Tetraspanin CD81 regulates HSV-1 infection

Different members of the tetraspanin superfamily have been described to regulate different virus infectious cycles at several stages: viral entry, viral replication or virion exit or infectivity. In addition, tetraspanin CD81 regulates HIV reverse transcription through its association with the dNTP...

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Autores: Benayas, Beatriz, Sastre, Isabel, López-Martín, Soraya, Oo, Adrian, Kim, Baek, Bullido, María Jesús, Aldudo, Jesús, Yáñez-Mó, María
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2020
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/239168
Acceso en línea:http://hdl.handle.net/10261/239168
Access Level:acceso abierto
Palabra clave:Tetraspanin CD81
Herpes simplex-1
SAMHD1
Viral replication
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spelling Tetraspanin CD81 regulates HSV-1 infectionBenayas, BeatrizSastre, IsabelLópez-Martín, SorayaOo, AdrianKim, BaekBullido, María JesúsAldudo, JesúsYáñez-Mó, MaríaTetraspanin CD81Herpes simplex-1SAMHD1Viral replicationDifferent members of the tetraspanin superfamily have been described to regulate different virus infectious cycles at several stages: viral entry, viral replication or virion exit or infectivity. In addition, tetraspanin CD81 regulates HIV reverse transcription through its association with the dNTP hydrolase SAMHD1. Here we aimed at analysing the role of CD81 in Herpes simplex virus 1 infectivity using a neuroblastoma cell model. For this purpose, we generated a CD81 KO cell line using the CRISPR/Cas9 technology. Despite being CD81 a plasma membrane protein, CD81 KO cells showed no defects in viral entry nor in the expression of early protein markers. In contrast, glycoprotein B and C, which require viral DNA replication for their expression, were significantly reduced in CD81 KO infected cells. Indeed, HSV-1 DNA replication and the formation of new infectious particles were severely compromised in CD81 KO cells. We could not detect significant changes in SAMHD1 total expression levels, but a relocalization into endosomal structures was observed in CD81 KO cells. In summary, CD81 KO cells showed impaired viral DNA replication and produced greatly diminished viral titers.BIO2017-86500-R from Ministerio Español de Economía y Competitividad (MINECO) to MY-M and SAF2017-85747-R to MJB as well as USA NIH R01 AI136581 and AI150451 to BK. The institutional grants of Fundación Ramón Areces and Banco de Santander to the Centro de Biología Molecular Severo OchoaSpringer NatureMinisterio de Economía y Competitividad (España)Fundación Ramón ArecesBanco SantanderConsejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]2021202120202021info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_6501Publisher's versioninfo:eu-repo/semantics/publishedVersionhttp://hdl.handle.net/10261/239168reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)Ingléshttp://dx.doi.org/10.1007/s00430-020-00684-0Síinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/2391682026-05-22T06:33:51Z
dc.title.none.fl_str_mv Tetraspanin CD81 regulates HSV-1 infection
title Tetraspanin CD81 regulates HSV-1 infection
spellingShingle Tetraspanin CD81 regulates HSV-1 infection
Benayas, Beatriz
Tetraspanin CD81
Herpes simplex-1
SAMHD1
Viral replication
title_short Tetraspanin CD81 regulates HSV-1 infection
title_full Tetraspanin CD81 regulates HSV-1 infection
title_fullStr Tetraspanin CD81 regulates HSV-1 infection
title_full_unstemmed Tetraspanin CD81 regulates HSV-1 infection
title_sort Tetraspanin CD81 regulates HSV-1 infection
dc.creator.none.fl_str_mv Benayas, Beatriz
Sastre, Isabel
López-Martín, Soraya
Oo, Adrian
Kim, Baek
Bullido, María Jesús
Aldudo, Jesús
Yáñez-Mó, María
author Benayas, Beatriz
author_facet Benayas, Beatriz
Sastre, Isabel
López-Martín, Soraya
Oo, Adrian
Kim, Baek
Bullido, María Jesús
Aldudo, Jesús
Yáñez-Mó, María
author_role author
author2 Sastre, Isabel
López-Martín, Soraya
Oo, Adrian
Kim, Baek
Bullido, María Jesús
Aldudo, Jesús
Yáñez-Mó, María
author2_role author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Ministerio de Economía y Competitividad (España)
Fundación Ramón Areces
Banco Santander
Consejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]
dc.subject.none.fl_str_mv Tetraspanin CD81
Herpes simplex-1
SAMHD1
Viral replication
topic Tetraspanin CD81
Herpes simplex-1
SAMHD1
Viral replication
description Different members of the tetraspanin superfamily have been described to regulate different virus infectious cycles at several stages: viral entry, viral replication or virion exit or infectivity. In addition, tetraspanin CD81 regulates HIV reverse transcription through its association with the dNTP hydrolase SAMHD1. Here we aimed at analysing the role of CD81 in Herpes simplex virus 1 infectivity using a neuroblastoma cell model. For this purpose, we generated a CD81 KO cell line using the CRISPR/Cas9 technology. Despite being CD81 a plasma membrane protein, CD81 KO cells showed no defects in viral entry nor in the expression of early protein markers. In contrast, glycoprotein B and C, which require viral DNA replication for their expression, were significantly reduced in CD81 KO infected cells. Indeed, HSV-1 DNA replication and the formation of new infectious particles were severely compromised in CD81 KO cells. We could not detect significant changes in SAMHD1 total expression levels, but a relocalization into endosomal structures was observed in CD81 KO cells. In summary, CD81 KO cells showed impaired viral DNA replication and produced greatly diminished viral titers.
publishDate 2020
dc.date.none.fl_str_mv 2020
2021
2021
2021
dc.type.none.fl_str_mv info:eu-repo/semantics/article
http://purl.org/coar/resource_type/c_6501
Publisher's version
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10261/239168
url http://hdl.handle.net/10261/239168
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv http://dx.doi.org/10.1007/s00430-020-00684-0
Sí
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv Springer Nature
publisher.none.fl_str_mv Springer Nature
dc.source.none.fl_str_mv reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC
instname:Consejo Superior de Investigaciones Científicas (CSIC)
instname_str Consejo Superior de Investigaciones Científicas (CSIC)
reponame_str DIGITAL.CSIC. Repositorio Institucional del CSIC
collection DIGITAL.CSIC. Repositorio Institucional del CSIC
repository.name.fl_str_mv
repository.mail.fl_str_mv
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