Mehul S Suthar, PhD
Assistant Professor within the Emory Vaccine Center
Dr. Suthar is currently applying an innovative systems biology approach to understand the complex and dynamic signaling networks that control innate immunity to virus infection.Using a combination of high-throughput technology, computational analysis, and pathway-specific modeling, these studies are aimed at revealing tissue and cell-specific gene regulatory signaling networks and antiviral effector genes that control virus infection and regulate innate antiviral immunity.
His research has focused on defining the host innate immune response programs that control West Nile virus infection. His initial work, published in PLoS Pathogens, demonstrates the importance of the RIG-I like receptors in eliciting effective and integrated innate and adaptive immune responses to WNV infection. The key findings from this study show that: 1) RLR signaling through MAVS is required for triggering an innate response to WNV in the key target cells of infection; and 2) loss of RLR signaling causes dysregulation of cell-mediated and humoral adaptive immune responses, characterized by uncontrolled expansion of virus-specific CD8+ T cells, reduced T-regulatory cells, and altered humoral immunity. This study revealed that the RLR signaling pathway mediates an important interface in coordinating innate and adaptive immunity against viral infection by regulating both the quantity and quality of the immune response. Dr. Suthar has continued to study the role of the RLR pathway in directing immunity to WNV infection, focusing on the roles of each RLR within the RLR family, including RIG-I, MDA5, and LGP2. His recent work, published in Immunity, demonstrated that LGP2 functions in a cell-intrinsic manner to promote CD8+ T cell survival and effector functions in response to RNA virus infection. In addition, Dr. Suthar has published a number of collaborative studies describing the role of innate immune signaling factors, including IRF-1, IRF-3, IRF-5, IRF-7, TLR3, MyD88, and NOS2, in regulating WNV infection and immunity.