Hepatology research : the official journal of the Japan Society of Hepatology 2017 02 22() doi 10.1111/hepr.12878
25-hydroxy vitamin D (Vit D) plays a role in treatment outcomes in chronic hepatitis C virus (HCV) infection (CHC). We aimed to clarify 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 anti-viral therapy.
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-); Group C (RVR+/SVR+).
The viral load of Con1 cells decreased by 69%, 80%, and 86%, in 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% in 1 μM, 5 μM, and 10 μM Vit D, respectively (p < 0.0001). There was a significant increase of Vit D between CHC groups, ranging from 4.4 ± 5.6 ng/mL of group A (n = 44), 17.2 ± 11.6 ng/mL of group B (n = 44), to 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
Vit D decreases HCV replication and also contributes to early treatment viral kinetics.