There are 350 million people in the world chronically infected with hepatitis B virus (HBV), and about 93 million people are infected in our country. Chronic hepatitis B causes acute and chronic viral hepatitis, which is closely related to the development of liver fibrosis and liver cancer, and seriously threatens human health. After the virus infects the human body, the interaction between the virus and the host determines the outcome of the infection and the outcome of the disease. However, to date, the mechanism by which the virus escapes host defense and chronic hepatitis B is unclear. Therefore, studying the molecular mechanism of the interaction between the virus and the host factor and the persistent infection of the virus will help to design new targeted drugs for the treatment of chronic hepatitis B.
microRNA-122 (miR-122) is specifically expressed in the liver and is the most abundant small RNA in liver cells, playing an important role in liver function and pathology. With the support of "973" and the National Natural Science Foundation, Meng Songdong, a research group of the Institute of Microbiology, Chinese Academy of Sciences, has recently found that miR-122 as a host limiting factor significantly inhibits viral replication. In chronic hepatitis B infection, chronic inflammation and Viral infection caused miR-122 to be down-regulated. Further research revealed that miR-122 regulates viral replication through the cyclin G1 / p53 pathway.
Based on the above research, the research group proposed a new mechanism for chronic hepatitis B infection: chronic hepatitis B infection down-regulates host restricted small RNA and promotes the expression and replication of the virus through the miR-122-cyclin G1 / p53-virus enhancer pathway. This provides a new basis and explanation for further understanding the persistent infection mechanism of HBV virus and the pathogenesis of hepatocellular carcinoma. At the same time, it proposes the feasibility of miR-122 as a potential new generation drug for the treatment of chronic hepatitis B.
The research results were published online in the journal Hepatology.
In chronic hepatitis B infection, miR-122-cyclin G1 / p53-virus enhancer pathway promotes viral expression and replication
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