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16th International HIV Drug Resistance Workshop12-16 June 2007, Barbados |
FREQUENCY OF TRANSMITTED DRUG RESISTANCE AMONG ACUTE AND RECENTLY HIV-INFECTED PATIENTS IN NORTH CAROLINA IS SIMILAR TO REPORTS FROM MORE URBANIZED AREAS
Antivir Ther. 2007; 12:S55 (abstract no. 48)
C Hurt
1, S McCoy2, M Kerkau3, J Nelson3, J Sebastian4, J Kuruc1, K McGee5, J Lennox6, C Pilcher7, C Hicks5 and J Eron1,3
1Division of Infectious Diseases, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; 2Department of Epidemiology, School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; 3Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; 4LabCorp, Research Triangle Park, NC, USA; 5Division of Infectious Diseases, School of Medicine, Duke University, Durham, NC, USA; 6Division of Infectious Diseases, School of Medicine, Emory University, Atlanta, GA, USA; 7HIV/AIDS Division, School of Medicine, University of California at San Francisco,
San Francisco, CA, USA
BACKGROUND: Transmitted drug resistance (TDR) limits antiretroviral options, complicating the management of HIV-positive patients. The United States’ (US) epidemic is increasing fastest in non-urbanized areas and non-traditional risk groups, but available estimates of US TDR prevalence reflect only large metropolitan centers.
METHODS: Since 1998, we have collected clinical and behavioral data on HIV-1 antibody-negative, RNA-positive subjects (Ab–/RNA+) and others having enzyme immunoassay seroconversion (SC) within 45 days of prior negative testing. Protease and reverse transcriptase (RT) were sequenced using the earliest collected pre-treatment plasma sample for each subject. We analysed nucleotide data with the Stanford HIV Database and screened results with the International AIDS Society (IAS) Fall 2006 and Stanford Surveillance Drug Resistance Mutation (SDRM) lists of resistance mutations.
RESULTS: Analysis of 126 subjects (Ab–/RNA+, n=117; SC, n=9) revealed most are male (82.9%); 43.4% are white, 48.4% black, and 5.7% Hispanic; a minority (38.1%) selfidentified as men who have sex with men (MSM); and only 3 (2.4%) used injection drugs. Twenty-one (16.7%) had any IAS “major” protease inhibitor (PI), nucleos(t)ide RT inhibitor (NRTI), or non-nucleoside RT inhibitor (NNRTI) mutation; 20 (15.9%) had any SDRM mutation. With SDRM classifications applied, non-significant increasing trends were apparent for overall TDR (P=0.37) and NNRTIs in particular (P=0.21). NNRTI mutations were the most prevalent (7.9%, SDRM; 9.5%, IAS). Only four subjects (3.2%) had thymidine analogue mutations (TAMs). The most frequent single-codon changes conferring resistance were K103N (n=8, 6.4%) and L90M (n=3, 2.4%). Two subjects had two-class drug resistance (1.6%); none had triple-class resistance. Sixteen had intermediate- to-high level TDR predicted for any class (12.7%). Univariate analyses of age, race, or MSM were not predictive of TDR, but female gender was (SDRM OR=3.42, 95%CI 1.16–10.06; IAS OR=4.21, 95%CI 1.47–12.11). Patients with acute retroviral symptoms seemed more likely to have TDR than asymptomatic patients (SDRM OR=3.74, 95%CI 0.47–30.07; IAS OR=4.00, 95%CI 0.50–32.08).
CONCLUSIONS: TDR among acutely HIV-infected patients in North Carolina’s largely rural, heterosexual epidemic is similar to estimates from US metropolitan areas with different demographics. These findings have implications for initial regimen selection and secondary prevention efforts in non-urban HIV epicenters.
2007-06-12
48
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