Kaposi’s sarcoma (KS), caused by KS-associated herpesvirus (KSHV), is the most common cancer among HIV-infected patients in Malawi and in the United States today. In Malawi, KSHV is endemic. We conducted a cross-sectional study of patients with HIV infection and KS with no history of chemo- or antiretroviral therapy (ART). Seventy patients were enrolled. Eighty-one percent had T1 (advanced) KS. Median CD4 and HIV RNA levels were 181 cells/mm3 and 138,641 copies/ml, respectively. We had complete information and suitable plasma and biopsy samples for 66 patients. For 59/66 (89%) patients, a detectable KSHV load was found in plasma (median, 2,291 copies/ml; interquartile range [IQR], 741 to 5,623). We utilized a novel KSHV real-time quantitative PCR (qPCR) array with multiple primers per open reading frame to examine KSHV transcription. Seventeen samples exhibited only minimal levels of KSHV mRNAs, presumably due to the limited number of infected cells. For all other biopsy samples, the viral latency locus (LANA, vCyc, vFLIP, kaposin, and microRNAs [miRNAs]) was transcribed abundantly, as was K15 mRNA. We could identify two subtypes of treatment-naive KS: lesions that transcribed viral RNAs across the length of the viral genome and lesions that displayed only limited transcription restricted to the latency locus. This finding demonstrates for the first time the existence of multiple subtypes of KS lesions in HIV- and KS-treatment naive patients.

Female sex workers (FSWs) have a notably high risk of acquiring human papillomavirus (HPV) infections. Relatively few studies address the type-specific prevalence and incidence of HPV among FSWs in sub-Saharan Africa. FSWs (n = 348) attending the Korogocho clinic in Nairobi, Kenya participated from August 2009 to March 2011. HPV DNA was detected using the SPF10-LiPA25 PCR assay. Baseline prevalence of HPV infection and cervical dysplasia were calculated, stratified by HIV-serostatus. Incidence rate (IR) of infection was calculated as number of new infections from baseline over person-months among 160 HPV-negative participants with complete 12-month follow-up. Baseline HPV prevalence was 23.6% for any HPV and 20.4% for high-risk HPV (hrHPV) types. Most prevalent types were HPV52 (10.1%), HPV35 (2.3%), and HPV51 (2.3%). A quarter (24%) of participants were HIV-positive. HPV prevalence was higher in HIV-positive (32.1%) than HIV-negative (20.8%) participants. hrHPV prevalence was higher in HIV-positive (27.4%) than HIV-negative (18.2%) women. During follow-up, HPV IR was 31.4 (95% CI: 23.8–41.5) for any HPV and 24.2 (95% CI: 17.9–32.8) for hrHPV types. HPV52 had the highest IR (6.0; 95% CI: 6.5–10.3). Overall HPV and hrHPV prevalence were lower than expected, but both prevalence and incidence were higher in HIV-positive than in HIV-negative women.

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