HCV Cure Shows No Effect on Markers of Preclinical Atherosclerosis in HIV/HCV Coinfection

Although hepatitis C virus (HCV) eradication was associated with a clinically relevant increase in serum low-density lipoprotein cholesterol (LDL-C), among patients coinfected with HIV/HCV there were no medium-term beneficial effects of sustained virologic response on markers of preclinical atherosclerosis and biomarkers of inflammation and endothelial dysfunction, according to study results published in the Journal of Acquired Immune Deficiency Syndrome.

The association between HCV infection and cardiovascular events is a controversial issue, with some observational studies evidencing a positive correlation but large studies failing to do so. In a previous study, this study’s authors found a sustained viral response after treatment for HCV and that patients coinfected with HIV and HCV had a reduction in the risk for diabetes and renal failure but had an increase in the risk for cardiovascular events.

Therefore, the investigators conducted this prospective study and collected data from 237 patients coinfected with HIV/HCV initiating treatment for chronic HCV between February 2012 and February 2016 at 14 centers in Spain. Clinical and laboratory variables were collected at baseline, every 4 weeks during HCV treatment, and every 12 weeks after discontinuation of therapy through 96 weeks.

Of the 237 patients, 62% patients achieved sustained virologic response. The median age of patients was 49.2 years, 75.9% were men, 65.8% were infected with HCV genotype 1, a significant majority of patients (97.9%) were receiving combination antiretroviral therapy, and 87.3% had an undetectable HIV viral load. At baseline, HCV-RNA was the only variable that showed significant differences between patients who demonstrated sustained virologic response vs those who did not (median, 6.2 vs 6.5 log10 IU/mL, respectively; P <. 05).

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Although there were no statistically significant differences at baseline in total cholesterol, LDL-C, and high-density lipoprotein cholesterol, total cholesterol and LDL-C were significantly higher between patients who demonstrated sustained virologic response vs those who did not at 96 weeks. Median increases in total cholesterol in patients who had sustained virologic response and those who did not were 15 mg/dL and 1 mg/dL, respectively (P =.001). Similarly, median increases in LDL-C were 14 mg/dL and 0 mg/dL (P =.024) among patients who showed a sustained virologic response and those who did not, respectively.

The rise in serum LDL-C in patients who responded to HCV treatment led to an increase in the Framingham 10-year general cardiovascular risk. At baseline, the least-squares mean of cardiovascular risk according the Framingham equation was 11.0% and 11.1% in patients with sustained viral response and those without, respectively. At 96 weeks, patients with sustained viral response had a 13.0% risk, compared with a 10.5% risk in patients who did not have a sustained response.

At 96 weeks, no significant effect of sustained virologic response was observed on carotid-femoral pulse wave velocity and carotid intima-media thickness (P =.446 and P =.320, respectively). Plasma concentrations of interleukin 6, interleukin 8, soluble intercellular adhesion molecule-1, and soluble vascular cell adhesion molecule-1 decreased from baseline to week 96, in both patients demonstrating sustained virologic response and those not; whereas increases were observed for tumor necrosis factor-α and interleukin-1β. However, no significant effect of sustained virologic response was identified for any of the biomarkers of inflammation or endothelial dysfunction.

Overall, the findings suggested that “evaluation of [cardiovascular risk] should be an integral part of care after the cure of chronic hepatitis C in patients with HIV,” concluded the researchers.


Carrero A, Berenguer J, Hontañón V, et al; GeSIDA 3603b Study Group. Effects of eradication of HCV on cardiovascular risk and preclinical atherosclerosis in HIV/HCV-coinfected patients. J Acquir Immune Defic Syndr. 2020;83(3):292-300.