Toll-like receptor 4 and hepatitis B infection: molecular mechanisms and pathogenesis.

Abstract

Hepatitis B virus (HBV) infection mainly causes liver disease, including inflammation, cirrhosis, and hepatocellular carcinoma (HCC). It has been documented that prolonged hepatitis B-infected patients are unable to clear HBV from hepatocytes completely. Previous investigations have suggested that various genetic and immunologic parameters may be responsible for the induction of prolonged infection forms. Toll-like receptors (TLRs), as members of pathogen recognition receptors (PRRs), play critical roles in the recognition of viruses and the induction of appropriate immune responses. Thus, TLRs may be considered as essential sensors for the recognition of HBV and the induction of immune responses against this virus. It has been documented that TLR4 plays key roles in the detection of several microbial pathogen-associated molecular pattern molecules, including bacterial lipopolysaccharide (LPS), as well as endogenous ligands (damage-associated molecular pattern molecules) and subsequently activates pro-inflammatory transcription factors in either MYD88 or TRIF dependent pathways. Previous investigations have proposed that TLR4 might be involved in appropriate immune responses against HBV. Therefore, the aim of this review is to present the recent data regarding the important roles of TLR4 in HBV recognition and regulation of immune responses against this virus, and also its roles in the pathogenesis of cirrhosis and HCC as complications of prolonged hepatitis B infections.

• Authors: Mohammad Zare-Bidaki, Kyoko Tsukiyama-Kohara, Mohammad Kazemi Arababadi
• Journal: Viral immunology (Viral Immunol) Vol. 27 Issue 7 Pg. 321-6 (Sep 2014) ISSN: 1557-8976 [Electronic] United States
• PMID: 25014492 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• TLR4 protein, human
• Toll-Like Receptor 4

Topics

• Gene Expression Regulation
• Hepatitis B (metabolism, pathology)
• Humans
• Signal Transduction
• Toll-Like Receptor 4 (genetics, metabolism)