The Immune Response Induced by Hepatitis B Virus Principal Antigens
Overview
Affiliations
Hepatitis B virus (HBV) infection occurs primarily in hepatocytes in the liver with release of infectious virions and non-infectious empty surface antigen particles into the bloodstream. HBV replication is non-cytopathic. Transient infections run a course of several months, and chronic infections are often life-long. Chronic infections can lead to liver failure with cirrhosis and hepatocellular carcinoma. It is generally accepted that neutralizing anti-HBs antibodies plays a key role in recovery from HBV infection by containing the spread of infection in the infected host and facilitating the removal and destruction of viral particles. However, the immune response initiated by the T-cell response to viral antigens is also important for viral clearance and disease pathogenesis in HBV infection. The three structural forms of the viral proteins, the HBsAg, the particulate HBcAg, and the nonparticulate HBeAg, may preferentially elicit different Th cell subsets. The different IgG subclass profiles of anti-HBs, anti-HBc, and anti-HBe in different HBV infection status were revealed. Moreover, the different IgG subclass profiles in chronic carriers did not change with different ALT and AST levels and may reflect the difference between stimulating antigens, immune response, and the stages of viral disease and provide the basis for the use of vaccines and prophylactic treatments for individuals at high risk of human HBV infection. This review elucidates the detailed understanding of the immune responses induced during transient and persistent infection, and the development of immunotherapy and immunodiagnosis in patients with HBV infection, and possible means of reducing the liver damage.
Huong N, Vu H, Luong B, Makram A, Elsheikh R, Huy N Gastro Hep Adv. 2024; 2(4):467-474.
PMID: 39132047 PMC: 11307456. DOI: 10.1016/j.gastha.2023.01.017.
Cullum E, Perez-Betancourt Y, Shi M, Gkika E, Schneewind O, Missiakas D PLoS Pathog. 2024; 20(6):e1012306.
PMID: 38843309 PMC: 11185455. DOI: 10.1371/journal.ppat.1012306.
Carcinogenic mechanisms of virus-associated lymphoma.
Zhang Y, Guo W, Zhan Z, Bai O Front Immunol. 2024; 15:1361009.
PMID: 38482011 PMC: 10932979. DOI: 10.3389/fimmu.2024.1361009.
de Almeida Ponde R Mol Biol Rep. 2023; 50(8):6435-6443.
PMID: 37326752 DOI: 10.1007/s11033-023-08546-7.
Hong J, Choi Y, Choi Y, Lee J, Hong H Vaccines (Basel). 2021; 9(7).
PMID: 34358170 PMC: 8310169. DOI: 10.3390/vaccines9070754.