Open AccessAnalysis of HIV‐1 mutation patterns in patients failing antiretroviral therapy
Author(s) -
QuirosRoldan Eugenia,
Signorini Simona,
Castelli Francesco,
Torti Carlo,
Patroni Andrea,
Airoldi Monica,
Carosi Giampiero
Publication year - 2001
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/1098-2825(2001)15:1<43::aid-jcla9>3.0.co;2-i
Subject(s) - antiretroviral therapy , human immunodeficiency virus (hiv) , mutation , medicine , virology , biology , genetics , viral load , gene
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. J. Clin. Lab. Anal. 15:43–46, 2001. © 2001 Wiley‐Liss, Inc.