| Hepatitis B virus(HBV),a global high-risk virus,has caused chronic infections in nearly 400 million people.Persistent infection of HBV in hepatocytes leads to a wide range of liver diseases,which often develop into cirrhosis and hepatocellular carcinoma.So far,no way has been found to completely cure HBV.The current antiviral treatment effect is not ideal,it can not completely eliminate the HBV genome,and it will bring great side effects.HBV triggers low levels of inflammatory cytokines during chronic infection to help viral replication and its immune escape.However,the current regulatory mechanisms that trigger low levels of inflammatory cytokine production by HBV are unclear.We found that glutamic-oxaloacetic transaminase 2(GOT2),which is highly expressed in the liver,interacts with lactate dehydrogenase(LDHB),and previous work in this laboratory showed that LDHB has the effect of inhibiting HBV replication,and GOT2 exerts resistance by inhibiting the degradation of the latter.The role of the virus.In principle,LDHB exerts the function of inhibiting viral replication by promoting the activation of MAPK,NF-κB and AKT signaling pathways induced by HBV and the production of pro-inflammatory cytokine TNF-α.The low level of HBV-induced inflammatory factor TNF-α downstream of the MAPK signaling pathway causes HBV to induce a low level of inflammatory response in the body,while overexpression of LDHB up-regulates TNF-α induced by HBV,which activates HBV-specific T cells.Inhibit HBV replication.Our work links virus-inducible innate immunity to metabolic and inflammatory responses.It provides a comprehensive and versatile discussion of the effects of HBV on hepatocytes and identifies some metabolic enzymes that may be resistant to host antiviral immunity or to viruses.The life cycle has an important impact and is quite innovative. |
