| Biography | |
|---|---|
 Prof. Limin Chen Chinese Academy of Medical Sciences, China |
|
| Title: Type I interferon signaling contributes to HCV and HBV persistent infections | |
| Abstract: Host innate immunity, characterized by the activation of type I interferon signaling and NK cells, poses the 1st line of defense in many virus infections. Using cDNA microarray gene expession profiling, we successfully identified an 18-gene response signature that predicts whether a given patient will respond to the interferon-based therapy or not with 96% accuracy. Most of these genes are interferon stimulated (sensitive) genes (ISGs) and they are all up-regulated in treatment non-responders. We therefore identified an “ISG high” non-responder phenotype characterized by the over-activation of type I IFN signaling leading to increased expression of ISGs, especially ISG15/USP18 ubiquitin-sigaling pathway. Similar findings were observed in HBV non-responders. Further evidence on how increased ISGs affect treatment response status will also be discussed. | |
| Biography: Dr. Limin Chen, a professor with Chinese Academy of Medical Sciences (CAMS)/Peking Union Medical College (PUMC) and also an affiliate scientist with the University of Toronto, now is the director and chief scientific officer of the center for transfusion transmitted infectious diseases, Institute of Blood Transfusion (IBT), CAMS/PUMC, Member of the American Association for Studies of Liver Diseases (AASLD) and Canadian Association for Studies of Liver (CASL). He got his MD, MSc in biochemistry and molecular biology in China, PhD in molecular genetics at the University of Toronto. Dr. Chen obtained his postdoctoral training both at Merck Research Laboratories (West Point, PA) and at the Harvard Medical School (MGH) . Currently Dr. Chen’s research focuses on the virus-host interaction of the transfusion-transmitted viruses, especially on HCV and HBV. He pioneered the work on identification of the response signature and proposed a novel mechanism on how HCV exploits host innate immune response to benefit its persistent infection and resistance to interferon-based therapy. | |
