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Minor Mutations in HIV Protease at Baseline and Appearance of Primary Mutation 90M in Patients for Whom Their First Protease‐Inhibitor Antiretroviral Regimens Failed
Author(s) -
Carlo Federico Perno,
Alessandro CozziLepri,
Federica Forbici,
Ada Bertoli,
Michela Violin,
María Stella Mura,
G. P. Cadeo,
Anna Orani,
Antonio Chirianni,
Carlo de Stefano,
Claudia Balotta,
Antonella d’Arminio Monforte
Publication year - 2004
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/386307
Subject(s) - protease , odds ratio , virology , protease inhibitor (pharmacology) , mutation , biology , confidence interval , clade , logistic regression , virus , immunology , medicine , viral load , genetics , gene , antiretroviral therapy , phylogenetics , biochemistry , enzyme
The association between minor mutations in human immunodeficiency virus (HIV) protease at baseline and development of common primary mutation 90M at virological failure (conferring some resistance to all protease inhibitors [PIs]) was evaluated in 93 previously drug-naive patients experiencing failure of their first PI-based antiretroviral regimens. In logistic regression analysis, the probability of accumulating a new 90M mutation at virological failure was associated with the presence at baseline of minor mutation 36I (naturally occurring in approximately 25% of HIV clade B and in >80% of HIV non-clade-B viruses) (adjusted odds ratio, 13.5 [95% confidence interval, 1.89-95.6]; P=.009) and, possibly, of 10I/V. This suggests a potential role for the presence of 36I at baseline in predicting the appearance of 90M at virological failure.

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