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dc.contributor.author | Matía, Alejandro | |
dc.contributor.author | Lorenzo, Maria M | |
dc.contributor.author | Romero-Estremera, Yolimar C | |
dc.contributor.author | Sánchez-Puig, Juana M | |
dc.contributor.author | Zaballos, Ángel | |
dc.contributor.author | Blasco, Rafael | |
dc.date.accessioned | 2023-05-08T09:30:27Z | |
dc.date.available | 2023-05-08T09:30:27Z | |
dc.date.issued | 2022-12 | |
dc.identifier.citation | PLoS Pathog. 2022 Dec 27;18(12):e1010800. | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/16011 | |
dc.description.abstract | Genome-wide genetic screens are powerful tools to identify genes that act as host factors of viruses. We have applied this technique to analyze the infection of HeLa cells by Vaccinia virus, in an attempt to find genes necessary for infection. Infection of cell populations harboring single gene inactivations resulted in no surviving cells, suggesting that no single gene knock-out was able to provide complete resistance to Vaccinia virus and thus allow cells to survive infection. In the absence of an absolute infection blockage, we explored if some gene inactivations could provide partial protection leading to a reduced probability of infection. Multiple experiments using modified screening procedures involving replication restricted viruses led to the identification of multiple genes whose inactivation potentially increase resistance to infection and therefore cell survival. As expected, significant gene hits were related to proteins known to act in virus entry, such as ITGB1 and AXL as well as genes belonging to their downstream related pathways. Additionally, we consistently found β2-microglobulin, encoded by the B2M gene, among the screening top hits, a novel finding that was further explored. Inactivation of B2M resulted in 54% and 91% reduced VV infection efficiency in HeLa and HAP1 cell lines respectively. In the absence of B2M, while virus binding to the cells was unaffected, virus internalization and early gene expression were significantly diminished. These results point to β2-microglobulin as a relevant factor in the Vaccinia virus entry process. | es_ES |
dc.description.sponsorship | This work was supported by grants ERTA2014-00006, RTA2017-0066 and PID2021-128466OR-I00 funded by Ministerio de Ciencia e Innovación MCIN/AEI/10.13039/501100011033 as part of the Plan Estatal de Investigación Científica, Desarrollo e Innovación (https://www.ciencia.gob.es) to R.B. A.M. was recipient of a predoctoral contract from Subprograma Estatal de Formación, Programa Estatal de Promoción del Talento y su Empleabilidad en I+D+I, Spain from the Ministerio de Ciencia e Innovación, grant number PRE2018-085415. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Public Library of Science (PLOS) | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject.mesh | Vaccinia | es_ES |
dc.subject.mesh | Vaccinia virus | es_ES |
dc.subject.mesh | Humans | es_ES |
dc.subject.mesh | Clustered Regularly Interspaced Short Palindromic Repeats | es_ES |
dc.subject.mesh | Genetic Testing | es_ES |
dc.subject.mesh | HeLa Cells | es_ES |
dc.subject.mesh | Virus Replication | es_ES |
dc.subject.mesh | beta 2-Microglobulin | es_ES |
dc.title | Identification of β2 microglobulin, the product of B2M gene, as a Host Factor for Vaccinia Virus Infection by Genome-Wide CRISPR genetic screens | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución 4.0 Internacional | * |
dc.identifier.pubmedID | 36574441 | es_ES |
dc.format.volume | 18 | es_ES |
dc.format.number | 12 | es_ES |
dc.format.page | e1010800 | es_ES |
dc.identifier.doi | 10.1371/journal.ppat.1010800 | es_ES |
dc.contributor.funder | Ministerio de Ciencia e Innovación (España) | es_ES |
dc.contributor.funder | Plan Nacional de I+D+i (España) | es_ES |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1553-7374 | es_ES |
dc.relation.publisherversion | https://doi.org/10.1371/journal.ppat.1010800 | es_ES |
dc.identifier.journal | PLoS pathogens | es_ES |
dc.repisalud.centro | ISCIII::Centro Nacional de Microbiología | es_ES |
dc.repisalud.institucion | ISCIII | es_ES |
dc.rights.accessRights | open access | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/ERTA2014-00006 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/RTA2017-0066 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2021-128466OR-I00 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/MCIN/AEI/10.13039/501100011033 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PRE2018-085415 | es_ES |