Hepatitis C virus (HCV) is only detectable in the semen of a minority of HIV-positive gay men co-infected with both viruses, and even then at very low levels, a small study presented at the second joint BHIVA/BASHH Conference has found. Seminal HCV viral load, it discovered, is no higher in men recently infected than in men with chronic infection.
This study adds to the weight of evidence that transmission of HCV during sex is via blood, not via semen. Behavioural research had already suggested this was the case – see Blood rather than semen mode of HCV transmission in HIV-positive gay men – and leaves researchers looking for a explanation as to why HIV-positive men are approximately 50 times more likely to acquire HCV than HIV-negative men.
Dr Joanne Turner from Mortimer Market Clinic in London told the conference that other studies had shown that between 10 and 40% of men with HCV have detectable virus in their semen and that HIV-positive gay men are more likely to have detectable seminal virus than HIV-negative men.
However no study had previously investigated whether HCV seminal viral load was higher in acutely infected men. The hypothesis was that high HCV viral loads in the semen of recently infected men, coupled with behavioural factors, led to the rapidly developing clusters of infections in HIV-positive men that have been seen in urban communities from New York to Sydney.
The study recruited men from the HCV cohort at Mortimer Market who had been diagnosed less than six months after initial infection. Paired samples of blood and semen were collected from HIV-positive men presenting with acute HCV at baseline, one month and six months. These were then compared with samples from men with chronic untreated HCV infection.
A sensitive viral load assay was used capable of detecting HCV down to ten international units per millilitre (IU/ml) and the assay was initially tested with semen ‘spiked’ with HCV.
This is a small pilot study with only ten acute cases and ten chronic controls. HIV-negative men were eligible to join the study, but with HCV infection being so much rarer in negative men, none have been recruited so far.
Detectable viral load in fact turned out to be non-significantly more common in the chronic controls. Two out of ten had a detectable viral load at baseline (37 and 230 IUs/ml). None of the acutely infected men did, though one developed a very low viral load (14 IUs/ml) at one month.
At six months two acutely infected men had had a detectable viral load at some point in the study compared with four chronically infected men, but all very low, with no measurement over 230 IUs/ml compared with figures in the millions for blood viral load. In addition, no correlation was seen in this study between seminal and blood viral loads.
Dr Turner said that the recruitment method meant that the peak of seminal and blood viraemia might have been missed in the acutely infected men, but said that the results mean that “The increased transmission of acute HCV in HIV-positive men remains unexplained”.
Turner J et al. Hepatitis C viral load in semen of HIV-positive men during acute and chronic hepatitis infection. Second joint BHIVA/BASHH Conference, Manchester. Abstract O5. 2010.