维生素D减少HCV细胞复制，有助于病毒学反应

StephenW

Vitamin D decreases HCV cell replication, aids virologic response

Huang JF, et al. Hepatol Res. 2017;doi:10.1111/hepr.12878.
February 27, 2017

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

StephenW

维生素D减少HCV细胞复制，有助于病毒学反应

Huang JF，et al。 Hepatol Res。 2017; doi：10.1111 / hepr.12878。
2017年2月27日

根据Hepatology Research发表的研究结果，维生素D减少丙型肝炎细胞复制并且显示与抗病毒治疗中的快速病毒学应答显着相关。

研究人员写道：“肝长期以来一直被认为是操纵复杂生化代谢的关键参与者，这对维持体内平衡是至关重要的。 “[维生素] D，具有多效性的类固醇激素，是一种重要的生理调节因子，参与肝脏疾病的各种生物学，免疫学和代谢功能。这些非骨骼效应与慢性肝病的许多原因的发病机理相关。

研究人员登记了132名患者来评估持续的病毒学反应，如果它与维生素D水平相关。用聚乙二醇化的基于IFN的个体化策略治疗患者，并分成三组：44名没有实现快速病毒学应答的无应答者（RVR; A组，RVR- / SVR-），44名具有RVR的非应答者（B组，RVR + / SVR-）和44，具有RVR和SVR（组C，RVR + / SVR +）。

三组的维生素D水平为A组为4.4±5.6ng / mL，B组为17.2±11.6ng / mL，C组为32.5±37.5ng / mL（P <0.001）。晚期纤维化（F3和F4）（OR = 0.13; 95％CI，0.04-0.41）和小于10ng / mL（OR = 0.11; 95％CI，0.03-0.43）的维生素D缺乏预示持续病毒学应答。

研究人员写道：“我们进一步指出[维生素D]可能在病毒减少的早期阶段发挥重要作用。 “未来前瞻性研究探讨[维生素D]对有效的直接抗病毒药物的疗效的影响在临床环境中是至关重要的。

在另一个细胞研究中，制备复制子细胞Con1（基因型1b）和J6 / JFH（基因型2a），然后暴露于增加浓度的维生素D 48小时。

在Con1细胞中，在第1天观察到显着的剂量依赖性抑制，其中病毒载量分别以1M，5M和10M的剂量分别减少69％，80％和86％（P <0.0001 ）。研究人员观察到1 M和5 M维生素D在细胞存活中没有显着差异，但他们确实观察到10％的显着回收率为80％。

在J6 / JFH细胞的第1天存在类似的显着复制减少。病毒载量在1μM（P = 0.014），5M（P <0.0001）和50μM（P <0.0001）中下降12％。 J6 / JFH细胞基线和用不同剂量的维生素D处理的细胞之间的细胞存活没有显着差异。

“我们的研究是一致的，表明，在细胞存活没有显着差异，HCV复制被维生素D治疗以剂量依赖的方式显着抑制，”研究人员总结。 “此外，在不同基因型的细胞系中观察到抑制效应。因此，目前的研究提供了另一个窗口的HCV翻译研究阐明HCV感染的基因组和蛋白质组学方面。“ - 通过Talitha Bennett

披露：研究人员报告没有相关的财务披露

llau_lhf

好像有一些医学研究说维生素d浓度跟癌症有关系，但不知普遍的定论如何。

StephenW

回复 llau_lhf 的帖子

是的，有，但结果不一致.
所以最好保持正常水平，避免不足.

llau_lhf

回复 StephenW 的帖子

谢谢！

antiHBVren

回复 StephenW 的帖子

之前有看到维生素C来治疗的

东野菰

好像有一些医学研究说维生素d浓度跟癌症有关系，但不知普遍的定论如何。