Role of proteolipid protein in HSV-1 entry in oligodendrocytic cells

Herpes simplex virus type 1 (HSV-1) has the ability to enter many different hosts and cell types by several strategies. This highly prevalent alphaherpesvirus can enter target cells using different receptors and different pathways: fusion at a neutral pH, low-pH-dependent and low-pH-independent endo...

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Bibliographic Details
Authors: Bello-Morales Arroyo, Ángeles Raquel, Tabares López, Enrique, López Guerrero, José Antonio, Crespillo, Antonio Jesús, Praena García, Beatriz, Revilla, Yolanda, García, Elena, Fraile Ramos, Alberto, Baron, Wia, Krummenacher, Claude
Format: article
Publication Date:2016
Country:España
Institution:Universidad Autónoma de Madrid
Repository:Biblos-e Archivo. Repositorio Institucional de la UAM
Language:English
OAI Identifier:oai:repositorio.uam.es:10486/715533
Online Access:http://hdl.handle.net/10486/715533
https://dx.doi.org/10.1371/journal.pone.0147885
Access Level:Open access
Keyword:Viral entry
Herpes simplex virus-1
Flow cytometry
Antibodies
Transfection
Virions
Immunofluorescence
Endocytosis
Biología y Biomedicina / Biología
Medicina
Description
Summary:Herpes simplex virus type 1 (HSV-1) has the ability to enter many different hosts and cell types by several strategies. This highly prevalent alphaherpesvirus can enter target cells using different receptors and different pathways: fusion at a neutral pH, low-pH-dependent and low-pH-independent endocytosis. Several cell receptors for viral entry have been described, but several observations suggest that more receptors for HSV-1 might exist. In this work, we propose a novel role for the proteolipid protein (PLP) in HSV-1 entry into the human oligodendrocytic cell line HOG. Cells transfected with PLP-EGFP showed an increase in susceptibility to HSV-1. Furthermore, the infection of HOG and HOG-PLP transfected cells with the R120vGF virus-unable to replicate in ICP4-defficient cells-showed an increase in viral signal in HOG-PLP, suggesting a PLP involvement in viral entry. In addition, a mouse monoclonal antibody against PLP drastically inhibited HSV-1 entry into HOG cells. PLP and virions colocalized in confocal immunofluorescence images, and in electron microscopy images, which suggest that PLP acts at the site of entry into HOG cells. Taken together these results suggest that PLP may be involved in HSV-1 entry in human oligodendrocytic cells