1504. HIV Antiretroviral Drug Resistance in Virginia: a Descriptive Analysis Comparing Genotype Data from Two Different Time Periods
Session: Poster Abstract Session: HIV Drug Resistance
Friday, October 28, 2016
Room: Poster Hall
  • MHS Poster FINAL.pdf (971.4 kB)
  • Background: Antiretroviral drug (ARV) resistance is conferred via mutations in the HIV genome. ARV-resistant strains can be spread through transmitted drug resistant mutations (TDRMs) and are associated with treatment failure. Evaluating Virginia (VA) TDRMs and ARV resistance patterns can help guide treatment decisions and direct public health interventions. TDRMs and ARV resistance patterns in circulating HIV strains were monitored in VA from 2004-2007 as part of the Variant, Atypical, and Resistant HIV Surveillance (VARHS) program and from 2013-2015 as part of the Molecular HIV Surveillance (MHS) program. The objective of this study was to compare circulating TDRMs and ARV resistance patterns identified during two different timeframes in VA.

    Methods: HIV genotypes collected from patients within 3 months of initial HIV diagnosis were included. The Stanford HIVDB genotypic resistance interpretation algorithm was used to identify ARV-resistant mutations and ARV resistance. ARV drug classes of interest included protease inhibitors (PI), nucleoside reverse transcriptase inhibitors (NRTI), and non-nucleoside reverse transcriptase inhibitors (nNRTI). Common mutations and ARV resistance were compared between the two timeframes.

    Results: A total of 1,360 HIV genotypes (493 VARHS, 867 MHS) were analyzed. TDRMs were identified in 190 (39%) VARHS and 393 (45%) MHS genotypes. The most common PI mutation was L10I (32% for VARHS and MHS) for both timeframes. The most common nNRTI mutation was K103N for both timeframes (40% VARHS, 36% MHS), while the most common NRTI mutation was M41L for VARHS (23%) and M184V and T215L for MHS (12% each). VARHS genotypes had more instances of high level resistance to PI ARVs. Both timeframes saw high levels of resistance to the nNRTIs Efavirenz and Nevirapine.

    Conclusion: Although there were some differences observed in the HIV strains collected between the two timeframes, overall mutation and resistance patterns were similar. There was an increased frequency of high-level resistance to PI ARVs seen in the earlier time frame that was not observed in MHS; however, the later time frame had a higher percentage of observed TDRMs. Continued reporting of genotype data will assist in further investigating ARV resistance patterns and provide valuable data on HIV disease in VA.

    Carrie Walker, MPH, Sahithi Boggavarapu, MPH, Kristen Kreisel, PhD, Celestine Buyu, MPH, MHSA and Anne Rhodes, PhD, Division of Disease Prevention, Virginia Department of Health, Richmond, VA


    C. Walker, None

    S. Boggavarapu, None

    K. Kreisel, None

    C. Buyu, None

    A. Rhodes, None

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