Glial cell response to Epstein-Barr Virus infection: A plausible contribution to virus-associated inflammatory reactions in the brain.

Epstein-Barr Virus (EBV) is clinically related to various neurological ailments. The manipulation of neural homeostasis through altered glial cells functions is enigmatic. We investigated EBV mediated nuances in glial cells through direct infection (group-1) or by supplementing them with EBV-infected lymphocytes (PBMCs) supernatant (group-3). Also, the cells were co-cultured with infected PBMCs (group-2). Upon confirmation of infection in U-87 MG through qRT-PCR, the gene expression of crucial molecules was analysed. We reported enhanced expression of IL6 in group-1 and 3 unlike group-2. PBMCs migrated and invaded the matrigel significantly when exposed to group-1 and 3 conditions. Thus, EBV may aid neuroinflammatory reactions through PBMCs infiltration. Also, the exposure of neurons to conditioned supernatant from group-2 caused reduced neuronal healing. Additionally, group-1 milieu contained chemical modulators that induced glial cells death and reduced NF-κB. Conclusively, the three modes of EBV infection can influence glial cells' functions to maneuver the microenvironment distinctly.