HIV-1 proviral DNA loads (as determined by quantitative PCR) in patients subjected to structured treatment interruption after antiretroviral therapy failure.

The impact of Structured Treatment Interruption (STI) in peripheral blood mononuclear cell (PBMC) proviral reservoirs in 41 highly active antiretroviral therapy (HAART)-treated viremic individuals at baseline and 12 weeks after STI was determined using quantitative PCR (qPCR). Viral load increased 0.7 log(10) and CD4 decreased 97.5 cells/mm(3) after 12 weeks. A total of 28 of the 41 individuals showed an increased proviral load, 19 with a statistically significant increase above 10%. An increase in active viral replication is an important factor in the replenishment of the proviral reservoir even for short time periods.

HIV type 1 antiretroviral resistance mutations in subtypes B, C, and F in the City of São Paulo, Brazil.

In Brazil, where three distinct HIV-1 subtypes (B, F, and C) cocirculate, a significant portion of the HIV-infected population has been exposed to antiretroviral drugs. This study analyzes the antiretroviral resistance profiles of HIV-1-infected individuals failing antiretroviral therapy. Genotypic resistance profiles of 2474 patients presenting virologic failure to antiretroviral therapy in the city of São Paulo, Brazil, were generated and analyzed. Resistance mutations to protease inhibitors and nucleoside reverse transcriptase inhibitors were less common in subtype C viruses, whereas nonnucleoside reverse transcriptase inhibitor resistance mutations were less common in subtype F viruses. The thymidine analog mutation pathway known as pathway 1 was more prevalent in subtype B viruses than in subtype C viruses, whereas pathway 2 was more prevalent in subtype C viruses. Selected resistance mutations varied according to subtype for all three classes of antiretrovirals. We describe two distinct pathways of nonnucleoside reverse transcriptase inhibitor resistance (to nevirapine and efavirenz). Although cross-resistance to etravirine should occur more frequently among individuals failing nevirapine treatment, the prevalence of cross-resistance to etravirine, darunavir, and tipranavir was found to be low. We found that increases in the number of resistance mutations will be related to increases in the viral load. Special attention should be given to resistance profiles in non-B subtype viruses. The accumulation of knowledge regarding such profiles in the developing world is desirable.