Immunopathogenesis of hepatitis C virus infection

Abstract

Summary Hepatitis C virus, a recently identified member of the family Flaviviridae, is an important cause of chronic viral hepatitis and cirrhosis. There are similarities in the nature of the immune response to this pathogen with immunity in other flavivirus and hepatotropic virus infections, such as hepatitis B. However, the high rate of viral persistence after primary hepatitis C infection, and the observation that neutralizing antibodies are not protective, would suggest that there are a number of important differences between hepatitis C, other flaviviruses, and hepatitis B. The phenomenon of quasispecies evolution and other viral factors have been proposed to contribute to immune evasion by hepatitis C virus. In the face of established persistent infection, virus-specific cytotoxic T lymphocytes may exert some control over viral replication. However, these same effectors may also be responsible for the progressive liver damage characteristic of chronic hepatitis C infection. The nature of protective immunity, including the role of innate immune responses early after hepatitis C exposure, remains to be defined.

Novel Plant Virus-Based Vaccine Induces Protective Cytotoxic T-Lymphocyte-Mediated Antiviral Immunity through Dendritic Cell Maturation

“…Most vaccines promote the production of neutralizing antibodies that offer protection against acute viral infections (24,47). In the context of chronic infections (e.g., hepatitis C virus and human immunodeficiency virus [HIV] infections), neutralizing antibodies are potent in controlling free viral particles but are usually inefficient at eliminating infected cells (4,9,19). Recognition and destruction of infected cells by specific cytotoxic T lymphocytes (CTLs) are essential for carrying out an effective battle against such viruses.…”

Liver Diseases from Lab to Clinic

“…Antigenic peptides derived from the cleavage of exogenous viral proteins are recognized by CD4+ T-helper cells in association with MHC class II molecules on the surface of APC. T-helper lymphocytes have an immunoregulatory function through the secretion of lymphokines that support either Cytotoxic T Lymphocyte (CTL) generation (the T-helper type 1 cytokine profile: IL-2, IFN-γ) or B-cell function and antibody production (the type 2 profile: IL-4, IL-5, IL-10) [6].…”

The functional avidity of virus‐specific CD8+ T cells is down‐modulated in Borna disease virus‐induced immunopathology of the central nervous system

“…However, a number of viruses like Theiler's murine encephalomyelitis virus or the neurotropic JHM strain of mouse hepatitis virus are able to establish a persistent infection in the central nervous system (CNS) despite strong primary CD8 + T cell responses in mice [1][2][3]. In humans, hepatitis B virus (HBV) and hepatitis C virus as well as HIV are able to maintain a chronic infection in the face of high numbers of antiviral CD8 + T cells, leading to liver immunopathology or immune system dysfunction [4][5][6][7]. In patients persistently infected with HIV, it was shown that HIV-specific CD8 + T cells have impaired cytolytic activity [8].…”