Abstract
BackgroundPersistent hepatitis B virus (HBV) infection causes liver cirrhosis and hepatocellular carcinoma and constitutes a major worldwide health problem. Currently, anti-HBV drugs are limited to peginterferon and nucleos(t)ide analogs, which are costly and have considerable side effects; the development of novel, effective anti-HBV agents is crucial.MethodsCatechins are a major group of compounds found in green tea extract and epigallocatechin gallate (EGCG) has been shown to have antiviral properties, including inhibition of cellular entry by HBV. FRG (Fah−/−/ Rag2−/−/ IL-2Rγ/−) mice were used in this study to generate chimeras carrying human primary hepatocytes, to facilitate investigation of the inhibitory effect of EGCG on HBV infection.ResultsHere, we show the inhibitory effect of EGCG on HBV infection and replication in HuS-E/2 cells. The inhibitory effect of EGCG on HBV infection in vivo was confirmed by monitoring HBV DNA and HBsAg in serum and immunostaining the liver tissues of the human liver chimeric mice.ConclusionsThe effects of EGCG suggest a robust strategy for the treatment of HBV infection and EGCG may have therapeutic potential for the treatment of HBV-associated liver diseases.
Highlights
Persistent hepatitis B virus (HBV) infection causes liver cirrhosis and hepatocellular carcinoma and constitutes a major worldwide health problem
We found that epigallocatechin gallate (EGCG), a flavonoid that belongs to the subclass of catechins and is present in green tea extract, has antiviral and anti-oncogenic properties [14,15,16] and is able to inhibit HBV entry and contribute to decreased HBV replication in vitro [17]
Inhibitory effect of EGCG on HBV infection To evaluate the effects of EGCG on HBV infectivity and replication, HuS-E/2 cells were infected with HBV derived from HepG2.2.15 cells in the presence of EGCG
Summary
Persistent hepatitis B virus (HBV) infection causes liver cirrhosis and hepatocellular carcinoma and constitutes a major worldwide health problem. Hepatitis B virus (HBV) infection is a major cause of acute and chronic viral hepatitis in humans, with the risk of development of cirrhosis and hepatocellular carcinoma (HCC) [1]. The nucleocapsid is surrounded by an envelope, which contains three types of hepatitis B surface antigen (HBsAg), the small (S), medium (M) and large (L) forms, with distinct functions [5]. These proteins are encoded by one open reading frame, with three in-phase start codons. The LHBsAg protein plays pivotal roles in the viral entry process [7, 8] and, recently, sodium
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