CROI 2016 Abstract eBook

Abstract Listing

Poster Abstracts

546 Prevalence and Factors of HCV Infection Among HIV-Negative and HIV-Positive MSM Nathan J. Lachowsky 1 ; Kristine Stephenson 2 ; Zishan Cui 3 ; Susan Shurgold 3 ;Troy Grennan 4 ; JasonWong 4 ; Julio Montaner 3 ; Eric A. Roth 5 ; Robert S. Hogg 6 ; David M. Moore 1 ; for the Momentum Health Study 1 Univ of British Columbia, Vancouver, BC, Canada; 2 Vancouver Coastal Hlth, Vancouver, BC, Canada; 3 BC Cntr for Excellence in HIV/AIDS, Vancouver, BC, Canada; 4 BC Cntr for Disease Control, Vancouver, BC, Canada; 5 Univ of Victoria, Victoria, BC, Canada; 6 Simon Fraser Univ, Burnaby, BC, Canada Background: Given recent treatment advances for and HIV-related implications of hepatitis C virus (HCV) infection, we sought to identify factors associated with past/current and incident HCV infection within a prospective cohort of gay, bisexual, and other men who have sex with men (MSM) in Metro Vancouver, Canada. Methods: Eligible participants were recruited from 2012-2015 using respondent-driven sampling, were aged ≥16 years of age and reported recent sex with another man. Participants completed study visits every 6 months that included a computer-assisted self-interview on demographics, sexual and substance use behaviors, and a nurse- administered clinical questionnaire. A rapid HIV test was administered and a venous blood sample was taken for HCV-antibody serology. We used logistic regression and generalized estimating equations to identify factors associated with prevalent HCV antibodies at enrolment and incident HCV infection at follow-up, respectively. Relative risks (RR) and 95% confidence intervals (CI) are shown. RDS-adjusted population parameters are provided for baseline data. Results: Of 774 participants, 2.0% (15/551) of HIV-negative and 28.3% (50/223) of HIV-positive MSM were HCV seropositive at enrollment. Of these, 56/65 (86.2%) were aware of their diagnosis, but only 5 HIV-negative and 17 HIV-positive MSM reported prior HCV treatment, with only 2 and 7 of those reporting treatment success. Factors associated with HCV seropositive at enrolment, stratified by HIV status are shown in Table 1. Of 534 participants with follow-up data, we observed 5 HCV-seroconversions for a calculated incidence rate of 0.50 per 100 person-years (95% CI: 0.21-1.21). All incident HCV infections were among single, HIV-positive, gay-identified MSM who did not work as escorts and had never been treated for HCV. Incident HCV infections were associated with older age (RR=1.06, 95% CI: 1.01-1.12), recent crystal methamphetamine use (RR=10.62, 95% CI: 1.77-63.64), and a greater number of recent anal sex partners (RR=1.01, 95% CI: 1.01-1.02). Notably, only 1 of 5 with HCV seroincidence reported recent injection drug use, and as such was not associated with HCV seroincidence (RR=3.01, 95% CI: 0.35–26.15, p=0.32). Conclusions: New cases of HCV infection indicate a potential shift to sexual transmission among HIV-positive gay men based on the lack of association with recent injecting behavior. Crystal methamphetamine use remains a strong factor associated with HCV seropositivity and predictor of new infection.

Poster Abstracts

547

The Impact of Host Genes on the Risk of Acquiring Hepatitis C Virus Infection Gaby S. Steba 1 ; Sylvie M. Koekkoek 1 ; JoostW.Vanhommerig 2 ; Kees Brinkman 3 ; JanT. van der Meer 4 ; Maria Prins 2 ;William A. Paxton 5 ; Richard Molenkamp 1 ; Janke Schinkel 1 ; for the MOSAIC Study Group and ACS 1 Academic Med Cntr, Amsterdam, Netherlands; 2 PH Service of Amsterdam, Amsterdam, Netherlands; 3 OLVG Hosp, Amsterdam, Netherlands; 4 Cntr of Infectious Diseases and Immunology Amsterdam, Academic Med Cntr, Amsterdam, Netherlands; 5 Univ of Liverpool, Liverpool, UK Background: Injecting drug use (IDU), receiving unscreened blood (-products) as well as high risk sexual behavior amongst HIV-1 infected men having sex with men (MSM) are major risk factors for acquiring HCV. Approximately 10-20% of HCV multiple exposed individuals remain uninfected (MEU), whilst the remainder become infected (MEI). We hypothesize that host factors play a role in HCV susceptibility. Aim of our study was to identify polymorphisms in host genes and their promoters that encode for proteins that modulate virus entry into cells; CD81, Scavenger receptor 1, low-density lipoprotein receptor, Claudin-1, Occludin and Niemann-Pick C1–like 1 (NPC1L1). In addition, we studied two genes that are thought to be involved in HCV transmission, the dendritic cell specific ICAM-grabbing non-integrin (DC-SIGN) and DC-SIGN related (DC-SIGNR), since they have been reported to capture and transfer HCV to hepatocytes. Methods: HCV exposed Individuals from two observational cohorts were selected. From the MSM observational study of acute infection with HCV (MOSAIC) 30 HIV-1 infected MEU cases and 32 HIV-1 infected MEI controls were selected based on reported high risk sexual risk behavior. From the Amsterdam Cohorts Studies (ACS) IDU cohort, 40 MEU cases and 22 MEI controls were selected who injected drugs for ≥2 years. 65 SNPs in the selected genes were determined by sequencing or SNP assays. Results: In the MSM cohort, we observed an association of three DC-SIGN promoter SNPs with HCV infection; rs2287886 GG, rs735240 AA and rs735239 GG are the protective genotypes (OR: 0.35 95% CI= 0.12 to 0.97, OR: 0.23 95% CI= 0.07 to 0.69 and OR: 0.23 95% CI= 0.06 to 0.85, respectively). No associations were found within the IDU cohort. Additionally, we found three SNPs in NPC1L1 to be associated with HCV susceptibility. When combining the MSM and IDU cohorts, rs217434 TT, rs2072183 CC and rs41279633 CC appeared as protective genotypes (OR: 0.38 95% CI=0.17-0.83, OR: 0.31 95% CI= 0.14-0.68, OR: 0.43 95% CI= 0.19-0.99, respectively). This association was maintained when the cohorts were analyzed separately. Conclusions: Our results support the hypothesis that DC-SIGN plays a role in HCV acquisition and indicates for the first time that this may relate to infection via sexual but not IDU exposure. Additionally, our results identify that variations within the NPC1L1 gene associate with HCV susceptibility, independent of the transmission route.

215

CROI 2016