Interplay between hepatitis B virus and the type Ⅰ interferon system and new therapeutic strategies / 复旦学报（医学版）

Hepatitis B virus (HBV) infection has been one of the most important public health problems,however,no complete cure is currently available.Although interferon (IFN)-α has been clinically used as a drug for chronic hepatitis B therapy because of its advantages including a higher rate of HBsAg/HBeAg seroconversion and a lower rate of recurrence after cessation of treatment,only 20％ -40 ％ of patients respond well to IFN therapy,thus hampering its clinical application.In recent years,based on the in vitro HBV replication and infection cell models,animal models and patient cohort with hepatitis B and by using a variety of methods,studies have been made.On the one hand,to identify new mechanisms underlying the IFN-and IFN-induced genes-mediated anti-HBV activities and signaling transduction,on the other hand,to reveal the effect and mechanisms of HBV replication and viral proteins in regulating the innate immune signaling pathways and IFN induction and antiviral action,based on which new strategies and approaches for optimization of IFN-based therapy and for a HBV cure have been further explored.This review mainly introduces the research findings of author's group and the future development is prospected.

Interferon inducible transmembrane proteins on influenza a virus infection: Research advances / 国际药学研究杂志

Interferon inducible transmembrane proteins (IFITM) were identified by small interference RNA(siRNA) screening method n 1980s. Its antiviral effect and mechanism have become a research hotspot in recent years. Recent studies have shown that IFITM could block the entry of viruses by multiple pathways. It could restrict the endosomal pathway in influenza A viral replication cycle after viral host binding but prior to viral RNA release. In the endosomal pathway, IFITM nhibited the viral RNA release to cytoplasm by decreasing the expression of clathrin, disturbing the acidified function of vacuolar(v)-ATPase, and disrupting intracellular cholesterol homeostasis. Some reports showed that IFITM could restrict the hemifusion between infectious cells and uninfectious cells. Moreover, IFITM could also nduce the memory CD8 + T cells to selectively maintaining the expression of themselves, thus enhancing the survival of cells.