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Trends in genotypic and phenotypic HIV-1 drug resistance among recent clinical samples submitted for resistance testing



Trends in genotypic and phenotypic HIV-1 drug resistance among recent clinical samples submitted for resistance testing



Abstracts of the Interscience Conference on Antimicrobial Agents & Chemotherapy 43: 324



Background: Resistance to antiretroviral drugs is a major factor contributing to failure of HIV-1 therapy. Patterns of drug resistance are likely to evolve over time with changes in treatment strategies and the introduction of new antiviral agents. Methods: Genotypes of >60,000 routine clinical samples submitted to Virco between 1998 and 2002 were surveyed for trends in resistance associated mutations and predicted phenotypic resistance assessed by VirtualPhenotypeTM. Results: In 2002, RT gene mutations 184V (40%) and 103N (27%) were most common, followed by the nucleoside analog resistance mutations (NAMs, 12-22%). Between 1998 and 2002, the proportion of isolates with NAMs declined, 184V remained almost constant and 103N increased by 32%. The largest increases (>2 fold) included mutations associated with NNRTI resistance (225H, 101P, 190Q and S, 103S, and 106I) as well as the 65R mutation. In the protease gene, mutations 77I, 36I, 10I, and 90M were most common in 2002 (32%-21% of isolates), although 10I and 90M had declined by 38% and 45% since 1998. Increases >2 fold were observed for mutations 50V, 54M and L, 33F, and 47V. VirtualPhenotypeTM analysis predicted that 70% of samples in 2002 were resistant to one or more drugs (60% to NRTIs, 45% to NNRTIs and 36% to PIs) with 18% of samples resistant to drugs in all three classes. Changes in phenotypic resistance since 1998 included decreases in resistance to all three classes (29%) and to NRTIs plus PIs (51%), and increases in resistance to NNRTIs (133%) and to NNRTIs plus NRTIs (114%). The proportion of isolates without resistance increased (27%). Conclusions: Resistance remained extensive throughout the period 1998-2002. The prevalence of NAMS and resistance to PIs declined while NNRTI resistance increased. Changing treatment practices, increased use of resistance testing and evolution of the patient population may have contributed to the observed changes in patterns of genotypic and phenotypic resistance.

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Accession: 035985344

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