From the Journals

Vitamin D–binding protein polymorphisms affect HCV susceptibility



Two specific polymorphisms within the vitamin D–binding protein (VDBP) gene may contribute to susceptibility to hepatitis C virus (HCV) infection in a high-risk Chinese Han population, according to the results of a case-control study published in Gene.

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Previous research has indicated that vitamin D deficiency may have an impact on the antiviral response in chronic HCV, and VDBP has been shown to transport vitamin D and its metabolites, thereby influencing vitamin D status. This made VDBP a valid candidate for study as to its effects on HCV infection.

The current study initially recruited around 2,500 Chinese subjects over the period October 2008 to January 2016. The majority were women, and the average age of the subjects was 49-50 years.

The researchers genotyped seven genetic variants in the VDBP gene in 886 patients with HCV persistent infection, 539 subjects with spontaneous clearance, and 1,081 uninfected controls, according to Chao-Nan Xie of the department of epidemiology and biostatistics, Nanjing (China) Medical University, and colleagues.

The researchers found that two variants (rs7041-G and rs3733359-T alleles) were significantly associated with an increased susceptibility of HCV infection. In addition, the combined effect of having the two unfavorable alleles was related to an elevated risk of HCV infection in a locus-dosage manner (P = .000816).

Haplotype analysis suggested that the GT haplotype showed an increased risk effect of HCV infection (odds ratio, 1.464), compared with the most frequent TC haplotype.

“Taken together, polymorphisms within the VDBP gene (rs4588 and rs3733359) may contribute to susceptibility to HCV infection in a high-risk Chinese Han population, which implicates a role of VDR genetic polymorphisms and vitamin D levels in the immune regulation and course of HCV infection,” the researchers concluded.

The authors reported that they had no conflicts of interest.

SOURCE: Xie C-N et al. Gene 2018;679:405-11.

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