In the Journals

Vitamin D decreases HCV cell replication, aids virologic response

Vitamin D decreased hepatitis C cell replication and appeared significantly associated with rapid virologic response in anti-viral therapy, according to study results published in Hepatology Research.

“Liver has long been regarded as the key player manipulating complex biochemical metabolism, which is essential to maintenance of homeostasis,” the researchers wrote. “[Vitamin] D, the secosteroid hormone with pleiotropic effects, is an important physiological regulator contributed into various biological, immunological and metabolic functions in liver diseases. These non-skeletal effects are relevant in the pathogenesis of many causes of chronic liver disease.”

The researchers enrolled 132 patients to assess sustained virologic response and if it correlated with vitamin D levels. The patients were treated with pegylated IFN-based individualized strategies and divided into three groups: 44 non-responders who did not achieve rapid virologic response (RVR; group A, RVR–/SVR–), 44 non-responders with RVR (group B, RVR+/SVR–) and 44 with both RVR and SVR (group C, RVR+/SVR+).

The vitamin D levels for the three groups were 4.4 ± 5.6 ng/mL for group A, 17.2 ± 11.6 ng/mL for group B and 32.5 ± 37.5 ng/mL for group C (P < .001). Advanced fibrosis (F3 and F4) (OR = 0.13; 95% CI, 0.04-0.41) and vitamin D deficiency of less than 10 ng/mL (OR = 0.11; 95% CI, 0.03-0.43) were predictive of sustained virologic response.

“We addressed further that [vitamin] D may play an important role in the early phase of viral decline,” the researchers wrote. “Future prospective study in exploring the impact of [vitamin] D on the efficacy of potent direct antiviral agents will be essential in clinical setting.”

In another study of cells, replicon cells Con1 (genotype 1b) and J6/JFH (genotype 2a) were prepared and then exposed to increasing concentrations of vitamin D for 48 hours.

In the Con1 cells, there was a significant dose-dependent suppression seen at day 1, in which viral load decreased by 69%, 80% and 86% with doses of 1 M, 5 M and 10 M, respectively (P < .0001). Researchers observed no significant difference in cell survival with 1 M and 5 M of vitamin D, but they did observe a significant recovery rate of 80% with 10 M.

There was a similarly significant replication decrease at day 1 for the J6/JFH cells. Viral load decreased by 12% in 1 M (P = .014), 55% in 5M (P < .0001) and 80.5% in 10 M (P < .0001). There was no significant difference in cell survival between the J6/JFH cell baseline and the cells treated with different doses of vitamin D.

“Our study is a concordant one demonstrating that, without significant difference in cell survival, HCV replication was significantly suppressed by vitamin D treatment in a dose-dependent manner,” the researchers concluded. “Furthermore, the suppressive effects were observed in cell lines of different genotypes. The current study thus provided another window of HCV translational research in elucidating the genomic and proteomic aspects of HCV infection.” – by Talitha Bennett

Disclosure: The researchers report no relevant financial disclosures.

Vitamin D decreased hepatitis C cell replication and appeared significantly associated with rapid virologic response in anti-viral therapy, according to study results published in Hepatology Research.

“Liver has long been regarded as the key player manipulating complex biochemical metabolism, which is essential to maintenance of homeostasis,” the researchers wrote. “[Vitamin] D, the secosteroid hormone with pleiotropic effects, is an important physiological regulator contributed into various biological, immunological and metabolic functions in liver diseases. These non-skeletal effects are relevant in the pathogenesis of many causes of chronic liver disease.”

The researchers enrolled 132 patients to assess sustained virologic response and if it correlated with vitamin D levels. The patients were treated with pegylated IFN-based individualized strategies and divided into three groups: 44 non-responders who did not achieve rapid virologic response (RVR; group A, RVR–/SVR–), 44 non-responders with RVR (group B, RVR+/SVR–) and 44 with both RVR and SVR (group C, RVR+/SVR+).

The vitamin D levels for the three groups were 4.4 ± 5.6 ng/mL for group A, 17.2 ± 11.6 ng/mL for group B and 32.5 ± 37.5 ng/mL for group C (P < .001). Advanced fibrosis (F3 and F4) (OR = 0.13; 95% CI, 0.04-0.41) and vitamin D deficiency of less than 10 ng/mL (OR = 0.11; 95% CI, 0.03-0.43) were predictive of sustained virologic response.

“We addressed further that [vitamin] D may play an important role in the early phase of viral decline,” the researchers wrote. “Future prospective study in exploring the impact of [vitamin] D on the efficacy of potent direct antiviral agents will be essential in clinical setting.”

In another study of cells, replicon cells Con1 (genotype 1b) and J6/JFH (genotype 2a) were prepared and then exposed to increasing concentrations of vitamin D for 48 hours.

In the Con1 cells, there was a significant dose-dependent suppression seen at day 1, in which viral load decreased by 69%, 80% and 86% with doses of 1 M, 5 M and 10 M, respectively (P < .0001). Researchers observed no significant difference in cell survival with 1 M and 5 M of vitamin D, but they did observe a significant recovery rate of 80% with 10 M.

There was a similarly significant replication decrease at day 1 for the J6/JFH cells. Viral load decreased by 12% in 1 M (P = .014), 55% in 5M (P < .0001) and 80.5% in 10 M (P < .0001). There was no significant difference in cell survival between the J6/JFH cell baseline and the cells treated with different doses of vitamin D.

“Our study is a concordant one demonstrating that, without significant difference in cell survival, HCV replication was significantly suppressed by vitamin D treatment in a dose-dependent manner,” the researchers concluded. “Furthermore, the suppressive effects were observed in cell lines of different genotypes. The current study thus provided another window of HCV translational research in elucidating the genomic and proteomic aspects of HCV infection.” – by Talitha Bennett

Disclosure: The researchers report no relevant financial disclosures.