Dephosphorylation of eIF2α Mediated by the γ 1 34.5 Protein of Herpes Simplex Virus 1 Facilitates Viral Neuroinvasion-Reference-Cited by-同舟云学术

Dephosphorylation of eIF2α Mediated by the γ 1 34.5 Protein of Herpes Simplex Virus 1 Facilitates Viral Neuroinvasion

Published:2009-12 Issue:23 Volume:83 Page:12626-12630
ISSN:0022-538X
Container-title:Journal of Virology
language:en
Short-container-title:J Virol

Author:

Verpooten Dustin¹,Feng Zongdi¹,Valyi-Nagy Tibor²,Ma Yijie¹,Jin Huali¹,Yan Zhipeng¹,Zhang Cuizhu³,Cao Youjia³,He Bin¹

Affiliation:

1. Department of Microbiology and Immunology

2. Department of Pathology, College of Medicine, University of Illinois, Chicago, Illinois 60612

3. Tianjin Key Laboratory of Protein Sciences, College of Life Sciences, Nankai University, Tianjin 300071, People's Republic of China

Abstract

ABSTRACT The γ 1 34.5 protein, a virulence factor of herpes simplex viruses, redirects protein phosphatase 1 to dephosphorylate the α subunit of translation initiation factor 2 (eIF2α). Additionally, it inhibits the induction of antiviral genes by TANK-binding kinase 1. Nevertheless, its precise role in vivo remains to be established. Here we show that eIF2α dephosphorylation by γ 1 34.5 is crucial for viral neuroinvasion. V 193 E and F 195 L substitutions in γ 1 34.5 abrogate viral replication in the eye and spread to the trigeminal ganglia and brain. Intriguingly, inhibition of antiviral gene induction by γ 1 34.5 is not sufficient to exhibit viral virulence.

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

Link

https://journals.asm.org/doi/pdf/10.1128/JVI.01431-09

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