Dengue virus (DNV) is an arthropod-borne virus that infects near to 400 million humans per year. To establish a productive infection in the host, DENV needs to counteract the host innate immune system, particularly the type I interferon (IFN) system. DENV interferes with both the production and signaling of type I IFN pathways through the expression of viral proteins that specifically target adaptor molecules involved in these essential host responses to pathogens.
Our group showed that the DENV protease complex NS2B3 is able to interact and cleave the adaptor STING to inhibit the activation of IRF3 in infected cells. Recent reports have shown anti flavivirus activity of the newly described pattern recognition receptor (PRR) cGAS, which after activation generate a second messenger (cGAMP) that in turn activates the adaptor STING and subsequently the induction of type I IFN. We are investigating how the cGAS/STING pathway is triggered during DENV infection and the role of the NS2B3 protease complex in the inhibition of type I IFN induction induced by cGAS. Our group also investigates the role of the DENV untranslated regions (UTR) in triggering type I IFN responses in the host and developing novel model systems to study DENV infection.Event Contact: