Abstract
Among seven human hepatitis viruses (A to E, G and TT virus), hepatitis B (HBV) and C (HCV) viruses are able to persist in the host for years and principally contribute to the establishment of chronic hepatitis. During the course of persistent infection, continuous intrahepatic inflammation maintains a cycle of liver cell destruction and regeneration that often terminates in hepatocellular carcinoma (HCC). While the expression and retention of viral proteins in hepatocytes may influence the severity and progression of liver disease, the mechanisms of liver injury in viral hepatistis are defined to be due not to the direct cytopathic effects of viruses, but to the host immune response to viral proteins expressed by infected hepatocytes. In the process of liver injury, hepatocellular death (apoptosis) induced by the proapoptotic molecules of T cells activated following antigen recognition triggers a cascade of antigen nonspecific effector systems and causes necroinflammatory disease. Accordingly, the regulation of the immune response, e.g., via the cell death pathways, in chronically infected patients should prevent the development of HCC.
Keywords: viral hepatitis, hepatitis viruses, hepatitis b, hepatocellular carcinoma
Current Molecular Medicine
Title: Mechanisms of Viral Hepatitis Induced Liver Injury
Volume: 3 Issue: 6
Author(s): Yasunari Nakamoto and Shuichi Kaneko
Affiliation:
Keywords: viral hepatitis, hepatitis viruses, hepatitis b, hepatocellular carcinoma
Abstract: Among seven human hepatitis viruses (A to E, G and TT virus), hepatitis B (HBV) and C (HCV) viruses are able to persist in the host for years and principally contribute to the establishment of chronic hepatitis. During the course of persistent infection, continuous intrahepatic inflammation maintains a cycle of liver cell destruction and regeneration that often terminates in hepatocellular carcinoma (HCC). While the expression and retention of viral proteins in hepatocytes may influence the severity and progression of liver disease, the mechanisms of liver injury in viral hepatistis are defined to be due not to the direct cytopathic effects of viruses, but to the host immune response to viral proteins expressed by infected hepatocytes. In the process of liver injury, hepatocellular death (apoptosis) induced by the proapoptotic molecules of T cells activated following antigen recognition triggers a cascade of antigen nonspecific effector systems and causes necroinflammatory disease. Accordingly, the regulation of the immune response, e.g., via the cell death pathways, in chronically infected patients should prevent the development of HCC.
Export Options
About this article
Cite this article as:
Nakamoto Yasunari and Kaneko Shuichi, Mechanisms of Viral Hepatitis Induced Liver Injury, Current Molecular Medicine 2003; 3 (6) . https://dx.doi.org/10.2174/1566524033479591
DOI https://dx.doi.org/10.2174/1566524033479591 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Rationalizing the Study of Plants for the Treatment of Oral Pain
Current Chemical Biology Targeting Mammalian Target of Rapamycin: Prospects for the Treatment of Inflammatory Bowel Diseases
Current Medicinal Chemistry Pathogenic Bacterial Proteins and their Anti-Inflammatory Effects in the Eukaryotic Host
Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry Evaluation of Hyperforin Analogues for Inhibition of 5-lipoxygenase
Medicinal Chemistry FDA-approved Drugs Selected Using Virtual Screening Bind Specifically to G-quadruplex DNA
Current Pharmaceutical Design Treatment of MDR1 Mutant Dogs with Macrocyclic Lactones
Current Pharmaceutical Biotechnology The Interplay Between Inflammation and Oxidative Stress in Carcinogenesis
Current Molecular Medicine Chemoprevention with Phytonutrients and Microalgae Products in Chronic Inflammation and Colon Cancer
Current Pharmaceutical Design Poor Safety and Tolerability Hamper Reaching a Potentially Therapeutic Dose in the Use of Thalidomide for Alzheimer’s Disease: Results from a Double-Blind, Placebo-Controlled Trial
Current Alzheimer Research Avian Cytokines - An Overview
Current Pharmaceutical Design Elicitation of Immune Responsiveness Against Antigenic Challenge in Age- Related Diseases: Effects of Red Wine Polyphenols
Current Pharmaceutical Design Mobile Phone Based Biomedical Imaging Technology: A Newly Emerging Area
Recent Patents on Biomedical Engineering (Discontinued) An Aggressive Medical Approach for Inflammatory Bowel Disease: Clinical Challenges and Therapeutic Profiles in a Retrospective Hospitalbased Series
Current Clinical Pharmacology Dysregulated Post-Transcriptional Control of COX-2 Gene Expression in Cancer
Current Pharmaceutical Design Bombacaceae Between the Ethnomedical Uses and Pharmacological Evidences: A Review
The Natural Products Journal Vesicovaginal Fistula
Current Women`s Health Reviews Design of Lanthanide Complex Probes for Highly Sensitive Time-Resolved Fluorometric Detection Methods and Its Application to Biochemical, Environmental and Clinical Analyses
Current Analytical Chemistry Modification of Decoy Oligodeoxynucleotides to Achieve the Stability and Therapeutic Efficacy
Current Topics in Medicinal Chemistry Bevacizumab for Malignant Brain Gliomas. Which is the Current Evidence?
Recent Patents on Inflammation & Allergy Drug Discovery Applications of Nucleic Acid Drugs for Organ Transplantation
Current Topics in Medicinal Chemistry