Abstract
Background: Recently, several studies have reported that the host immune response can be related to the RANKL/RANK/OPG signaling pathway. However, the associations of TNFSF11, TNFRSF11A, and TNFRSF11B gene polymorphisms in the RANKL/RANK/OPG pathway with hepatitis C virus (HCV) infection outcomes remain unclear.Methods: In this case-control study, 768 persistent HCV infection and 503 spontaneous HCV clearance cases, and 1,259 control subjects were included. The Taman-MGB probe method was utilized to detect TNFSF11 rs9525641, TNFRSF11A rs8686340, and TNFRSF11B rs2073618 genotypes. The distribution of three single nucleotide polymorphisms (SNPs) genotypes was analyzed using stata14.0.Results: SNPs rs9525641, rs8086340, and rs2073618 genotype frequencies followed the Hardy-Weinberg natural population equilibrium (p = 0.637, 0.250, and 0.113, respectively). Also, rs9525641 was significantly associated with HCV chronicity risk in recessive (OR = 1.203, 95% CI: 1.018–1.420, p = 0.030) and additive models (OR = 1.545, 95% CI: 1.150–2.075, p = 0.004). The stratified analysis showed that rs9525641 variant genotypes were associated with HCV chronicity among people older than 50 years (OR =1.562, 95% CI: 1.079–2.262, p = 0.018), females (OR = 1.667, 95% CI: 1.145–2.429, p = 0.008), ALT <40 U/L (OR = 1.532, 95% CI: 1.074–2.286, p = 0.018), and AST < 40 U/L (OR = 1.552, 95% CI: 1.095–2.201, p = 0.014).Conclusion: TNFRSF11 rs9525641 was significantly associated with HCV chronicity in the Chinese population.
Highlights
With the introduction of all-oral direct-actingantiviral therapy, a substantial breakthrough has been made in chronic hepatitis C virus (HCV) infection treatment during the past decades [1]
Rs9525641 was significantly associated with HCV chronicity risk in recessive (OR = 1.203, 95% CI: 1.018–1.420, p = 0.030) and additive models (OR = 1.545, 95% CI: 1.150–2.075, p = 0.004)
The stratified analysis showed that rs9525641 variant genotypes were associated with HCV chronicity among people older than 50 years (OR =1.562, 95% CI: 1.079–2.262, p = 0.018), females (OR = 1.667, 95% CI: 1.145–2.429, p = 0.008), ALT < 40 U/L (OR = 1.532, 95% CI: 1.074–2.286, p = 0.018), and AST < 40 U/L (OR = 1.552, 95% CI: 1.095–2.201, p = 0.014)
Summary
With the introduction of all-oral direct-actingantiviral therapy, a substantial breakthrough has been made in chronic HCV infection treatment during the past decades [1]. The activation of NF-κB and NF-κB-dependent inflammatory pathways are important to chronic HCV infection and its related cirrhosis and HCC. The communication pathways mediated by TNFSF/TNFRSF are essential for numerous developmental, homeostatic, and stimulus-responsive processes. Many studies have identified that immune cytokines SNPs were significantly associated with HCV spontaneous clearance and virological response, except for viral and environmental factors [6,7,8,9]. Studies have shown that multiple TNFSF and TNFRSF gene SNPs are related to autoimmune diseases, suggesting that these SNPs play an important role in immunity. Several studies have reported that the host immune response can be related to the RANKL/RANK/OPG signaling pathway. The associations of TNFSF11, TNFRSF11A, and TNFRSF11B gene polymorphisms in the RANKL/RANK/OPG pathway with hepatitis C virus (HCV) infection outcomes remain unclear
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