LAUSR

Purpose of review Although viral infections of the central nervous system (CNS) are known to acutely cause pathology in the form of cytokine-mediated neural tissue damage and inflammation, the pathophysiology of neurologic sequelae after viral clearance is incompletely understood. Recent findings Alterations in microglial and glial biology in response to initial infiltration of immune cells that persist within the CNS have recently been shown to promote neuronal dysfunction and cognitive deficits in animal models of viral encephalitis. Summary The current review summarizes the current knowledge on the possible role of innate immune signaling during acute infections as triggers of neurologic sequelae that persist, and may even worsen, after clearance of viral infections within the CNS.