25-Hydroxy vitamin D suppresses hepatitis C virus replication and contributes to rapid virological response of treatment efficacy.

ABSTRACT

AIM: 25-Hydroxy vitamin D (Vit D) plays a role in treatment outcomes in chronic hepatitis C virus (HCV) infection. We aimed to clarify whether HCV replication is inhibited by Vit D in HCV replicon cells. Clinical implication was assessed for rapid virological response (RVR) and sustained virological response (SVR) among those patients receiving antiviral therapy. METHODS: Cell survival and viral loads were observed in Con1 (genotype 1b) and J6/JFH (genotype 2a) cells treated with different doses of Vit D. Three groups of patients with different treatment responses were recruited to assess their Vit D levels group A, RVR-/SVR-; group B, RVR+/SVR-; and group C, RVR+/SVR+. RESULTS: The viral load of Con1 cells decreased by 69%, 80%, and 86% following treatment with 1 µM, 5 µM, and 10 µM Vit D, respectively (P < 0.0001). In J6/JFH cells, it decreased by 12%, 55%, and 80.5% following treatment with 1 µM, 5 µM, and 10 µM Vit D, respectively (P < 0.0001). There was a significant increase of Vit D between chronic hepatitis C groups, ranging from 4.4 ± 5.6 ng/mL in group A (n = 44), to 17.2 ± 11.6 ng/mL in group B (n = 44), and 32.5 ± 37.5 ng/mL of group C (n = 44) (P < 0.001). Advanced fibrosis (odds ratio = 0.13, 95% confidence interval = 0.04-0.41, P < 0.001) and Vit D deficiency (<10 ng/mL) (odds ratio = 0.11, 95% confidence interval = 0.03-0.43, P = 0.001) were predictive of SVR in the multivariate regression analysis. CONCLUSION: Vitamin D decreases HCV replication and also contributes to early treatment viral kinetics.