Low Prevalence of Antiretroviral Resistance Among HIV Type 1-Positive Prisoners in the Southeast United States

Abstract

Drug-resistant HIV complicates management of HIV infection. Although an estimated 14% of all HIV-positive persons pass through a prison or jail in the United States each year, little is known about the overall prevalence of antiretroviral (ARV) resistance in incarcerated persons. All genotypic sequence data on HIV-positive prisoners in the North Carolina (NC) Department of Corrections (DOC) were obtained from LabCorp. Screening for major resistance mutations in protease (PI) and reverse transcriptase (NRTI and NNRTI) was done using Genosure and the Stanford HIV Database. For subjects with multiple genotype reports, each mutation was counted only once and considered present on all subsequent genotypes. Between October 2006 and February 2010, the NC DOC incarcerated 1,911 HIV(+) individuals of whom 19.2% (n=367) had at least one genotype performed. The overall prevalence of a major resistance mutation was 28.3% (95% CI 23.7, 33.0). Among prisoners ever exposed to an ARV during incarceration (n=329) prevalence of a major resistance mutation was 29.8% (95% CI 24.9, 34.7); resistance by class was 20.4% (95% CI 16.0, 24.7) for NRTIs, 19.8% (95% CI 15.5, 24.1) for NNRTIs, and 8.8% (95% CI 5.8,11.9) for PIs. Single class drug resistance was most prevalent at 14.2% (10.2,17.7) followed by dual 12.5% (I8.9,16.0) and triple class 3.3% (1.4,5.3) resistance. The three most prevalent mutations were K103N 15.8% (12.0, 20.2), M184V 14.3% (10.7,18.5), and M41L 4.9% (2.8,7.8). In the NC DOC ARV resistance prevalence, dual and triple class drug resistance was moderate over the study period. Resistance to PIs was lower than NNRTIs and NRTIs, likely reflecting higher usage of these two classes or a lower barrier to resistance.

Incarceration of People Living with HIV/AIDS: Implications for Treatment-as-Prevention

“…A large observational study of testing and linkage to care in 10 cities in the United States demonstrated improved HIV treatment outcomes at six-months post release [87]. Evidence on viral resistance to antiretrovirals among incarcerated populations was mixed [100,101], however incarceration was associated with elevated VL and associated risk factors among illicit drug users in Vancouver, Canada [99]. …”

“…A molecular phylogeny inferred from the analysis of viral RNA sequences from 40 individuals did not find any evidence of between-prisoner transmission; however, analysis of sequences from the pol gene evidenced high rates of HIV primary and secondary resistance [100]. In contrast, a survey of 367 viral sequences from individuals incarcerated in the state prison system of North Carolina found moderate levels of drug resistance, comparable to non-incarcerated populations [101]. …”

Prevalence of Pretreatment and Acquired HIV-1 Mutations Associated with Resistance to Lamivudine or Rilpivirine: A Systematic Review

“…In North America, data were available for pretreatment DRMs from 19,563 individuals with HIV (Supplemental Tables 18 and 19 in Additional file 1) [52,[86][87][88][89][90][91][92][93][94][95][96][97][98][99]; 6% (n=1,062/17,951) and 8% (n=1,413/17,951) had mutations resistant to the NRTI and NNRTI classes, respectively. The most frequent pretreatment 3TC/FTC DRMs were at position M184 (1%; n=216/15,401); the most frequent pretreatment RPV DRMs were at positions E138 (2%; n=5/317) and V179 (1%; n=43/6,380).…”

Current Assays for HIV-1 Diagnostics and Antiretroviral Therapy Monitoring: Challenges and Possibilities

“…The Trugene ® HIV-1 Genotyping Kit (Siemens Healthcare Diagnostics, USA) and the ViroSeq™ HIV-1 Genotyping System (Celera Diagnostics, USA) are both CE-IVD-marked in Europe and approved by the FDA in the USA [61,62]. Many other commercial genotyping assays, such as GenoSure ® MG (Monogram, future science group USA), and less-expensive in-house genotyping assays have also been well evaluated worldwide [63][64][65][66]. The major limitation of both widely validated kits is that they were designed based on the HIV-1 subtype B viral genome, and their performance on HIV-2 or other HIV-1 genotypes remains uncertain.…”