Theme: Epidemiology & Public Health Research Year: 2018
Opioid agonist therapy (OAT) has been shown to reduce hepatitis C virus (HCV) incidence by
50% among people who inject drugs (PWID). Recent research suggests that the protective
effects of OAT may be attenuated in females compared to males. This study aimed to assess
differences in HCV incidence by sex among PWID engaged in OAT and to identify factors
independently associated with decreased efficacy.
Inc3 pooled biological and behavioural data from 10 prospective observational studies
examining incident HIV and HCV infections in high-risk cohorts. This study synthesised data
from seven of the ten cohorts. Cox proportional hazards regression models with random
effects for handling clustered survival data were used to identify predictors of incident HCV
infection. Entry in each study to the estimated date of HCV infection was used to calculate
person-year observation (PYO) and adjusted hazard ratios (aHRs) among participants who
reported recent (last 12 months) OAT (methadone, buprenorphine or buprenorphinenaloxone).
701 participants reported engagement in OAT (observed over 3,003 visits). HCV incidence
(per 100 PYO) among females engaged in OAT was 16.5 PYO (95% CI 13.1-20.7), and 7.6
PYO (95% CI 6.0-9.5) among males. The female to male aHR was 1.77 (95% CI 1.45-2.17,
p<0.001). Factors associated with decreased efficacy of OAT among females included nonwhite race (aHR 1.72, 95% CI 1.21-2.44, p=0.002), recent unstable housing (aHR 3.04, 95% CI 1.98-4.67, p<0.001) and injecting daily or more frequently (aHR 2.10, 95% CI 1.15-3.83, p=0.016). Conclusion: Among respondents engaged in OAT, HCV incidence among females was twice that compared to males. Independent associations with attenuated effect included bio-social (nonwhite race), structural (unstable housing), and behavioural (frequent injecting) factors. Structural and behavioural interventions that target women are needed to bolster the efficacy of OAT in females in order to prevent HCV transmission. Disclosure of Interest Statement: InC3 was funded by the National Institute on Drug Abuse (NIDA) R01DA031056. JB, MH, PD, GD and JG have received funding from Gilead Sciences Inc. and/or AbbVie and/or BristolMyers Squibb and/or Cepheid and/or Merck/MSD for work on HCV treatment unrelated to this study. PD has received funding from Indivior for work unrelated to this study. Authors (LG, AE, JI, JT, NS, MP, MDM, AL, LM and KP) have no commercial or other associations that might pose a conflict of interest. LG is supported through an Australian Government Research Training Program Scholarship. JI, PD, MH, AL, GD, JG and LM are supported by Australian National Health and Medical Research Council (NH&MRC) Fellowships. KP is supported by 3R01DA016017, 1ULTR001449 and U54GM104944.