Fig. 2

Microglia rapidly respond to CNS viral infection and play critical roles in orchestrating innate and adaptive responses to protect the host. Upon infection and damage, cells secrete nucleotides that microglia sense via purinergic receptors, inducing their subsequent migration to damaged cells. The sensing of damage-associated molecular patterns (DAMPs) leads to microglial activation, which enhances their capacity to sense viral pathogen-associated molecular patterns (PAMPs) and resulting cell damage. Interacting with infected cells allows microglia to sense viral PAMPs and acquire antigens for presentation to T cells. PAMP sensing leads to cytokine responses by microglia. Peli1, which regulates the NF-kB pathway, seems to be critical in inflammatory responses after CNS viral infection. Antigen presentation by microglia is thought to be critical for T-cell responses in the CNS and host protection. Very few studies have been able to assess the cross talk between components of these important functions of microglia. Furthermore, whether one microglial cell is able to perform diverse functions or whether labor is divided among cells in this context remains unknown.