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Possible Mechanism of Double-Stranded DNA on Replication of Hepatitis B Virus

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Possible Mechanism of Double-Stranded DNA on Replication of Hepatitis B Virus

Chronic hepatitis B remains a substantial public health burden affecting approximately 350 million individuals worldwide. It is presently much more prevalent in China where the hepatitis B virus (HBV) carriers are almost 10% in the general population. These patients have an elevated risk of liver cirrhosis, hepatocellular carcinoma (HCC), and other severe clinical sequelae. It is therefore a global health priority to cure chronic HBV infection and prevent its dire consequences. Currently approved drugs for treatment of chronic hepatitis B, including alpha interferon and nucleos(t)ide analogue inhibitors, despite get the good therapeutic effect in clinic, but still exhibit limited response, adverse effects, and emergence of drug resistance, and are rarely curative. Therefore, scientists have not stopped their efforts for looking for better drugs to cure this virus infectious disease. Many groups focus on the development of therapy measures using an immunotherapeutic approach such as therapeutic HBV vaccine. The gene delivery vectors for specifically target hepatitis B virus or cellular molecules are often utilized. dsDNA may regulate the replication of HBV in hepatoma cell line HepG2.2.15 in which HBV replicates stably.

 

Yang Y, Liu A, Liu S, Zhang C, Liu X, Huang H, et al. (2013) The Effect and Possible Mechanism of Double-Stranded DNA on Replication of Hepatitis B Virus. J Mol Genet Med 7:89. doi: 10.4172/1747-0862.1000089

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