Abstract
Chronic hepatitis B virus (HBV) infection remains a major global health problem. The immunopathology of the disease, especially the interplay between HBV and host innate immunity, is poorly understood. Moreover, inconsistent literature on HBV and host innate immunity has led to controversies. However, recently, there has been an increase in the number of studies that have highlighted the link between innate immune responses, including Toll-like receptors (TLRs), and chronic HBV infection. TLRs are the key sensing molecules that detect pathogen-associated molecular patterns and regulate the induction of pro- and anti-inflammatory cytokines, thereby shaping the adaptive immunity. The suppression of TLR response has been reported in patients with chronic hepatitis B (CHB), as well as in other models, including tree shrews, suggesting an association of TLR response in HBV chronicity. Additionally, TLR agonists have been reported to improve the host innate immune response against HBV infection, highlighting the potential of these agonists as immunomodulators for enhancing CHB treatment. In this study, we discuss the current understanding of host innate immune responses during HBV infection, particularly focusing on the TLR response and TLR agonists as immunomodulators.
Highlights
Hepatitis B virus (HBV) infection, which causes chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC), remains a major global health problem despite the availability of an effective preventive vaccine for HBV [1,2]
In our previous study, we observed a significant suppression of interferon regulatory factor 7 (IRF-7) and ISG15, as well as no increase in IFN-β production at 1- or 3-days post-infection in the tree shrew model [23], which was suggestive of the inhibition of innate immune response at early stage of infection in this model
Recent studies have highlighted HBV as a cunning virus, which raises questions about stealth properties of HBV and shows the ability of the virus to interfere with the innate immune response and establish an infection
Summary
Hepatitis B virus (HBV) infection, which causes chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC), remains a major global health problem despite the availability of an effective preventive vaccine for HBV [1,2]. TLRs, retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), nucleotide-binding oligomerization domain (NOD)like receptors (NLRs), and C-type lectin receptors play an essential role in sensing the invading pathogens, including viruses, and initiating an innate immune response. This leads to the synthesis of IFNs and cytokines through several distinct signaling pathways, thereby limiting infection and promoting adaptive immune responses [27,28]. Activation of innate immune response by TLR agonists may play a significant role in modulating the outcome of chronic HBV infection. We have addressed the immunomodulatory potential of TLR agonists for improving host innate immune responses during chronic HBV infection
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