In this study, the mechanism by which Suramin inhibits the replication of epidemic encephalitis B virus was explored to provide a theoretical basis for its further application in clinical practice. After viral infecti...In this study, the mechanism by which Suramin inhibits the replication of epidemic encephalitis B virus was explored to provide a theoretical basis for its further application in clinical practice. After viral infection of HepG2 and IMR 32 cells, different concentrations of Suramin were added to the culture media, and then the cultural supernatants and infected cells were collected 48 h later. For the evaluation of the curative effect, cytopathic effect (CPE), virus titers, the expression of viral protein and viral RNA were determined by Western blot, RT PCR and in vitro RNA synthesis, respectively. At the concentration of 50 μg/ml of Suramin, HepG2 and IMR 32 infected with epidemic encephalitis B virus decreased by 51.8 % and 0.03 % respectively, as compared with controls. It was suggested that expression of encephalitis B virus proteins NS3 and E was notably reduced by Suramin. This is especially true of E protein. At RNA level, however, no difference in RNA virus was found between Suramin treated virus and non treated cells. Our results suggest that Suramin can inhibit viral replication by blocking the production of viral proteins.展开更多
基金ThisprojectwassupportedbythefundofChineseServiceCenterforScholarlyExchange (No .1999- 36 3)
文摘In this study, the mechanism by which Suramin inhibits the replication of epidemic encephalitis B virus was explored to provide a theoretical basis for its further application in clinical practice. After viral infection of HepG2 and IMR 32 cells, different concentrations of Suramin were added to the culture media, and then the cultural supernatants and infected cells were collected 48 h later. For the evaluation of the curative effect, cytopathic effect (CPE), virus titers, the expression of viral protein and viral RNA were determined by Western blot, RT PCR and in vitro RNA synthesis, respectively. At the concentration of 50 μg/ml of Suramin, HepG2 and IMR 32 infected with epidemic encephalitis B virus decreased by 51.8 % and 0.03 % respectively, as compared with controls. It was suggested that expression of encephalitis B virus proteins NS3 and E was notably reduced by Suramin. This is especially true of E protein. At RNA level, however, no difference in RNA virus was found between Suramin treated virus and non treated cells. Our results suggest that Suramin can inhibit viral replication by blocking the production of viral proteins.
