Predictors of Retention among Men Attending STI Clinics in HIV Prevention Programs and Research: A Case Control Study in Pune, India

Retention is critical in HIV prevention programs and clinical research. We studied retention in the three modeled scenarios of primary prevention programs, cohort studies and clinical trials to identify predictors of retention.Men attending Sexually Transmitted Infection (STI) clinics (n = 10, 801) were followed in a cohort study spanning over a ten year period (1993-2002) in Pune, India. Using pre-set definitions, cases with optimal retention in prevention program (n = 1286), cohort study (n = 940) and clinical trial (n = 896) were identified from this cohort. Equal number of controls matched for age and period of enrollment were selected. A case control analysis using conditional logistic regression was performed. Being employed was a predictor of lower retention in all the three modeled scenarios. Presence of genital ulcer disease (GUD), history of commercial sex work and living away from the family were predictors of lower retention in primary prevention, cohort study and clinical trial models respectively. Alcohol consumption predicted lower retention in cohort study and clinical trial models. Married monogamous men were less likely to be retained in the primary prevention and cohort study models.Predicting potential drop-outs among the beneficiaries or research participants at entry point in the prevention programs and research respectively is possible. Suitable interventions might help in optimizing retention. Customized counseling to prepare the clients properly may help in their retention

Evaluation of a Cost Effective In-House Method for HIV-1 Drug Resistance Genotyping Using Plasma Samples

<div><p>Objectives</p><p>Validation of a cost effective in-house method for HIV-1 drug resistance genotyping using plasma samples.</p><p>Design</p><p>The validation includes the establishment of analytical performance characteristics such as accuracy, reproducibility, precision and sensitivity.</p><p>Methods</p><p>The accuracy was assessed by comparing 26 paired Virological Quality Assessment (VQA) proficiency testing panel sequences generated by in-house and ViroSeq Genotyping System 2.0 (Celera Diagnostics, US) as a gold standard. The reproducibility and precision were carried out on five samples with five replicates representing multiple HIV-1 subtypes (A, B, C) and resistance patterns. The amplification sensitivity was evaluated on HIV-1 positive plasma samples (n = 88) with known viral loads ranges from 1000–1.8 million RNA copies/ml.</p><p>Results</p><p>Comparison of the nucleotide sequences generated by ViroSeq and in-house method showed 99.41±0.46 and 99.68±0.35% mean nucleotide and amino acid identity respectively. Out of 135 Stanford HIVdb listed HIV-1 drug resistance mutations, partial discordance was observed at 15 positions and complete discordance was absent. The reproducibility and precision study showed high nucleotide sequence identities i.e. 99.88±0.10 and 99.82±0.20 respectively. The in-house method showed 100% analytical sensitivity on the samples with HIV-1 viral load >1000 RNA copies/ml. The cost of running the in-house method is only 50% of that for ViroSeq method (112$vs 300$), thus making it cost effective.</p><p>Conclusions</p><p>The validated cost effective in-house method may be used to collect surveillance data on the emergence and transmission of HIV-1 drug resistance in resource limited countries. Moreover, the wide applications of a cost effective and validated in-house method for HIV-1 drug resistance testing will facilitate the decision making for the appropriate management of HIV infected patients.</p></div

Pairwise sequence identity analysis between the in-house and the ViroSeq method.

<p>Pairwise sequence identity analysis between the in-house and the ViroSeq method.</p

Primers used in the In-house method for HIV-1 drug resistance genotyping.

<p>Primers used in the In-house method for HIV-1 drug resistance genotyping.</p

Phylogenetic analysis of the sequences generated during the evaluation of an in-house method.

<p>The phylogenetic tree was generated by using the PhyML software to create a maximum likelihood tree <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0087441#pone.0087441-Chaturbhuj1" target="_blank">[13]</a>. The reference sequences were obtained from the Los Alamos HIV Database (<a href="http://www.hiv.lanl.gov" target="_blank">www.hiv.lanl.gov</a>). IHDR- sequences generated by an in-house method; VSQ- sequences generated by the ViroSeq method; R1 to R5- sample used in the reproducibility study (hilighted in blue); P1 to P5- sample used in the precision study (hilighted in red); A, B, C, D, E are the replicates of the same sample.</p

Reproducibility and Precision of an in-house method.

<p>Reproducibility and Precision of an in-house method.</p

Drug resistance-associated amino acid positions in protease and reverse transcriptase from 26 proficiency testing panel plasma samples genotyped by the in-house and the ViroSeq methods.

<p>Note: Partial discordant positions are shown in bold.</p

HPV Genotype Distribution in Cervical Intraepithelial Neoplasia among HIV-Infected Women in Pune, India

<div><h3>Background</h3><p>The distribution of HPV genotypes, their association with rigorously confirmed cervical precancer endpoints, and factors associated with HPV infection have not been previously documented among HIV-infected women in India. We conducted an observational study to expand this evidence base in this population at high risk of cervical cancer.</p> <h3>Methods</h3><p>HIV-infected women (N = 278) in Pune, India underwent HPV genotyping by Linear Array assay. Cervical intraepithelial neoplasia (CIN) disease ascertainment was maximized by detailed assessment using cytology, colposcopy, and histopathology and a composite endpoint.</p> <h3>Results</h3><p>CIN2+ was detected in 11.2% while CIN3 was present in 4.7% participants. HPV genotypes were present in 52.5% (146/278) and ‘carcinogenic’ HPV genotypes were present in 35.3% (98/278) HIV-infected women. ‘Possibly carcinogenic’ and ‘non/unknown carcinogenic’ HPV genotypes were present in 14.7% and 29.5% participants respectively. Multiple (≥2) HPV genotypes were present in half (50.7%) of women with HPV, while multiple ‘carcinogenic’ HPV genotypes were present in just over a quarter (27.8%) of women with ‘carcinogenic’ HPV. HPV16 was the commonest genotype, present in 12% overall, as well as in 47% and 50% in CIN2+ and CIN3 lesions with a single carcinogenic HPV infection, respectively. The carcinogenic HPV genotypes in declining order of prevalence overall included HPV 16, 56, 18, 39, 35, 51, 31, 59, 33, 58, 68, 45 and 52. Factors independently associated with ‘carcinogenic’ HPV type detection were reporting ≥2 lifetime sexual partners and having lower CD4+ count. HPV16 detection was associated with lower CD4+ cell counts and currently receiving combination antiretroviral therapy.</p> <h3>Conclusion</h3><p>HPV16 was the most common HPV genotype, although a wide diversity and high multiplicity of HPV genotypes was observed. Type-specific attribution of carcinogenic HPV genotypes in CIN3 lesions in HIV-infected women, and etiologic significance of concurrently present non/unknown carcinogenic HPV genotypes await larger studies.</p> </div