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Pathogen Page
Hepatitis B virus
I. General Information
1. NCBI Taxonomy ID:
10407
2. Disease:
Hepatitis B
3. Introduction
Hepatitis B virus is a DNA virus that infects the liver of hominoidae (including humans) and causes hepatitis. It has caused epidemics in parts of Asia and Africa. About a third of the world's population, more than 2 billion people, have been infected with the hepatitis B virus. The acute illness causes liver inflammation, vomiting, jaundice and - rarely - death. Chronic hepatitis B may eventually cause liver cirrhosis and liver cancer. This disease is preventable by vaccination (Wiki: Hepatitis B).
4. Microbial Pathogenesis
HBV primarily interferes with the functions of the liver by replicating in hepatocytes. HBV virions bind to the host cell via the preS domain of the viral surface antigen, leading to subsequent internalization through endocytosis. HBV-preS specific receptors are primarily expressed on hepatocytes. During HBV infection, the host immune response causes both hepatocellular damage and viral clearance. The innate immune response does not play a significant role in these processes. The adaptive immune response, particularly virus-specific cytotoxic T lymphocytes (CTLs), contributes to most of the liver injury associated with HBV infection. Liver damage is initiated and mediated by the CTLs. Antigen-nonspecific inflammatory cells can worsen CTL-induced immunopathology (Wiki: Hepatitis B).
5. Host Ranges and Animal Models
Hepatitis B virus infects the liver of apes including humans (Wiki: Hepatitis B).
6. Host Protective Immunity
During HBV infection, the host immune response causes both hepatocellular damage and viral clearance. Although the innate immune response does not play a significant role in these processes, the adaptive immune response, particularly virus-specific cytotoxic T lymphocytes (CTLs), contributes to most of the liver injury associated with HBV infection. By killing infected cells and by producing antiviral cytokines capable of purging HBV from viable hepatocytes, CTLs eliminate the virus. Although liver damage is initiated and mediated by the CTLs, antigen-nonspecific inflammatory cells can worsen CTL-induced immunopathology, and platelets activated at the site of infection may facilitate the accumulation of CTLs in the liver (Wiki: Hepatitis B).
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