Journal
WORLD JOURNAL OF GASTROENTEROLOGY
Volume 20, Issue 35, Pages 12462-12472Publisher
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v20.i35.12462
Keywords
Hepatitis B virus; Hepatitis B virus genotype; Hepatocellular carcinoma; Woodchuck hepatitis virus; Ground squirrel hepatitis virus; Peripheral blood mononuclear cells; Interferon regulatory factor 7; Interleukin-1 receptor-associated kinase 4; TNF receptor-associated factor 3
Categories
Funding
- King Fahd Medical Research Ceneter
- Center of Genomic Medicine
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Chronic active hepatitis (CAH) is acknowledged as an imperative risk factor for the development of liver injury and hepatocellular carcinoma. The histological end points of CAH are chronic inflammation, fibrosis and cirrhosis which are coupled with increased DNA synthesis in cirrhotic vs healthy normal livers. The potential mechanism involved in CAH includes a combination of processes leading to liver cell necrosis, inflammation and cytokine production and liver scaring (fibrosis). The severity of liver damage is regulated by Hepatitis B virus genotypes and viral components. The viral and cellular factors that contribute to liver injury are discussed in this article. Liver injury caused by the viral infection affects many cellular processes such as cell signaling, apoptosis, transcription, DNA repair which in turn induce radical effects on cell survival, growth, transformation and maintenance. The consequence of such perturbations is resulted in the alteration of bile secretion, gluconeogenesis, glycolysis, detoxification and metabolism of carbohydrates, proteins, fat and balance of nutrients. The identification and elucidation of the molecular pathways perturbed by the viral proteins are important in order to design effective strategy to minimize and/or restore the hepatocytes injury. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.
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