Thomas Lane - December 2, 2020

Thomas Lane, PhD, Professor, Department of Neurobiology & Behavior, University of California, Irvine, United States, "Exploring the roles of microglia in host defense and disease in response to SARS-CoV-2 infection of the CNS"

SARS-CoV-2 infection in particular, compared to SARS-CoV-1 and MERS, results in neurological symptoms in COVID-19 patients. Dr. Lane’s group uses mouse models and single-cell sequencing studies to define how the microglia are affected during viral infection. In mice infected with mouse coronavirus the ablation of microglia results in increased mortality and viral load in the brain and spinal cord. Notably, the overall immunological landscape does not change but B cells do increase with microglial ablation and there is muted activation of CD4 T cells and decreased MHC Class II in macrophages. It was also noted that demyelination was increased in microglial ablated mice as well as a lack of remyelination. In SARS-CoV-2 infection, the lack of microglia did not result in increased clinical presentation but slightly more severe disease with a higher viral load in the brain. They also found that neurons were the primary cellular reservoir for SARS-CoV-2 in the brain. A large amount of the virus was present in the brain stem but differences in demyelination were not observed within the spinal cords. Future studies will interrogate the immune response in the brains of so called COVID-19 “long-haulers”.