The aim of the present study was to determine viral subtypes and resistance mutations to antiretroviral treatment (ART) in HIV-1-infected treatment-naive patients from Rabat, Morocco during the period 2005-2009. The protease and reverse transcriptase (RT) genes were sequenced, the phylogenetic trees were inferred, and the resistance-associated mutations to NRTIs, NNRTIs, and PIs were recorded according to the international list of surveillance drug resistance mutations (SDRMs). The viral subtypes were subtype B (74%), CRF02_AG (15%), A1 (6%), C (2%), F1 (1%), CRF09 (1%), and CRF25_cpx (1%). The presence of DRMs was found in four (5.06%) of 91 patients; resistance mutations to NRTIs were M184V and T215I/S revertant mutations; resistance to NNRTIs was associated with K103N and resistance to PIs with V82A. These findings have relevant implications for the local molecular mapping of HIV-1 and future ART surveillance studies in the region.
The emergence of viral-resistant strains is a major problem for the medical management of HIV-infected individuals. The aim of this study was to characterize viral subtypes and drug-resistance mutations (DRMs) in HIV-1 isolates from patients failing antiretroviral therapy (ART). A total of 45 HIV-1-infected patients failing ART were enrolled. The viral RT and Prot genes were amplified and sequenced to determine subtypes and potential DRMs. The subtype distribution was 74% subtype B, 11% subtype A, 9% CRF02-AG, 4% subtype G, and 2% subtype C. Virus samples from 34% of the patients had no DRM while 53%, 27%, and 2% of samples carried at least one DRM conferring resistance to drugs of one, two, or three classes, respectively. DRMs were observed in 50% of the patients infected with non-B strains. The prevalence of nucleoside transcriptase inhibitor (NRTI) mutations was 48%, M184V being largely predominant. The prevalence of nonnucleoside reverse transcriptase inhibitor (NNRTI) mutations was 13%, with K103N present in 57% of samples from NNRTIs-exposed patients. The prevalence of protease inhibitor (PI) mutations was 22%, with major mutations V82A and M46I seen in 16% and 11% of viruses from PI-exposed individuals, respectively. Our study shows the emergence of DRMs in HIV-1 isolates from Moroccan patients failing ART. Although not surprising, the data plead for longitudinal surveys of the dynamics of emergence of DRMs (with a focus on multidrug resistance) in treated patients and circulation of resistant HIV-1 strains in this country.
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