Immunopathogenesis of chronic hepatitis B

Abstract

Chronic hepatitis B (CHB) is a widespread infectious disease with unfavorable outcomes and life-threatening consequences for patients, in spite of modern vaccination and antiviral treatment modalities. Cutting-edge experimental approaches have demonstrated key pathways that involve cross-talk between viral particles and host immune cells. All events, including penetration of hepatitis B virus (HBV) particles into host cells, establishing persistence, and chronization of CHB infection, and possibility of complete elimination of HBV particles are controlled by the immune system. Researchers have paid special attention to the replication capacity of HBV in host cells, which is associated with cellular changes that reflect presentation of viral antigens and variability of HBV antigen features. In addition, specific HBV proteins have an immune-modulating ability to initiate molecular mechanisms that "avoid" control by the immune system. The relationship between immunological shifts and chronic infection stages has been intensively studied since it was recognized that the immune system is a direct participant in the recurrent (cyclic) nature of CHB. Understanding the wide diversity of molecular pathways and the crosstalk between innate and adaptive immune system components will provide fresh insight into CHB immune pathogenesis and the possibilities of developing new treatment strategies for this disease.

Genetic polymorphisms in Toll-like receptor 3 gene are associated with the risk of hepatitis B virus-related liver diseases in a Chinese population

“…It is known that SNPs may be implicated in various human diseases. TLR3 signaling takes part in the immunopathogenesis of HBV infection (Balmasova et al, 2014) and in TLR3-mediated antiviral response in control of HBV replication through IFN-β in liver cells (Wu et al, 2007;Zhang and Lu, 2015). Thus, we hypothesized that TLR3 polymorphisms (rs1879026 and rs3775290) may be associated with HBV infection and HBV-related liver diseases in the South Chinese population.…”

“…HBV infection and clearance depends on host immune responses (Balmasova et al, 2014). Additionally, it has been reported that TLR signaling contributes to immunopathogenesis of HBV infection (Wu et al, 2009).…”

“…The clinical course of HBV infection varies from spontaneous to chronic persistent infection, and persistent HBV infection will finally lead to severe liver injury. Most HCC cases in China are derived from initial HBV infection, followed by LC, and finally carcinogenesis (Chemin and Zoulim, 2009;Balmasova et al, 2014). Despite the poor prognosis and high relapse rates of HCC, targeted drugs and surgical treatment are still unsatisfactory.…”

Involvement of Interleukin 6 in Hepatitis B Viral Infection

“…HBV infection can lead to a great number of clinical consequences such as acute self-limited hepatitis, chronic hepatitis, liver failure, liver cirrhosis (LC) and hepatocellular carcinoma (HCC) [1]. These complications do not result from a direct cytopathic effect of the virus itself, but from the immune response of the host that affects both outcome and disease progression [2,3]. Cytokines have been shown to be engaged in regulating hepatocyte functions, and play a fundamental role in HBV infection immunopathogenesis [4].…”

Adenovirus Vector Harboring the HBcAg and Tripeptidyl Peptidase II Genes Induces Potent Cellular Immune Responses In Vivo

“…With the help of APCs, antigens are hydrolyzed into peptides by the proteasome [47]. Previous studies have indicated that HBcAg could activate the innate immunity [48]. Our previous study suggested that AdvHBcAg-TPPII could promote DC maturation and enhance HBcAg-specific CTLs in vitro.…”