Interplay between autophagy and herpes simplex virus type 1: ICP34.5, one of the main actors

Herpes simplex virus type 1 (HSV-1) is a neurotropic virus that occasionally may spread to the central nervous system (CNS), being the most common cause of sporadic encephalitis. One of the main neurovirulence factors of HSV-1 is the protein ICP34.5, which although it initially seems to be relevant...

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Authors: Ripa Peralta, Inés, Andreu Satué, Sabina, López Guerrero, José Antonio, Bello-Morales Arroyo, Ángeles Raquel
Format: article
Publication Date:2022
Country:España
Institution:Universidad Autónoma de Madrid
Repository:Biblos-e Archivo. Repositorio Institucional de la UAM
Language:English
OAI Identifier:oai:repositorio.uam.es:10486/706012
Online Access:http://hdl.handle.net/10486/706012
https://dx.doi.org/10.3390/ijms232113643
Access Level:Open access
Keyword:Autophagy
Herpes Simplex
Herpesvirus 1, Human
Virus Replication
Antivirus Agent
Viral Proteins
Biología y Biomedicina / Biología
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spelling Interplay between autophagy and herpes simplex virus type 1: ICP34.5, one of the main actorsRipa Peralta, InésAndreu Satué, SabinaLópez Guerrero, José AntonioBello-Morales Arroyo, Ángeles RaquelAutophagyHerpes SimplexHerpesvirus 1, HumanVirus ReplicationAntivirus AgentViral ProteinsBiología y Biomedicina / BiologíaHerpes simplex virus type 1 (HSV-1) is a neurotropic virus that occasionally may spread to the central nervous system (CNS), being the most common cause of sporadic encephalitis. One of the main neurovirulence factors of HSV-1 is the protein ICP34.5, which although it initially seems to be relevant only in neuronal infections, it can also promote viral replication in non-neuronal cells. New ICP34.5 functions have been discovered during recent years, and some of them have been questioned. This review describes the mechanisms of ICP34.5 to control cellular antiviral responses and debates its most controversial functions. One of the most discussed roles of ICP34.5 is autophagy inhibition. Although autophagy is considered a defense mechanism against viral infections, current evidence suggests that this antiviral function is only one side of the coin. Different types of autophagic pathways interact with HSV-1 impairing or enhancing the infection, and both the virus and the host cell modulate these pathways to tip the scales in its favor. In this review, we summarize the recent progress on the interplay between autophagy and HSV-1, focusing on the intricate role of ICP34.5 in the modulation of this pathway to fight the battle against cellular defensesMDPIDepartamento de Biología MolecularFacultad de Ciencias20222022-11-07research articlehttp://purl.org/coar/resource_type/c_2df8fbb1VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10486/706012https://dx.doi.org/10.3390/ijms232113643reponame:Biblos-e Archivo. Repositorio Institucional de la UAMinstname:Universidad Autónoma de MadridInglésengopen accesshttp://purl.org/coar/access_right/c_abf2info:eu-repo/semantics/openAccessoai:repositorio.uam.es:10486/7060122026-06-23T12:46:27Z
dc.title.none.fl_str_mv Interplay between autophagy and herpes simplex virus type 1: ICP34.5, one of the main actors
title Interplay between autophagy and herpes simplex virus type 1: ICP34.5, one of the main actors
spellingShingle Interplay between autophagy and herpes simplex virus type 1: ICP34.5, one of the main actors
Ripa Peralta, Inés
Autophagy
Herpes Simplex
Herpesvirus 1, Human
Virus Replication
Antivirus Agent
Viral Proteins
Biología y Biomedicina / Biología
title_short Interplay between autophagy and herpes simplex virus type 1: ICP34.5, one of the main actors
title_full Interplay between autophagy and herpes simplex virus type 1: ICP34.5, one of the main actors
title_fullStr Interplay between autophagy and herpes simplex virus type 1: ICP34.5, one of the main actors
title_full_unstemmed Interplay between autophagy and herpes simplex virus type 1: ICP34.5, one of the main actors
title_sort Interplay between autophagy and herpes simplex virus type 1: ICP34.5, one of the main actors
dc.creator.none.fl_str_mv Ripa Peralta, Inés
Andreu Satué, Sabina
López Guerrero, José Antonio
Bello-Morales Arroyo, Ángeles Raquel
author Ripa Peralta, Inés
author_facet Ripa Peralta, Inés
Andreu Satué, Sabina
López Guerrero, José Antonio
Bello-Morales Arroyo, Ángeles Raquel
author_role author
author2 Andreu Satué, Sabina
López Guerrero, José Antonio
Bello-Morales Arroyo, Ángeles Raquel
author2_role author
author
author
dc.contributor.none.fl_str_mv Departamento de Biología Molecular
Facultad de Ciencias
dc.subject.none.fl_str_mv Autophagy
Herpes Simplex
Herpesvirus 1, Human
Virus Replication
Antivirus Agent
Viral Proteins
Biología y Biomedicina / Biología
topic Autophagy
Herpes Simplex
Herpesvirus 1, Human
Virus Replication
Antivirus Agent
Viral Proteins
Biología y Biomedicina / Biología
description Herpes simplex virus type 1 (HSV-1) is a neurotropic virus that occasionally may spread to the central nervous system (CNS), being the most common cause of sporadic encephalitis. One of the main neurovirulence factors of HSV-1 is the protein ICP34.5, which although it initially seems to be relevant only in neuronal infections, it can also promote viral replication in non-neuronal cells. New ICP34.5 functions have been discovered during recent years, and some of them have been questioned. This review describes the mechanisms of ICP34.5 to control cellular antiviral responses and debates its most controversial functions. One of the most discussed roles of ICP34.5 is autophagy inhibition. Although autophagy is considered a defense mechanism against viral infections, current evidence suggests that this antiviral function is only one side of the coin. Different types of autophagic pathways interact with HSV-1 impairing or enhancing the infection, and both the virus and the host cell modulate these pathways to tip the scales in its favor. In this review, we summarize the recent progress on the interplay between autophagy and HSV-1, focusing on the intricate role of ICP34.5 in the modulation of this pathway to fight the battle against cellular defenses
publishDate 2022
dc.date.none.fl_str_mv 2022
2022-11-07
dc.type.none.fl_str_mv research article
http://purl.org/coar/resource_type/c_2df8fbb1
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/10486/706012
https://dx.doi.org/10.3390/ijms232113643
url http://hdl.handle.net/10486/706012
https://dx.doi.org/10.3390/ijms232113643
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv reponame:Biblos-e Archivo. Repositorio Institucional de la UAM
instname:Universidad Autónoma de Madrid
instname_str Universidad Autónoma de Madrid
reponame_str Biblos-e Archivo. Repositorio Institucional de la UAM
collection Biblos-e Archivo. Repositorio Institucional de la UAM
repository.name.fl_str_mv
repository.mail.fl_str_mv
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