Special Issue "Hepatitis Viruses"

Guest Editor
Dr. Birke Bartosch
Centre de recherche en cancérologie de Lyon, UMR 5286, UMR_S 1052, Equipe 15, 151 cours Albert Thomas, 69424 Lyon Cedex 03, France
E-Mail:
Phone: +33 472681975
Fax: +33 472681971
Interests: flavivirus; hepatitis C virus; hepatitis B virus; virus-host cell interactions; hepatology; liver physiopathology; antivirals

Dear Colleagues,

Chronic infection with hepatitis viruses B and C (HBV and HCV) has become a significant burden to world health with ca 6% and 3% of the world population being chronic carriers of HBV and HCV, respectively. Acute viral infection progresses to chronicity in 50% to 80% of HCV cases and 5 to 10% of adult HBV cases. Chronic hepatitis is characterized by inflammatory lesions in the liver, in the case of HCV often accompanied by intrahepatic lipid accumulation (steatosis), and progressive fibrosis of variable intensity. Each year, 4 to 5% of chronic hepatitis patients develop cirrhosis and primary liver cancer (hepatocellular carcinoma, HCC). Hepatitis B and C have become the main indications for liver transplantation in industrialised countries and will soon be the leading cause of HCC in Western Europe. The only available treatment of chronic hepatitis C is based on a combination of pegylated interferon (IFN)-a, and ribavirin, and cures only about 50% of cases. However, this rate varies widely with the viral genotype and is most likely a too optimistic estimation, because in most studies patients with advanced fibrosis are excluded. Treatment for HBV is more advanced and consists of nucleoside analogues, but is often complicated by the emmergence of viral resistance.

Due to severe limitations in available in vitro study systems, the biology of HBV and HCV has for a long time remained elusive. With the recent advances in cell culture systems the life cycles of HBV and HCV are now under intense investigation. Clinical observations and in vitro studies imply that HBV and HCV replication induce, in the context of a persistent inflammation, the formation of hepatic lesions and on the long term the development of HCC. While the pathological mechanisms underlying HBV induced liver cirrohsis and hepatocarcinogenesis are thought to share common features with those associated with HCV, they still remain largely ill refined. Chronic HCV infection is commonly associated with insulin resistance, hepatocellular steatosis and fibrosis, phenomena which are suspected to be induced either directly by the virus and/or to require metabolic predispositions. The interplay of insulin resistance, oxidative or ER stress and steatosis are thought to trigger and/or contribute to the formation of hepatic lesions and on the long term the development of HCC. This editorial aims to cover basic information on the life cycle of HBV and HCV and how the replication and assembly of these viruses in their host cells may trigger pathological alterations that lead to liver cancer on the long term.

Dr. Birke Bartosch
Guest Editor

Submission Information

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• Hepatitis C virus
• Hepatitis B virus
• Viral cell entry
• Replication and assembly
• Disease progression and virus induced pathology,
• Hepatocarcinogenesis
• Antivirals and viral escape
• Therapy
• Vaccination