Association of toll-like receptors single nucleotide polymorphisms with HBV and HCV infection: research status

PeerJ. 2022 Apr 19:10:e13335. doi: 10.7717/peerj.13335. eCollection 2022.

Abstract

Background: Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections have become increasingly severe worldwide and are a threat to public health. There have been a number of studies conducted recently on the relationship of single nucleotide polymorphisms (SNPs) to innate immune receptor genes such as toll-like receptors (TLRs). Some literature suggests that SNPs of TLRs are associated with HBV and HCV infection. We summarized the role of TLRs gene polymorphisms associated with HBV and HCV infections and explored their possible mechanisms of action.

Methodology: PubMed and Web of Science were used to perform the literature review. Related articles and references were identified and used to analyze the role of TLRs gene polymorphism in HBV and HCV infection.

Results: TLRs gene polymorphisms may have beneficial or detrimental effects in HBV and HCV infection, and some SNPs can affect disease progression or prognosis. They affect the disease state by altering gene expression or protein synthesis; however, the mechanism of action is not clearly understood.

Conclusions: Single nucleotide polymorphisms of TLRs play a role in HBV and HCV infection, but the mechanism of action still needs to be explored in future studies.

Keywords: HBV; HCV; Single nucleotide polymorphisms (SNPs); Toll-like receptors (TLRs).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Hepacivirus / genetics
  • Hepatitis B virus* / genetics
  • Hepatitis C* / genetics
  • Humans
  • Polymorphism, Single Nucleotide / genetics
  • Toll-Like Receptors / genetics

Substances

  • Toll-Like Receptors

Grants and funding

This study was supported by the Lanzhou Science and technology project (grant no.2021-1-104). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.