Home Acta Virologica 2020 Acta Virologica Vol.64, No.4, p.490-495, 2020

Journal info


Quarterly,
Founded: 1957
ISSN 0001-723X
E-ISSN 1336-2305

Published in English

Aims and Scope
Editorial Info

Abstracted and Indexed
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Acta Virologica Vol.64, No.4, p.490-495, 2020

Title: Neuropathogenic and non-neuropathogenic EHV-1 strains induce the accumulation of hyperphosphorylated Tau in primary murine neurons
Author: J. Cymerys, A. Słońska, M. Chodkowski, A. Golke, M. Krzyżowska, M. W. Bańbura

Abstract: Equid herpesvirus 1 (EHV-1) causes respiratory disease, abortion and neurological disorders in horses. Similarly, to other alphaherpesviruses, EHV-1 is neurotropic and establishes latency in the neurons of its natural host. Despite the fact that many studies have been devoted to the pathogenesis of various clinical forms of EHV-1 infection, mechanisms of the neuronal damage are still not fully understood. The aim of this study was to define the phosphorylation status of tau protein in neuronal cell culture infected with EHV-1. Phosphorylation of tau was tested at tau-ser199/ser202, tau-ser404, tau-ser262, tau-thr181, tau-thr217 and tau-thr205 sites. We described, for the first time, that EHV-1 infection leads to the accumulation of hyperphosphorylated tau in primary murine neurons. We showed that non-neuropathogenic and neuropathogenic EHV-1 strains specifically induce hyperphosphorylation of tau-ser199/ser202, tau-ser404 and tau-thr205 during long-term infection and after a controlled activation of productive infection.

Keywords: tau protein; hyperphosphorylation; equid herpesvirus 1 (EHV-1); neuronal cell culture
Published online: 26-Oct-2020
Year: 2020, Volume: 64, Issue: 4 Page From: 490, Page To: 495
doi:10.4149/av_2020_407


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.