Please use this identifier to cite or link to this item: https://dspace.iiti.ac.in/handle/123456789/3854
Title: Glial cell response to Epstein-Barr Virus infection: A plausible contribution to virus-associated inflammatory reactions in the brain
Authors: Jakhmola, Shweta
Jha, Hem Chandra
Keywords: immunoglobulin enhancer binding protein;interleukin 6;Article;controlled study;Epstein Barr virus infection;glia cell;human;human cell;nerve cell necrosis;nonhuman;peripheral blood mononuclear cell;priority journal;protein expression;virus encephalitis
Issue Date: 2021
Publisher: Academic Press Inc.
Citation: Jakhmola, S., & Jha, H. C. (2021). Glial cell response to epstein-barr virus infection: A plausible contribution to virus-associated inflammatory reactions in the brain. Virology, 559, 182-195. doi:10.1016/j.virol.2021.04.005
Abstract: 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. © 2021 Elsevier Inc.
URI: https://doi.org/10.1016/j.virol.2021.04.005
https://dspace.iiti.ac.in/handle/123456789/3854
ISSN: 0042-6822
Type of Material: Journal Article
Appears in Collections:Department of Biosciences and Biomedical Engineering

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