Navegando por Palavras-chave "reverse transcriptase"

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    Prevalence of mutations related to HIV-1 antiretroviral resistance in Brazilian patients failing HAART
    (Elsevier B.V., 2002-07-01) Tanuri, A.; Caridea, E.; Dantas, M. C.; Morgado, M. G.; Mello, DLC; Borges, S.; Tavares, M.; Ferreira, S. B.; Santoro-Lopes, G.; Martins, CRF; Esteves, ALC; Diaz, R. S.; Andreo, SMS; Ferreira, LAP; Rodrigues, R.; Reuter, T.; Cavalcanti, AMS; Oliveira, S. M. de; Barbosa, H. B. de; Teixeira, P. R.; Chequer, P. N.; Universidade Federal do Rio de Janeiro (UFRJ); Brazilian Minist Hlth; Fiocruz MS; Univ Fed Espirito Santos; Universidade de Brasília (UnB); Lab Cent Saude Publ; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP); Universidade Federal de Santa Catarina (UFSC)
    Background: Current guidelines for antiretroviral (ARV) therapy recommend at least triple-drug combination, the so-called highly active antiretroviral therapy (HAART). Not all patients respond to HAART and the development of drug resistance remains one of the most serious obstacles to sustained suppression of HIV. Objective: in an attempt to correlate the HIV therapeutic failure with reverse transcriptase (RT) and protease resistance mutations, we describe the ARV resistance profile in patients failing HAART in Brazil. We studied 267 Brazilian HIV-1 infected patients failing HAART looking for mutations in RT and protease genes. the mutation profile of the viruses infecting these individuals were deduced and correlated to laboratorial parameters. Study Design: Two different HIV-1 genomic regions were targeted for PCR amplification, the protease (pro) and pal RT (palm finger region) genes. the mutations related to drug resistance in RT gene was analyzed using a line probe assay (LIPA(R)) and pro amino acids positions 82 and 90 were screened through RFLP using HincII restriction digestion. Results: There was strong correlation between the mutation in the pro and RT genes and therapeutic failure. the main mutation found in RT gene was the M184V (48%) followed by T69D/N (47%), T215Y/F (46%), M41L (39%), and L74V (7%). in the pro gene the main mutation found was L90M (26%) followed by dual substitution in L90M and V82A (6%). All mutations profiles matched very well with the patients drug regimen. Conclusions: This study has shown that 84.7% of HIV infected subjects failing HAART for more than 3 months presented viral genomic mutations associated with drug resistance. (C) 2002 Elsevier Science B.V. All rights reserved.
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    Sexual transmission of HIV-1 isolate showing G -> A hypermutation
    (Elsevier B.V., 2002-01-01) Caride, E.; Brindeiro, R. M.; Kallas, Esper Georges [UNIFESP]; Sa, CAM de; Eyer-Silva, W. A.; Machado, E.; Tanuri, A.; Universidade Federal do Rio de Janeiro (UFRJ); Universidade Federal de São Paulo (UNIFESP); Hosp Univ Gaffree & Guinle
    Retroviral genomes with a high frequency of G --> A mutations are thought to originate during reverse transcription (RT). Here we present a case report of an AIDS patient infected with a subtype F variant where extensive G --> A hypermutation (G --> A Hypm) sequences were found in the protease gene. This patient was failing HAART at the time the hypermutation was found. These sequences were basically encountered in the proviral compartment on two occasions and were persistently absent in the plasma viral population. the patient's viral genotype showed several mutations related to antiretroviral drug resistance in RT (T69N, N184V, T215F, K219Q) and protease (M36I, G48V, I54V, T63L, V82A) genes. the drug regimen was changed and the viral load dropped 0.9 Logs and CD4 count increased by 200 cells/ml. the hypermutation was not found any more in a 1-year follow up. the patient's wife was infected with a similar virus strain and G A Hypm sequences were also detected in the RT gene. This is the first report of sexual transmitted G --> A Hypermutation in HIV-1 and suggest that this phenomenon can be genetically coded by the viral RT molecule. (C) 2002 Elsevier Science B.V. All rights reserved.