Eliminating HIV/HCV co-infection in gay and bisexual men: is it achievable through scaling up treatment?

ABSTRACT

Introduction: Broad availability of direct-acting antiviral therapy for hepatitis C virus (HCV) raises the possibility that HCV prevalence and incidence can be reduced through scaling-up treatment, leading to the elimination of HCV. High rates of linkage to HIV care among HIV-infected gay and bisexual men may facilitate high uptake of HCV treatment, possibly making HCV elimination more achievable in this group.

Areas covered: This review covers HCV elimination in HIV-infected gay and bisexual men, including epidemiology, spontaneous clearance and long term sequelae in the absence of direct-acting antiviral therapy; direct-acting antiviral therapy uptake and effectiveness in this group; HCV reinfection following successful treatment; and areas for further research.

Expert commentary: Early data from the direct-acting antiviral era suggest that treatment uptake is increasing among HIV infected GBM, and SVR rates are very promising. However, in order to sustain current treatment rates, additional interventions at the behavioral, physician, and structural levels may be required to increase HCV diagnosis, including prompt detection of HCV reinfection. Timely consideration of these issues is required to maximize the population-level impact of HCV direct-acting antiviral therapy. Potential HCV transmissions from HIV-uninfected GBM, across international borders, and from those who are not GBM also warrant consideration.

KEYWORDS:

• Men who have sex with men
• HIV
• hepatitis C
• coinfection
• elimination

Declaration of interest

R Sacks-Davis receives fellowship support from the Australian National Health and Medical Research Council and acknowledges the Victorian Operational Research Infrastructure Support Program for their support to the Burnet Institute. A Pedrana receives funds from Merck to support investigator-initiated research and acknowledges the Victorian Operational Research Infrastructure Support Program for their support to the Burnet Institute. N Scott acknowledges the Victorian Operational Research Infrastructure Support Program for their support to the Burnet Institute. J Doyle receives fellowship support from the Australian National Health and Medical Research Council and funds from Gilead Sciences, Abbvie, Merck, and BMS to support investigator initiated research and acknowledges the Victorian Operational Research Infrastructure Support Program for their support to the Burnet Institute. M Hellard receives fellowship support from the Australian National Health and Medical Research Council and funds from Gilead Sciences, Abbvie, Merck, and BMS to support investigator-initiated research and acknowledges the Victorian Operational Research Infrastructure Support Program for their support to the Burnet Institute. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

The manuscript was not funded.