Dr. Matthew Cain joined the Department of Medicine, Division of Infectious Diseases as an Assistant Professor in July, 2018.
Dr. Cain received his bachelor’s degree from Rhodes College in Memphis, TN. He received his PhD from Washington University in St. Louis. His graduate work with Dr. Kendall Blumer focused on the identification of inner retinal circuits that are sensitive to regulation by Gi/o signaling. Additionally, he characterized the in vivo function of two components of the regulator of G protein signaling 7 (R7-RGS) complex, RGS6 and R7 RGS-binding protein (R7BP), in retinal biology and vision. As a postdoctoral researcher under Dr. Robyn Klein, his research focused on neuroinvasion and host-virus interactions at the blood-brain barrier during Venezuelan equine encephalitis virus infection.
Neurotropic arboviruses, including encephalitic alphaviruses and flaviviruses, are at potential high risk of emergence and increased disease burden both domestically and globally. Despite the potential to cause fatal neuroinvasive disease in subsets of patients, many such viruses currently lack effective vaccines or specific therapies. The blood-brain barrier (BBB) is a structurally and functionally specialized vasculature that limits pathogen infiltration from the periphery into the central nervous system (CNS). Both viral infection and the host-virus interactions that comprise the CNS innate immune response are capable of modulating the functional and structural properties of the BBB. These alterations in the BBB potentially lead to both anti-viral and immunopathogenic outcomes by affecting BBB permeability, viral neuroinvasion, immune cell infiltration, neuroinflammation, and viral clearance during the course of infection. Using mouse models of encephalitic alphavirus and flavivirus infection, we will investigate how neurotropic viral infection is shaped by the interaction between the BBB and the innate immune response. We have specific interests in the mechanisms underlying 1) viral sensing by pattern recognition receptors, 2) BBB-leukocyte interaction, and 3) anti-viral and immunopathogenic cytokine signaling. Greater understanding of these mechanisms are necessary for the identification of potential therapeutic interventions to improve patient outcomes.