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The presence of hepatitis C virus (HCV) RNA in semen among two of six (33%) HIV negative and six of 15 (40%) HIV infected males, reported recently suggests that HIV may facilitate genital shedding and subsequent sexual transmission of HCV.1 We determined HCV prevalence and examined evidence for its sexual transmission in a cohort of STD patients with observed HIV prevalence of 21.2%.
Consecutive serum samples (n=9141) collected between January 1994 and December 1999 were batched, pooled, and tested for anti-HCV antibody (Ortho HCV 3.0, Ortho-clinical Diagnostic, Germany). As previously described,2 25 μl aliquots of five samples were pooled and 20 μl of each pool was screened. Samples from positive pools were then tested individually. Positive sera were tested by HCV RNA polymerase chain reaction (PCR) using standard primers.3 HIV antibody status of each sample was ascertained using the algorithm described previously.4 Data were analysed using statistical package SPSS version 10.0. This study was a part of a prospective cohort study that was approved by ethics committee/institutional review boards of the collaborating organisations and blood samples were collected after counselling and informed consent.
Overall prevalence of anti-HCV antibodies was 0.68 % (62/9141, 95% CI 0.52 to 0.87). The prevalence among HIV infected individuals (1.5%, 95% CI 1.0 to 2.1) was higher (p=<0.01) than that in those not infected (0.44 %, 95% CI 0.3 to 0.6). The annual anti-HCV antibody prevalence rate between 1994 and 1999 was 0.57%, 0.46%, 1.10%, 0.81%, 0.37%, and 0.61%, which did not change significantly over time (table 1). Of the 55 anti-HCV antibody positive sera tested, 27 (49%) were HCV RNA PCR positive.
Univariate analysis revealed that history of past or current STD was not associated with HCV, whereas female sex (OR=2.07, 95% CI 1.17 to 3.66), prevalent HIV infection (OR=3.38, 95% CI 2.05 to 5.58), history of tattoo (OR=2.18, 95% CI 1.31 to 3.63), and being a sex worker (OR=2.35, 95% CI 1.27 to 4.35) were significantly associated with presence of anti-HCV antibody. However, multivariate analysis revealed that prevalent HIV infection and tattooing increased the likelihood of presence of anti-HCV antibodies by 3.08-fold (AOR 3.08, 95% CI 1.86 to 5.11, p=<0.00) and 1.87-fold (AOR 1.87, 95% CI 1.12 to 3.13, p=0.017), respectively (table1).
A rapid spread and high HCV prevalence of 80% has been reported recently among a cohort of injecting drug users from Kolkata, India.5 In contrast, we observed a low and stable prevalence of anti-HCV antibody among STD clinic attendees over the past 6 years in an urban setting where HIV transmission was predominantly sexual. Given that a high HIV prevalence was reported among female sex workers (FSWs) in this population4 and about 70% of males attending STD clinic had visited FSWs in the past 3 months, stable HCV prevalence over 6 years suggests that HCV is not efficiently transmitted sexually. Additionally, no association was found between past or current STD and HCV prevalence, and a high prevalence and incidence of HBV, a known sexually transmitted infection, has been reported in this population.6 Our analysis failed to identify any evidence that could support sexual transmission of HCV.