The HSV-1 ubiquitin ligase ICP0: modifying the cellular proteome to promote infection

Collados Rodríguez, M. , Dybas, J. M., Hughes, J. , Weitzman, M. D. and Boutell, C. (2020) The HSV-1 ubiquitin ligase ICP0: modifying the cellular proteome to promote infection. Virus Research, 285, 198015. (doi: 10.1016/j.virusres.2020.198015) (PMID:32416261)

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Herpes simplex virus 1 (HSV-1) hijacks ubiquitination machinery to modify the cellular proteome to create an environment permissive for virus replication. HSV-1 encodes its own RING-finger E3 ubiquitin (Ub) ligase, Infected Cell Protein 0 (ICP0), that directly interfaces with component proteins of the Ub pathway to inactivate host immune defences and cellular processes that restrict the progression of HSV-1 infection. Consequently, ICP0 plays a critical role in the infectious cycle of HSV-1 that is required to promote the efficient onset of lytic infection and productive reactivation of viral genomes from latency. This review will describe the current knowledge regarding the biochemical properties and known substrates of ICP0 during HSV-1 infection. We will highlight the gaps in the characterization of ICP0 function and propose future areas of research required to understand fully the biological properties of this important HSV-1 regulatory protein.

Item Type:Articles
Glasgow Author(s) Enlighten ID:Hughes, Dr Joseph and Boutell, Dr Chris and Collados Rodriguez, Dr Milagros
Authors: Collados Rodríguez, M., Dybas, J. M., Hughes, J., Weitzman, M. D., and Boutell, C.
College/School:College of Medical Veterinary and Life Sciences > Institute of Infection Immunity and Inflammation
Journal Name:Virus Research
ISSN (Online):1872-7492
Published Online:13 May 2020
Copyright Holders:Copyright © 2020 The Authors
First Published:First published in Virus Research 285:198015
Publisher Policy:Reproduced under a Creative Commons License

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Project CodeAward NoProject NamePrincipal InvestigatorFunder's NameFunder RefLead Dept
656521The role of ubiquitin and ubiquitin-like proteins during viral infectionChris BoutellMedical Research Council (MRC)MC_UU_12014/5MVLS III - CENTRE FOR VIRUS RESEARCH