Key result
DAA therapy in HIV/HCV co-infection linked to ~13 mg/dL higher total cholesterol without altering ASCVD risk.
Why the study?
Does direct acting antiviral therapy initiation alter HbA1c, lipid levels, or ASCVD risk score at 12 months in people with HIV and HCV co-infection?
Cohort (n=3,418)
Yes
Does direct acting antiviral therapy initiation alter HbA1c, lipid levels, or ASCVD risk score at 12 months in people with HIV and HCV co-infection?
Answers are grounded in this paper and cite their sources.
In people with HIV and HCV co-infection, initiating direct-acting antiviral therapy is associated with increased total and LDL cholesterol at 12 months, though HbA1c and overall ASCVD risk scores remain unchanged compared to non-initiators.
Objectives Among people with HIV with hepatitis C virus (HCV) co‐infection, we examined differences in haemoglobin A1c (HbA1c), total cholesterol (TC), low‐density lipoprotein (LDL), high‐density lipoprotein (HDL) and atherosclerotic cardiovascular disease (ASCVD) risk score at 12‐months following direct acting antiviral (DAA) initiation, comparing people with HIV who initiated DAA with those who did not to explore the utility of DAAs beyond HCV elimination. Methods Utilizing a nested exposure‐matched study of people with HIV age 18 years, on antiretroviral therapy from the NA‐ACCORD and the Mass General Brigham HIV cohorts between 01/1/2014 and 12/31/2022, people with HIV with HCV co‐infection were identified by detectable plasma HCV RNA. People with HIV who initiated DAA were matched 1:1 with people with HIV who did not initiate DAA. Multivariable linear regression models estimated HbA1c ( N = 2374), TC ( N = 3418) and ASCVD risk score ( N = 488) at 12‐months comparing people with HIV who initiated DAAs versus did not. Results We identified no significant difference in the mean HbA1c at 12‐months comparing DAA initiators to DAA non‐initiators (β: 0.00%, 95% confidence interval [CI] −0.09% to 0.08%). The mean TC at 12‐months was 13 mg/dL (95% CI 11–16 mg/dL) higher in DAA initiators and largely due to increases in LDL. There was no significant difference in the mean ASCVD risk score at 12‐months when comparing DAA initiators with those who did not initiate DAAs (β: 1.10, 95% CI −0.09 to 2.20). Conclusion People with HIV with HCV who initiated DAA demonstrated no statistically significant difference in HbA1c or ASCVD risk score at 12‐months compared to HIV/HCV co‐infected persons who did no initiate DAA. However, TC and LDL levels increased 12 months following DAA treatment.
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Lang et al. (2026) conducted a cohort in HIV with hepatitis C virus (HCV) co-infection (n=3,418). Direct acting antiviral (DAA) therapy initiation vs. No DAA initiation was evaluated on Mean total cholesterol (TC), HbA1c, and ASCVD risk score at 12 months (MD 13 mg/dL (TC); β 0.00% (HbA1c); β 1.10 (ASCVD score), 95% CI 11-16). Direct acting antiviral initiation in HIV/HCV co-infection increased total cholesterol by 13 mg/dL (95% CI 11-16) at 12 months without altering HbA1c (β 0.00%) or ASCVD risk score (β 1.10).
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