Forty samples collected from HIV-1 AIDS and asymptomatic patients in 2002 and 2003 before the initiation of antiretroviral treatment (ART), most in poorly investigated regions of Ghana were retrospectively examined. For baseline data on genetic diversity before therapy, env, gagand pol phylogenetic analysis was generated. pol was further analysed for potential resistance to antiretroviral drugs. Plasma viral load was also quantified. HIV-1 subtypes A1 and G constituted a minority, while simple and/or complex recombinant strains dominated by CRF02_AG and including CRF06_cpx, CRF09 and CRF10 was observed. Major mutations,protease (PR) L33F and reverse transcriptase (RT) M41L, associated with high levels of phenotypic resistance or clinical evidence for reduced virological response were identified. In the protease-coding domain, positions 10 and 11 were mutated in 21% (5/24) of patients examined, carrying putative resistance to PIs. In the reverse transcriptase-coding domain, seven mutations were detected in 6/35 patients (17%). Of these, 8.5% (3/35) had either double or single mutations possibly affecting NRTIs or NNRTIs respectively. Within PR and RT regions, the mutation rate ranged between 2.6 and 7.0%. Position 10 had 57% mutation frequency. The mutational profile of our non-B HIV-1 strains were identical with subtype B strains at documented DR-related positions. Therefore, drug resistance (DR) pathways of non-B strains were presumed similar to subtype B viruses. Although antiretroviral therapy was expected to be successful, patients presenting resistance-related mutations prior to the initiation of ART could develop clinically relevant resistance earlier than wild-type strains.
Key words: HIV-1 genotyping, antiretroviral therapy, drug-naive HIV-1 patients, drug resistance.
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