Deletions in the beta3-beta4 hairpin loop of HIV-1 reverse transcriptase are observed in HIV-1 isolated from subjects during long-term antiretroviral therapy.

Autor: Ross L; Department of Virology, Glaxo Wellcome Inc., Research Triangle Park, North Carolina 27709, USA. llr8156@glaxowellcome.com, Johnson M, Ferris RG, Short SA, Boone LR, Melby TE, Lanier R, Shaefer M, St Clair M
Jazyk: angličtina
Zdroj: Journal of human virology [J Hum Virol] 2000 May-Jun; Vol. 3 (3), pp. 144-9.
Abstrakt: Objectives: To examine the effect of in-frame deletions in human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) on plasma viremia and phenotypic resistance to antiretroviral drugs.
Study Design/methods: Plasma HIV-1 RNA was isolated from 168 antiretroviral therapy-experienced subjects for quantification of plasma viremia, RT sequence analysis, and phenotypic resistance assays.
Results: Four patients were found to harbor HIV-1 strains possessing in-frame, 3-nucleotide deletions at RT codons 67, 69, and 70. In these subjects, phenotypic resistance and high plasma viremia were observed only in a background of multiple resistance mutations. A recombinant virus engineered with an in-frame deletion of RT codon 67 did not have increased resistance to nucleoside reverse transcriptase inhibitors (NRTIs).
Conclusions: Selection for deletions within the beta3-beta4 hairpin loop of the HIV-1 RT is an uncommon event most likely to occur in subjects with long-term antiretroviral experience. The codon 67 deletion does not appear to cause increased phenotypic resistance or increased viremia in the absence of concomitant RT mutations.
Databáze: MEDLINE