Association of TGF-ß1 polymorphisms and chronic hepatitis C infection: a Meta-analysis

Abstract

Background Although several researches have reported the connection between the transforming growth factor-beta 1 ( TGF-β1 ) gene polymorphisms and chronic hepatitis C virus (HCV) infection, the conclusions of these studies were not always consistent. Here, this paper proposed a meta-analysis to evaluate whether the TGF-ß1 gene polymorphisms, −509C/T (rs1800469), codon 10 T/C (rs1982073) and codon 25G/C (rs1800471), were associated with chronic HCV infection. Methods The summary odds ratios (ORs) of chronic HCV infected patients and controls with all SNPs were obtained by adaptive fixed or random effect model. A series of statistical tools were employed to guarantee the accuracy of related pooling ORs, including the Hardy-Weinberg equilibrium (HWE) test, sensitivity analysis and publication bias test. Results This paper analyzed 18 case-control studies in 17 articles which totally contains 2718 chronic HCV infection cases corresponding to 1964 controls. The results of the meta-analysis indicated that the −509C/T polymorphism effected an increased risk of chronic HCV infection in all gene models. More specifically by ethnicity stratification, the Egyptians shared the similar association with the above overall study. Moreover, the meta-fusion of healthy control studies showed that − 509 T allele carriers (TT + TA) had nearly 2.00 and 3.36 fold higher risk of chronic HCV infection in the total and Egyptian populations, respectively (OR = 2.004, 95% CI = 1.138–3.528, P = 0.016; OR = 3.363, 95% CI = 1.477–7.655, P = 0.004, respectively). However, our meta-analysis did not find any significant association between the codon 10 T/C or codon 25G/C polymorphisms and chronic HCV infection. Conclusions Our results suggested that the TGF-ß1 –509C/T polymorphism may effect an increased risk of chronic HCV infection, especially in Egyptian population. Electronic supplementary material The online version of this article (10.1186/s12879-019-4390-8) contains supplementary material, which is available to authorized users.

TGF-Β1 & PNPLA3 Genetic Variants and the Risk of Hepatic Fibrosis and HCC in Egyptian Patients with HCV-Related Liver Cirrhosis

“…Although several epidemiological studies have examined the association of TGF-β1 Arg25Pro (G>C) variant with the chronic HCV infection susceptibility, and fibrosis progression, controversial results still exist (Gewaltig et al, 2002;Pereira et al, 2008;Guo et al, 2019). In the current study we did not find significant difference in genotyping distribution or allele frequency of TGF-β1 (Arg25Pro) variant when comparing total cirrhosis patients with controls.…”

“…However, the subjects with codon 25 G allele which was associated with high TGF-β1 production displayed over suppression in the human immune response. This mechanism may elucidate the correlation of the polymorphism of Arg25Pro (G>C) and chronic HCV infection (Guo et al, 2019).…”

Cytokine (IL-10, IL-6, TNF-α and TGF-β1) Gene Polymorphisms in Chronic Hepatitis C Virus Infection among Malay Male Drug Abusers

“…These findings are different with some past studies that indicated an association of the gene polymorphism of the TGF-β1 genotype with the outcome of HCV infection [ 14 ]. By contrast, several studies that explored the role of TGF-β1 rs1800471 (the codon 25G) polymorphism in chronic HCV infection in Asian, Caucasian, and Brazilian populations found no significant association between the codon 25G/C polymorphism and chronic HCV infection in all subgroup analyses [ 16 , 34 , 35 ]. The human TGF-β1 gene located on chromosome 19q13 is mainly expressed by regulatory T cells [ 36 ].…”

Role of Inflammatory/Immune Response and Cytokine Polymorphisms in the Severity of Chronic Hepatitis C (CHC) before and after Direct Acting Antiviral (DAAs) Treatment

“…Transforming growth factor-beta (TGF-β) is a cytokine secreted by hepatic stellate cells, fibroblasts, Kupffer cells, and M2 macrophages that regulate cell growth, differentiation, and proliferation [ 29 , 30 ].…”