Abstract
The cytotoxic T-lymphocyte antigen 4 (CTLA-4) gene is a negative regulator of T lymphocyte activation and proliferation. Single nucleotide polymorphisms (SNPs) occurring on the CTLA-4 gene can modify the ability to control the proliferation of T lymphocytes, thereby impacting the clearance of hepatitis B (HBV) and hepatitis C (HCV) virus infections. The -319C/T and +49A/G SNPs of CTLA-4 gene have been associated with autoimmune disorders and liver infections. Studies show that the +49G allele confers susceptibility to HBV and HCV infection in chronic disease (without cirrhosis), associates with the risk of chronic HCV infection in males, confers protective effect against the development of hepatocellular carcinoma, and favors viral elimination. Furthermore, the +49G allele alone or in haplotype with the -319C favors chronic infection with genotype 3 HCV; has an inverse association with HCV genotype 1; and decreases viral load in chronic hepatitis C associated with sustained viral response (SVR). These findings support an important role of the SNPs of CTLA-4 gene in viral hepatitis; however, the mechanisms by which they influence immune response against viral infections is not fully understood. This review gives an overview of the current understanding of the association between CTLA4 SNPs and HBV/HCV infections.
Highlights
Chronic viral hepatitis is most commonly caused by hepatitis B (HBV) or hepatitis C (HCV) viruses
This review aims to discuss the results of research evaluating how single nucleotide polymorphisms (SNPs) in cytotoxic T-lymphocyte antigen 4 (CTLA-4) gene may affect the course of HBV and HCV infections through their role in immune function
We previously found that the +49G allele is associated with HCV chronic infection but not with the presence of liver cirrhosis in the Mexican population [30]
Summary
Chronic viral hepatitis is most commonly caused by hepatitis B (HBV) or hepatitis C (HCV) viruses. It is estimated that 5–10% of individuals infected are unable to eliminate the virus; of these, 15–40% will develop cirrhosis or HCC [6,7,8] Both HBV and HCV have a similar natural history but with different propensities for chronic complications. The interaction between the virus and the immune response of the host is responsible for liver damage and the clinical manifestations of disease [10, 11]. This demonstrates the importance of the immune system in determining how the body will respond to these pathogens. This review aims to discuss the results of research evaluating how single nucleotide polymorphisms (SNPs) in CTLA-4 gene may affect the course of HBV and HCV infections through their role in immune function
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