Sexual transmission and response to treatment in acute HCV infection in HIV-positive gay men coinfected with HIV

15 June 2005. Related: Conference reports, Hepatitis coinfection, BHIVA/BASHH 1st Dublin 2005.

Simon Collins, HIV i-Base

Several presentations previous meetings have documented a significant number of sexual transmission of HCV to HIV-positive gay men. In an oral presentation at this years meeting, Danta and colleagues from HIV and Acute HCV group characterised HCV transmission in 90 gay men seen at the Royal Free Hospital, Chelsea and Westminster Hospital or Brighton Hospital. Transmission factors were accessed by questionnaire, and compared in a case control study to mono-infected patients, matched by age, duration of infection and duration of HAART. [1]

Phylogenetic analysis indicated that multiple independent lineages were circulating, with the largest single clade including 21 patients.

Group sex was practiced by 87% cases vs 52% controls, and recreational drug use during sex occurred in 100% cases vs 64% of controls (p=0.01 and p<0.003 respectively).

As with previous reports, unprotected anal receptive and insertive anal intercourse, fisting, and use of sex toys were statistically associated with HCV transmission (all p< 0.001).

Two presentations at the meeting detailed the response to PEG IFN plus RBV in coinfeced patients treated in acute HCV infection.

Gilleece and colleagues presented results from 50 HIV-positive gay men (mean age 37) diagnosed with acute HCV at the Chelsea and Westminster Hospital, London. [2]

Patients with detectable HCV RNA at 12 weeks after their HCV diagnosis were offered PEG interferon (PEG IFN) plus weight-adjusted ribavirin (RBV); patients with rising HCV RNA were offered treatment earlier. The majority of HCV infections (44/50) were identified through abnormal ALT, with four men tested after exposure to know HCV-positive partner, and two men were diagnosed with HIV and HCV at the same time.

The significant factors associated with spontaneous clearance of HCV in almost one quarter of the men (12/50) included high baseline CD4 count, CD4 count > 500 cells/mm3 and lower HCV RHA. However, only 59% of the men who accepted HCV treatment (16/27) had a sustained virological response six months after the end of treatment. Usually, genotype was not a predictive factor in treatment outcome.

Hopkins and colleagues presented results from a mixed group of 59 HIV/HCV coinfected patients treated during chronic HCV infection at either the Royal Free Hospital or the Mortimer Market Clinic. [3]

Median age was 40 years and 70% were on ARV treatment. 32% were IDU, 39% MSM, 14% women. 44% were genotype 2 or 3. Median baseline and nadir CD4 count was 468 and 220 cells/mm3 respectively.

SVR rates were 24% with genotype 1 or 4 and 65% with genotype 2 or 3. In this study genotype clearly related to treatment response (p=0.008).

Given that HAART is often started prior to HCV treatment to boost CD4 count when HCV in treated in chronic infection, it was surprising to see that nadir CD4 count in this study also predicted response (p=0.04). Age, sex or duration of HCV therapy did not predict response. There was a 19% discontinuation rate in the study.

Comment

Most reports of sexual transmitted HCV are in men who already ‘sero-sort’ – ie men who chose partners who are also HIV-positive. This is a long established and valid choice for these men not to use condoms.

However, the mechanism for HCV transmission is unclear. Whether the key factor is exposure to blood or to semen, and the degree to which HIV-infection increases susceptibility to HCV needs further research. HIV-positive men have higher rates of HCV RNA in acute HCV infection, and this factor would also increase infection risk for other HIV-positive men. As a blood-born virus, HCV infection can be tranmitted indirectly from a source partner, without necessarily infecting the active partner, on to a third partner.

HCV has not been reported as a sexually transmitted virus in HIV-negative men. Although HIV-negative men attending sexual health clinics are not routinely screened for HCV, data from anonymous sample testing has indicated the rate of HCV in MSM that are not injecting drug users is approximately 1%. [3]

The optimum time to treat HCV is still not defined in this patient group. Higher age is a significant risk factor for faster HCV progression in co-infected individuals, and this should be considered. The results from the C+W study showed a higher rate of spontaneous HCV clearance and lower SVR compared to historical data in HIV negative individuals.

The last issue of HTB (May 2005) included a case report of sexual reinfection with a second HCV infection in a gay man receiving PEG INF plus RBV. A heightened awareness of HCV transmission in HIV-positive men clearly requires informed health information and new prevention messages.

‘Sero-sorting’ HIV-positive gay men are unlikely to be helped by the same prevention messages that have held little relevance since their HIV diagnosis. This is complicated by the lack of any clear data to explain HCV sexual transmission risks, if activities associated with the higher risk of mucosal trauma (fisting), shared sex toys, and sex parties are all avoided.

References:

1. Danta M, Brown D, Pybus O et al. Evidence for sexual transmission of HCV in recent epidemic in HIV-infected men in South-East England. 11th Annual BHIVA Conference, 20-23 April 2005, Dublin. Oral abstract O25.
2. Browne RE, Gilleece YC, Asboe D et al. Is the treatment of acute hepatitis C in HIV-positive individuals effective? 11th Annual BHIVA Conference, 20-23 April 2005, Dublin. Oral abstract O26.
3. Hopkins S, Turner J, Mahungu T et al. Does nadir CD4 count in HIV-HCV co-infected patients predict HCV treatment response to pegylated interferon and ribavirin. 11th Annual BHIVA Conference, 20-23 April 2005, Dublin. Oral abstract O27.
4. Balogun MA, Ramsay ME, Parry JV et al. A national survey of genitourinary medicine clinic attenders provides little evidence of sexual transmission of hepatitis C virus infection. Sex Transm Infect 2003;79:301–306.