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1.
Braz. j. infect. dis ; 14(4): 360-371, July-Aug. 2010. ilus, tab
Article in English | LILACS | ID: lil-561208

ABSTRACT

Antiretroviral therapy (ART) has reduced morbidity and mortality related to human immunodeficiency virus (HIV) infection, but in spite of this advance, HIV mutations decrease antiretroviral susceptibility, thus contributing to treatment failure in patients. Genotyping HIV-1 allows the selection of new drugs after initial drug failure. This study evaluated the genotypic profile of HIV-1 isolates from treated (drug-experienced) patients in Paraná, Brazil. The prevalence of mutations in reverse transcriptase (RT) and protease (PR) genes were assessed. We analyzed 467 genotypes of patients with HIV-1 viral loads above 1,000 copies/mL. Mutations at HIV-1 RT and PR genes and previously used ART regimens were recorded. The most prevalent RT mutations were: 184V (68.31 percent), 215YF (51.6 percent), 103NS (46 percent), 41L (39.4 percent), 67N (38.54 percent), 210W (23.5 percent), 190ASE (23.2 percent), and 181C (17.4 percent). PR mutations were 90M (33.33 percent), 82ATFS (29 percent), 46I (26.8 percent) and 54V (22.2 percent). The prevalence of mutations was in line with previous national and international reports, except to nonnucleoside analogue reverse transcriptase inhibitors related mutations, which were more prevalent in this study. Previous exposure to antiretroviral drugs was associated with genotypic resistance to specific drugs, leading to treatment failure in HIV patients.


Subject(s)
Adult , Female , Humans , Male , Anti-HIV Agents/therapeutic use , HIV Infections/drug therapy , HIV Protease/genetics , HIV Reverse Transcriptase/genetics , HIV-1 , Mutation/genetics , Antiretroviral Therapy, Highly Active , Brazil , Drug Resistance, Viral/genetics , Genotype , HIV Infections/virology , HIV-1 , Treatment Failure , Viral Load
2.
Braz. j. infect. dis ; 14(3): 230-236, May-June 2010. ilus, tab
Article in English | LILACS | ID: lil-556834

ABSTRACT

OBJECTIVE: Because epidemiological data on circulating HIV subtypes among HIV-positive patients in the state of Paraná were not known until now, the aims of this study were to describe the genetic diversity profile of HIV-1 in treated patients in Paraná, Brazil, and report the differences in protease (PR) and reverse transcriptase (RT) mutations in HIV-1 subtypes. PATIENTS AND METHODS: A cross-sectional study was conducted from 2003 to 2006. Plasma viral RNA of 389 patients was extracted and PR and RT genes were polymerase chain reaction-amplified and sequenced. Sequences were subtyped and examined for antiretroviral resistance mutations. Data on gender of patient harboring the viruses and past history of antiretroviral treatment were also collected. RESULTS: Most viruses were either subtype B (61.44 percent) or subtype C (20.57 percent). Subtype C and F were more frequent in women (p < 0.00). The prevalence of subtypes was similar over the years studied. The most frequent RT mutations in all subtypes were M184V and mutations at codons 215, 41, 103, 67, 219, and 190. Mutations 41L, 210W, 215YF, and 74V were significantly more prevalent on subtype B, and the mutation 106M was significantly more prevalent on subtype C. The most frequent major PI mutations in all subtypes occurred at codons 46, 82, and 90. PR mutations 32I, 46I, and 84V were significantly more prevalent on subtype B. The minor PI mutations on codons 36, 93, and 63 were more prevalent on subtypes F, C, and B, respectively. CONCLUSION: We concluded that the predominant strain of HIV-1 in Paraná is subtype B, followed by subtype C. Some mutations at PR and TR had subtype predominance in accordance with other authors' report.


Subject(s)
Adult , Female , Humans , Male , Drug Resistance, Viral/genetics , Genetic Variation/genetics , HIV Infections/virology , HIV Protease/genetics , HIV Reverse Transcriptase/genetics , HIV-1 , Mutation/genetics , Antiretroviral Therapy, Highly Active , Cross-Sectional Studies , Genotype , HIV Infections/drug therapy , HIV-1 , Polymerase Chain Reaction , RNA, Viral/genetics
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