Hepatitis C virus is found significantly more frequently in the semen of men who are coinfected with HIV than in the semen of men who are only infected with hepatitis C (HCV), according to research published in the November 4th edition of AIDS. Sexual transmission of hepatitis C virus has recently been observed in HIV-positive gay men and the investigators write, “our results partly illustrate how the recent increase in sexually transmitted hepatitis C virus in homosexual men could arise.”
The investigators also found that hepatitis C virus in semen originated in the blood with no evidence of hepatitis C replication in the genitals.
Sexual transmission of hepatitis C is a controversial subject. There is little evidence of transmission of the virus between heterosexual couples and large studies involving HIV-negative gay men have failed to find any evidence of sexual transmission of hepatitis C. In recent years there have been a number of studies reporting sexual transmission of hepatitis C amongst HIV-positive gay men, with evidence from the UK, Switzerland and France suggesting that unprotected anal sex, concurrent sexually transmitted infections, and “hard” sex which may involve trauma are risk factors.
To further understand the sexual transmission of hepatitis C, French investigators compared the prevalence of hepatitis C virus in the semen of men who were coinfected with HIV and hepatitis C virus and men who were infected only with hepatitis C. They also wished to see if hepatitis C was reproducing in the genital tract of men.
A total of 120 men with hepatitis C were included in the investigators’ analysis. In addition to being infected with hepatitis C, 82 of the men were also HIV-positive.
Paired blood and semen samples were obtained from each of the men. Repeat semen samples were obtained from 45 men (35 of whom were coinfected). The blood and semen samples were tested for hepatitis C viral load.
None of the men were receiving anti-hepatitis C treatment. The HIV-positive individuals had a median CD4 cell count of 524 cells and a median viral load of below 50 copies/ml. All but seven HIV-positive patients were taking antiretroviral therapy.
A total of 191 semen samples were tested for hepatitis C and overall 27% were positive. In all, 32% of men provided at least one semen sample which was positive for hepatitis C.
Hepatitis C was detected with significantly greater frequency in the semen of HIV-positive men (38%) than HIV-negative men (18%, p = 0.033).
Amongst the HIV-positive men, neither CD4 cell count nor viral load were significantly associated with having detectable hepatitis C in semen.
Blood samples tested positive for hepatitis C in all 120 men. The investigators found that men who had detectable hepatitis C in their semen had hepatitis C viral loads in their blood. This difference was statistically significant for coinfected men (median 6.22 log10IU/ml versus 5.95 log10IU/ml, p = 0.038).
Samples of blood and semen were further studies in two men (one HIV-positive and one HIV-negative) to see if there was any evidence of hepatitis C reproduction in the genitals. No evidence was found of hepatitis C replication in the genitals with hepatitis C in semen being genetically similar to hepatitis C in the blood.
“In this study, hepatitis C virus RNA was more frequently found in the semen of HIV/hepatitis C virus coinfected men than in the semen of non-coinfected men”, write the investigators. They note that even in men who had hepatitis C in their semen, detection of the virus was intermittent and “close to the detection threshold.”
The investigators also observe that hepatitis C viral load was higher in the blood of coinfected men than in HIV-negative men (p = 0.017) and they believe that “this may partly explain why the coinfected men had a higher prevalence of hepatitis C in their semen.”
Rather than reproducing in the genitals, the investigators believe that hepatitis C was “transferring” between blood and semen.
Briat A et al. Hepatitis C virus in the semen of men coinfected with HIV-1: prevalence and origin. AIDS 19: 1827 – 1853, 2005.