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Analysis of HIV-1 mutation patterns in patients failing antiretroviral therapy

✍ Scribed by Eugenia Quiros-Roldan; Simona Signorini; Francesco Castelli; Carlo Torti; Andrea Patroni; Monica Airoldi; Giampiero Carosi

Publisher: John Wiley and Sons
Year: 2001
Tongue: English
Weight: 27 KB
Volume: 15
Category: Article
ISSN: 0887-8013
DOI: 10.1002/1098-2825(2001)15:1<43::aid-jcla9>3.0.co;2-i

No coin nor oath required. For personal study only.

✦ Synopsis

The emergence of mutations encoding drug resistance is supposed to be a significant limitation to the clinical efficacy of inhibitor compounds directed against specific HIV-1 enzymatic targets. We have used a commercial test (Visible Genetics Inc., Paris, France) to study the prevalence of mutations occurred in HIV-1 protease and reverse transcriptase (RT) genes in 93 HIV-1 infected patients treated with at least one regimen containing a protease inhibitor (PI) and failing to the current therapeutic regimen. Protease mutations conferring resistance to at least one PI were detected in 46/93 (49.4%) of strains, 25 (26.8%) of which showed resistance to all PIs. Reverse transcriptase mutations conferring resistance to at least one RT inhibitor were detected in 57/93 (61.2%) of strains, 18 (19.3%) of which showed resistance to all RT inhibitors. The most frequent RT mutations were T215Y/F, M41L, and M184V (41.9, 40.8, and 40.8%, respectively), while L63P, L10R/V, and A71V/T (58, 41.9, and 34.4%, respectively) were the most represented protease substitutions. We have found no mutations encoding for multiple dideoxynucleoside resistance (Q151M or T69SS). Twelve of our patients (12.9%) had no mutation encoding drug resistance and were completely sensitive to all RT and protease inhibitors. Therefore, not all virological failures are caused by HIV-1 genomic resistance.

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