Sexual transmission of HIV-1 isolate showing G -> A hypermutation

Sexual transmission of HIV-1 isolate showing G -> A hypermutation

Autor Caride, E. Google Scholar
Brindeiro, R. M. Google Scholar
Kallas, E. G. Google Scholar
Sa, CAM de Google Scholar
Eyer-Silva, W. A. Google Scholar
Machado, E. Google Scholar
Tanuri, A. Google Scholar
Instituição Universidade Federal do Rio de Janeiro (UFRJ)
Universidade Federal de São Paulo (UNIFESP)
Hosp Univ Gaffree & Guinle
Resumo 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.
Assunto HIV-1
G -> A hypermutation
reverse transcriptase
CD4+T cells
oligoclonal expansion
Idioma Inglês
Data 2002-01-01
Publicado em Journal of Clinical Virology. Amsterdam: Elsevier B.V., v. 23, n. 3, p. 179-189, 2002.
ISSN 1386-6532 (Sherpa/Romeo, fator de impacto)
Editor Elsevier B.V.
Extensão 179-189
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000173240800006

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