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Volume 6, Issue 2 (Suppl) Virol-mycol
ISSN: 2161-0517 VMID, an open access journal Virology Asia 2017
May 11-12, 2017
May 11-12, 2017 Singapore
10th World Congress on
Virology and Mycology
Unappreciated role of type-I interferon signaling in HBV and HCV persistent infections and resistance to
interferon therapy
Limin Chen1,2
1University of Toronto, Canada
2Peking Union Medical College, China
Activation of the type-I interferon (IFN) signaling pathway poses the first line of defense against many virus infections, including
HCV and HBV. With the activation of the Jak/STAT signaling leading to the increased expression of several hundred interferon-
stimulated genes (ISGs) in the liver microenvironment, an anti-viral state was established and the virus replication was suppressed.
However, over-activation of the type-I IFN signaling may actually benefit virus leading to its persistent infection. High throughput
gene expression profiling identified 18 differentially-expressed hepatic genes between treatment responders (Rs) and non-responders
(NRs) to IFN treatment of patients chronically infected with HCV. Many of these genes are ISGs and they all showed higher expression
levels in the pretreatment liver tissues of NRs, indicating that over-activation of type I IFN signaling contributes to treatment non-
response leading to persistent infection. Similar findings were observed in chronic HBV infection. Mechanistically, some of these
ISGs, such as ISG15 and ISG16 stimulated HCV replication and blunted IFN anti-HCV activity. In line with our observations, studies
from other labs demonstrated that blocking IFN signaling facilitated viral clearance in chronic infections, such as in LCMV. All these
data point out that type-I IFN signaling is a “double-edged” sword, while activation of this pathway is indeed necessary to control viral
spread, over-activation actually benefits virus to facilitate its persistent infection. Detailed molecular mechanisms warrant further
investigation.
Biography
Limin Chen is a Professor in the Chinese Academy of Medical Sciences (CAMS) and Peking Union Medical College (PUMC) and also an Affiliate Scientist with the
University of Toronto. He is now the Director and Chief Scientific Officer of the Center for Transfusion Transmitted 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 obtained his
MD, MSc in Biochemistry and Molecular Biology in China, PhD in Molecular Genetics at the University of Toronto. He obtained his Postdoctoral training both at the
Merck Research Laboratories and at the Harvard Medical School. Currently, his research focuses on the virus-host interaction of the hepatitis viruses, especially
HCV. 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.
Limin Chen, Virol-mycol 2017, 6:2 (Suppl)