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Rongtuan Lin

USA

Title: Manipulating the immune response to inhibit virus infection

Biography

Biography: Rongtuan Lin

Abstract

The innate immune response to virus infection plays a critical role in limiting virus multiplication and pathogenesis. Central to the innate antiviral response is the rapid induction of type I interferon (IFN) expression; IFN gene expression is tightly regulated by the recognition of extra- and intra-cellular signals, generated during primary infection.The viral genome or viral replicative intermediates containing 5’triphosphate (5’ppp) RNA binds to RIG-I and ultimately leads to the production of pro-inflammatory cytokines and anti-viral factors, as well as type I interferons (IFNs) that amplifies the antiviral immune response.Given that viral RNA-RIG-I interaction is the initial trigger of the innate and adaptive immune response, an attractive strategy for the development of an efficient and broad spectrumantiviral therapy to inhibit virus infection involves the use of RIG-I agonist that mimic viral RNA to activate the host defense. Our previous study demonstrated that treatment of various cell lines and primary cells with 5’pppRNA in vitro led to protection against infection and replication of a broad range of RNA and DNA viruses. In vivo, intravenous administration of 5’pppRNA protected mice from a challenge with H1N1 and H5N1 Influenza virus. Our recent study shown that5’pppRNA has the ability to counteract Ebola virus infectivity in vitro. We identified STING among a plethora of differentially expressed genes induced by the RIG-I agonist 5’ppp RNA. STING has been identified as an RIG-I signaling cofactor and a critical adaptor protein required for cytosolic DNA and cyclic dinucleotides (CDNs) triggered immune responses.We further detailthe mechanism of STING regulation.Furthermore, our results also unveiled an essential contribution of STING in the establishment of the 5’pppRNA induced antiviral responses during HSV1 infection.Taken together, these observations demonstrate that the STING is induced via RIG-I signaling and up-regulated STING is essential for 5’ppp RNA mediated HSV restriction.