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Immune responses and immunopathology in acute and chronic viral hepatitis
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Immune responses and immunopathology in acute and chronic viral hepatitis
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Journal Article
Immune responses and immunopathology in acute and chronic viral hepatitis
2016
Overview
Key Points
Hepatitis C virus (HCV) tends to establish a chronic persistent infection, whereas hepatitis A virus (HAV) does not develop into a chronic infection. Hepatitis B virus (HBV) is effectively controlled in adults, although it persists for a lifetime after neonatal infection.
HCV infection increases the expression of a large number of IFN-stimulated genes (ISGs), whereas HAV infection minimally induces ISG expression and HBV infection does not induce ISG expression. Patients with chronic HCV infection who have high baseline levels of ISGs in the liver respond poorly to interferon-α (IFNα)-based therapy due to an ISG15–ubiquitin-specific peptidase 18 (USP18)-mediated mechanism.
HAV-specific and hepatitis B surface antigen (HBsAg)-specific antibodies with virus neutralizing activity confer lifelong protective immunity to infection. By contrast, HCV-specific antibodies are not long-lasting even after spontaneous virus clearance, and the roles of HCV E1- and E2-specific antibodies in the control of infection and in protective immunity have not been clearly elucidated.
Robust and multiple epitope-specific CD8
+
T cell responses, which are helped by CD4
+
T cells, are crucial for the spontaneous resolution of acute HBV or HCV infection. In acute HCV infection, the induction of virus-specific T cell responses is remarkably delayed, which is not the case in acute HAV and HBV infections.
In chronic HBV or HCV infection, virus-specific T cells are exhausted and functionally impaired because of sustained antigenic stimulation. As a result, virus-specific T cells have a poor proliferation capacity, weak cytolytic activity and suppressed cytokine production.
In hepatitis virus infections, liver injury is caused by immune-mediated mechanisms. Both virus-specific T cells and nonspecific cells contribute to liver injury, and suppressor cells such as regulatory T cells and myeloid-derived suppressor cells control immune-mediated liver injury.
Comparing the immune responses to and immunopathogenesis of infection with hepatitis A virus (HAV), hepatitis B virus (HBV) and hepatitis C virus (HCV) provides insight into the distinct outcomes of each type of viral hepatitis.
Hepatitis A virus (HAV), hepatitis B virus (HBV) and hepatitis C virus (HCV) are responsible for most cases of viral hepatitis. Infection by each type of virus results in a different typical natural disease course and clinical outcome that are determined by virological and immunological factors. HCV tends to establish a chronic persistent infection, whereas HAV does not. HBV is effectively controlled in adults, although it persists for a lifetime after neonatal infection. In this Review, we discuss the similarities and differences in immune responses to and immunopathogenesis of HAV, HBV and HCV infections, which may explain the distinct courses and outcomes of each hepatitis virus infection.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ Antibodies, Neutralizing - immunology
/ Drug use
/ Epitopes
/ Hepatitis Antibodies - immunology
/ Hepatitis Viruses - immunology
/ Hepatitis, Viral, Human - immunology
/ Hepatitis, Viral, Human - metabolism
/ Hepatitis, Viral, Human - pathology
/ Hepatitis, Viral, Human - virology
/ Humans
/ Immunity
/ Killer Cells, Natural - immunology
/ Killer Cells, Natural - metabolism
/ Liver
/ Neonates
/ Proteins
/ Viruses
