analysed the cleavage sites p1/p7 and p1/p6-gag of 500 HIV-1 subtype B infected patients.