HIV/AIDS Drug Resistance: HIV-1 K65R mutation may emerge preferentially in absence of zidovudine and TAMs
AIDSWEEKLY Plus; Monday, July 31, 2006
Staff Medical Writers
According to recent research published in the journal HIV Medicine, "The K65R HIV-1 reverse transcriptase (RT) mutation is a multidrug resistance mutation which may be correlated with specific antiretroviral combinations and with the presence or absence of other RT resistance mutations.
"The aims of this study were: (1) to determine the prevalence of the K65R mutation in a cohort of antiretroviral-treated patients; (2) to study genotypic patterns and treatment characteristics in patients in whom the K65R mutation was present."
"We included in the study all antiretroviral-experienced patients followed up at the Bordeaux University Hospital in 2003 and 2004 for whom an HIV-1 genotypic resistance analysis was available.
"Information on RT resistance mutations was reported from a hospital database including therapeutic and biological parameters. The prevalence of K65R was investigated for all patients. Genotypic patterns and treatment characteristics were examined at the time of detection of the K65R mutation," researchers wrote.
"The prevalence of K65R was 1.9% (26 of 1404 patients). K65R was associated with nucleoside RT inhibitor-based regimens in 22 patients, and with tenofovir disoproxil fumarate, lamivudine, didanosine and abacavir in 23, 17, 17 and eight patients, respectively.
"The M184V and Q151M mutations were the most commonly coselected substitutions. Thymidine analogue mutations (TAMs) were rarely coselected with K65R and inversely associated with K65R," reported S. Boucher and colleagues at CHU de Bordeaux.
The authors concluded, "The K65R mutation may emerge preferentially in the absence of zidovudine and TAMs, suggesting the possibility of an antagonistic interaction between K65 and TAMs."
Boucher and colleagues published their study in HIV Medicine (HIV-1 reverse transcriptase (RT) genotypic patterns and treatment characteristics associated with the K65R RT mutation. HIV Med, 2006;7(5):294-298).
For additional information, contact B. Masquelier, Hopital Pellegrin, Dept. of Virology & Immunology Biology, Pl Amelie Raba Leon, F-33076 Bordeaux, France.
The publisher's contact information for the journal HIV Medicine is: Blackwell Publishing, 9600 Garsington Rd., Oxford OX4 2DQ, Oxon, England.
Keywords: Bordeaux, France, HIV/AIDS, Drug Resistance, K65R Mutation, Thymidine Analogue Mutation, Zidovudine.
This article was prepared by AIDS Weekly editors from staff and other reports.
2006-07-31
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