Literature DB >> 10630517

Rapid decline in detectability of HIV-1 drug resistance mutations after stopping therapy.

H L Devereux1, M Youle, M A Johnson, C Loveday.   

Abstract

OBJECTIVE: To investigate the rate of decline of drug resistant viruses after stopping therapy.
DESIGN: Twenty-five patients receiving multiple combination therapies (mean five; range three to nine drugs) for more than 3 months were tested for HIV-1 resistance on therapy and off therapy. The sample off therapy was tested 6-175 days after stopping therapy.
METHODS: Patients were tested for genotypic changes associated with drug resistance using an in-house automated DNA sequencing assay to detect resistance in the protease and reverse transcriptase genes.
RESULTS: All samples tested when patients were on therapy showed evidence of drug resistance (range 1-9 mutations). The patients were divided into three groups: <2 weeks after stopping therapy, median 1.1 weeks (n = 8, group A); 2 weeks-2 months, median 6.4 weeks (n = 7, group B) and 2 months-6 months, median 12.9 weeks (n = 10, group C). Of primary mutations (protease: 30N, 461/L, 82A, 90M; reverse transcriptase: 70R, 184I/V, 215 Y/F) detected on therapy 100% remained after stopping therapy in group A; 68% remained in group B and 15% remained in group C. For secondary mutations 98% remained in group A; 99% remained in group B and 57% in group C.
CONCLUSIONS: This study showed a rapid decline in detectability of the majority of primary mutations within 13 weeks of stopping combination therapy. From this data, HIV-1 resistance testing to direct patients' therapy should only be carried out when on existing therapy, or < 2 weeks off therapy, if reliable decisions are to be made relating to future combinations.

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Year:  1999        PMID: 10630517

Source DB:  PubMed          Journal:  AIDS        ISSN: 0269-9370            Impact factor:   4.177


  37 in total

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2.  Comparison of the dynamics of resistance-associated mutations to nucleoside reverse transcriptase inhibitors, nonnucleoside reverse transcriptase inhibitors, and protease inhibitors after cessation of antiretroviral combination therapy.

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Review 3.  Minority variants of drug-resistant HIV.

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4.  Evolution of drug-resistant viral populations during interruption of antiretroviral therapy.

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5.  The Genetic Basis of HIV-1 Resistance to Reverse Transcriptase and Protease Inhibitors.

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Authors:  Marie-Laure Chaix; Didier Koumavi Ekouevi; Gilles Peytavin; François Rouet; Besigin Tonwe-Gold; Ida Viho; Laurence Bequet; Clarisse Amani-Bosse; Hervé Menan; Valériane Leroy; Christine Rouzioux; François Dabis
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7.  Long-Range HIV Genotyping Using Viral RNA and Proviral DNA for Analysis of HIV Drug Resistance and HIV Clustering.

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8.  Comparison of DNA sequencing and a line probe assay for detection of human immunodeficiency virus type 1 drug resistance mutations in patients failing highly active antiretroviral therapy.

Authors:  J Servais; C Lambert; E Fontaine; J M Plesséria; I Robert; V Arendt; T Staub; F Schneider; R Hemmer; G Burtonboy; J C Schmit
Journal:  J Clin Microbiol       Date:  2001-02       Impact factor: 5.948

9.  Individual contributions of mutant protease and reverse transcriptase to viral infectivity, replication, and protein maturation of antiretroviral drug-resistant human immunodeficiency virus type 1.

Authors:  G Bleiber; M Munoz; A Ciuffi; P Meylan; A Telenti
Journal:  J Virol       Date:  2001-04       Impact factor: 5.103

10.  A multi-variant, viral dynamic model of genotype 1 HCV to assess the in vivo evolution of protease-inhibitor resistant variants.

Authors:  Bambang S Adiwijaya; Eva Herrmann; Brian Hare; Tara Kieffer; Chao Lin; Ann D Kwong; Varun Garg; John C R Randle; Christoph Sarrazin; Stefan Zeuzem; Paul R Caron
Journal:  PLoS Comput Biol       Date:  2010-04-15       Impact factor: 4.475

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