Microglia Do Not Restrict SARS-CoV-2 Replication following Infection of the Central Nervous System of K18-Human ACE2 Transgenic Mice
Gema M. Olivarria, Yuting Cheng, Susana Furman, Collin Pachow, Lindsay A. Hohsfield, Charlene Smith-Geater, Ricardo Miramontes, Jie Wu, Mara S. Burns, Kate I. Tsourmas, Jennifer Stocksdale, Cynthia Manlapaz, William H. Yong, John R. Teijaro, Robert A. Edwards, Kim N. Green, Leslie M. Thompson, Thomas E. Lane
Abstract
Understanding the immunological mechanisms contributing to both host defense and disease following viral infection of the CNS is of critical importance given the increasing number of viruses that are capable of infecting and replicating within the nervous system. With this in mind, the present study was undertaken to evaluate the role of microglia in aiding in host defense following experimental infection of the central nervous system (CNS) of K18-hACE2 with SARS-CoV-2, the causative agent of COVID-19. Neurologic symptoms that range in severity are common in COVID-19 patients and understanding immune responses that contribute to restricting neurologic disease can provide important insight into better understanding consequences associated with SARS-CoV-2 infection of the CNS.