Dissecting the Epstein–Barr virus entry pathway into astrocytes: unfolding the involvement of endosomal trafficking

Abstract

Aim: Previous reports have suggested successful infection by Epstein–Barr virus (EBV) in various brain cells

however, the entry mechanism is still elusive. In the present study, we investigated the entry pathway of EBV into astrocytes. Materials & methods: For virus entry, receptors are considered as a instrumental moieties for infection. Upon EBV infection, the expression of receptors such as Ephrin, neuropilin and nonmuscle myosin heavy chain-II were assessed in a time-dependent manner. Then, by using inhibitors, we investigated the role of membrane cholesterol, the dynamin protein and, eventually, EBV colocalization in endosomal vesicles. Results: EBV induced changes in the expression of numerous receptors, especially EphA4, EphA10 and NMHC-IIB. Upon binding to its receptor, the virus translocates into the lipid raft region of the plasma membrane, and its depletion results in decreased EBV internalization. The inhibition of dynamin also mitigated EBV entry. Subsequently, EBV colocalized in the endosomal compartment with markers such as EEA1, Rab5, Rab7 and LAMP1. Conclusion: The current work implicitly indicates that EBV follows the endocytic pathway to enter brain cells, although further validation by knocking down these proteins is needed. These findings will further enable us to pinpoint therapeutic targets. © 2024 Informa UK Limited, trading as Taylor & Francis Group.