Theme: Clinical Research Year: 2022
Background
Historically, hepatitis C virus (HCV) was difficult to treat among people with HIV, however treatment
with direct-acting antivirals (DAA) results in 90-95% of people being cured. There is a need to further
understand why 5-10% are not successfully cured in order to ensure no one is left behind in HCV
elimination efforts.
Methods
Data included people from Australia, Canada, France, the Netherlands, Spain, and Switzerland.
People who had interferon-free DAA HCV treatment data recorded between 2014 and 2019 and ≥
one HCV RNA test 12 or more weeks after end of treatment (EOT) were included in analyses. We
used mixed-effects logistic regression to examine factors associated with unsuccessful treatment,
defined as a positive RNA test at their first test 12+ weeks after EOT. Factors included in univariable
analyses were key population group, years since HIV diagnosis, HIV viral load, CD4 cell count, HCV
genotype, cirrhosis, and previous interferon-based HCV treatment. Factors significant at 90% in
univariable analyses, and age, were included in multivariable analyses.
Results
Overall, 4554 people had DAA treatment data; the majority were gay or bisexual males (46%) or had
a history of injection drug use (37%). Of these people, 4509 (99%) had HCV RNA test data recorded,
and 3844 (85%) had a test 12+ weeks following EOT, ranging from 83% to 86% across population
groups. Unsuccessful treatment was 5.5% (212/3844) overall, ranging from 4% to 8% across
population groups (Figure 1). Adjusted for age and population group, a CD4 cell count between 200-
350 cells/mm3 was the only factor associated with unsuccessful treatment (aOR 1.78, 95%CI 1.20-
2.63) compared to a CD4 cell count >350 cell/mm3
.
Conclusion
We found that 5.5% of people with an SVR12+ test were unsuccessfully treated with minimal
difference across key populations. Extra support through HCV treatment may be warranted among
people with markers of sub-optimal HIV treatment.
Disclosures
DKvS reports payment to their institution (Public Health Service of Amsterdam) for Liver Debate,
sponsored by Gilead, AbbVie, and Norgine. GM has received grants from Gilead Sciences and AbbVie
paid to their institute. MK has received research support and consulting fees from ViiV, AbbVie, and
Gilead Sciences. KL has received funding grants from Gilead, MSD, Abbie, Viiv Healthcare and
Janssen; has been on advisory boards for Gilead, MSD, Abbvie, ViiV Healthcare and Janssen; and
taken part in training and educational activities for Gilead, MSD, Abbvie, ViiV Healthcare and
Janssen. MvdV has received unrestricted research grants and consultancy fees from AbbVie, Gilead,
Johnson & Johnson, Merck Sharpe & Dohme, and ViiV Health Care which have been paid to their
institute. MP has received speaker fees and grants from Gilead Sciences, Merck Sharpe & Dohme,
and AbbVie paid to their institute. IJ reports honoraria for advice or public speaking from Gilead and
ViiV Healthcare. AR reports support to their institution for advisory boards and/or travel grants from
MSD, Gilead Sciences, Pfizer, and AbbVie, and an investigator-initiated trial grant from Gilead
Sciences. ME has received investigator-initiated funding from Gilead Sciences, Merck, AbbVie, and
BMS. JD has received investigator-initiated funding from AbbVie, BMS, Gilead Sciences, and Merck;
consultancies from Gilead Sciences and AbbVie; and support for attending meetings and/or travel
from Gilead Sciences. Other authors have no disclosures to declare.