The link between TLR7 signaling and hepatitis B virus infection

Toll-Like Receptors (TLRs) play crucial roles in recognition and induction of appropriate immune responses against viral infections, including hepatitis B. TLR7 detects intracellular viral single strand RNA which leads to the activation of several pro-inflammatory transcription factors via the MYD88 dependent pathway. Patients with prolonged infectious forms of hepatitis B, including active and inactive chronic forms, are unable to clear HBV from hepatocytes completely. It is believed that the differences in genetic and immunological parameters of the patients and clearance subjects, who successfully clear HBV infections, are the main factors responsible for allowing the long term infections to persist. It appears that defective expression of TLR7 may result in impaired immune responses against HBV. The aim of this review is to address the recent information regarding the crucial roles played by TLR7 in hepatitis B infection and also the main mechanisms used by HBV to escape from recognition by TLR7 in prolonged HBV infected patients. Considering that chronic hepatitis B infection is not yet curable, it could be possible to activate TLR7-related immunological pathways as a therapy directed towards persistent HBV infection. Hence, another aim of this study is to present recent developments of TLR7 agonists as a therapeutic strategy for chronic hepatitis B.

TLR7 signaling pathway plays key roles against HBV, and accordingly, the virus uses some mechanisms to inhibit the pathway. Using TLR7 agonists (Imidazoquinolines, Guanosine Analogues and GS-9620) can amplify TLR7 pathway and induce HBV clearance.Figure optionsDownload high-quality image (115 K)Download as PowerPoint slide