TLR3 plays significant roles against hepatitis B virus.
Hepatitis B virus (HBV) as the main prevalent infectious agent, play important roles in inducing severe liver diseases. Previous studies demonstrated that during prolonged forms of hepatitis B infection including chronic, asymptomatic and occult forms, patients are unable to eradicate HBV from hepatocytes completely. The main mechanisms responsible for development of the forms of hepatitis B are yet to be identified. Investigators suggested that the various genetic and immunological parameters of the patients may are responsible for resulting in the prolonged infection forms. It has been evidenced that TLRs play key roles in inducing appropriate immune responses, against viral infections. Therefore, these molecules can be considered as crucial sensors for HBV detection to induce immune responses against this virus. It has also been documented that the TLR3 detects intracellular viral dsRNA and subsequently activates NF-κB via the TRIF pathway. Therefore, impaired TLR3 expression may result in inappropriate immune responses against HBV which is reported in prolonged forms of hepatitis B. This review collected the recent information regarding the important roles of TLR3 in immune responses against HBV and also the status of TLR3 expression and its genetic variations in prolonged forms of HBV infections.
Department of Immunology, Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Masoud
M
Karimi-Googheri
Mohammad Kazemi
MK
Arababadi
D006515:Hepatitis B virus / Q000276:immunology / Q000378:metabolism*; D019694:Hepatitis B, Chronic / Q000276:immunology / Q000378:metabolism* / Q000628:therapy; D006801:Humans; D007167:Immunotherapy; D007370:Interferon Type I / Q000378:metabolism; D008024:Ligands; D015398:Signal Transduction; D051196:Toll-Like Receptor 3 / Q000378:metabolism*
D007370:Interferon Type I; D008024:Ligands; D051196:Toll-Like Receptor 3