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Shaping current European mitochondrial haplogroup frequency in response to infection: the case of SARS-CoV-2 severity.

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dc.contributor.authorCabrera-Alarcon, José Luis
dc.contributor.authorCruz, Raquel
dc.contributor.authorRosa-Moreno, Marina
dc.contributor.authorLatorre-Pellicer, Ana
dc.contributor.authorde Almeida, Silvia Diz
dc.contributor.authorRiancho, José A
dc.contributor.authorRojas-Martinez, Augusto
dc.contributor.authorFlores, Carlos
dc.contributor.authorLapunzina, Pablo
dc.contributor.authorSánchez-Cabo, Fátima
dc.contributor.authorCarracedo, Ángel
dc.contributor.authorEnriquez, José Antonio
dc.contributor.funderFondation Leducq
dc.contributor.funderUnión Europea. Comisión Europea. NextGenerationEU
dc.contributor.funderPlan de Recuperación, Transformación y Resiliencia (España)
dc.contributor.funderMinisterio de Ciencia e Innovación (España)
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
dc.contributor.funderBanco Santander
dc.contributor.funderInstituto de Salud Carlos III
dc.contributor.funderFundación ProCNIC
dc.contributor.funderMinisterio de Ciencia e Innovación. Centro de Excelencia Severo Ochoa (España)
dc.date.accessioned2025-06-16T15:04:19Z
dc.date.available2025-06-16T15:04:19Z
dc.date.issued2025-01-09
dc.description.abstractThe frequency of mitochondrial DNA haplogroups (mtDNA-HG) in humans is known to be shaped by migration and repopulation. Mounting evidence indicates that mtDNA-HG are not phenotypically neutral, and selection may contribute to its distribution. Haplogroup H, the most abundant in Europe, improved survival in sepsis. Here we developed a random forest trained model for mitochondrial haplogroup calling using data procured from GWAS arrays. Our results reveal that in the context of the SARS-CoV-2 pandemic, HV branch were found to represent protective factors against the development of critical SARS-CoV-2 in an analysis of 14,349 patients. These results highlight the role of mtDNA in the response to infectious diseases and support the proposal that its expansion and population proportion has been influenced by selection through successive pandemics.
dc.description.peerreviewedSí
dc.description.tableofcontentsThe authors thank M. M. Muñoz-Hernandez, R. Martínez de Mena and E.R. Martínez Jiménez, for technical assistance. Scheme figures were made with BioRender. We particularly acknowledge all the patients, Banco Nacional de ADN, Biobanco del Sistema de Salud de Aragón, Biobanc Fundació Institut d'Investigació Sanitària Illes Balears, Biobanco del Complexo Hospitalario Universitario de Santiago, Biobanco Vasco, for their collaboration and providing materials. JAE laboratory is supported by: RTI2018-099357-B-I00 and PID2021-1279880B-and TED2021-131611B-I00 funded by MCIN/AEI/10.13039/501100011033 and the, and CIBERFES (CB16/10/00282), Human Frontier Science Program (grant RGP0016/2018), and Leducq Transatlantic Networks (17CVD04). MR-M is supported by a FPI/PRE2021-097721 fellowship. JAE and FSC are supported by TED2021-131611B-I00 funded by MCIN/AEI/10.13039/501100011033 and the European Union “NextGenerationEU”/Plan de Recuperación Transformación y Resiliencia -PRTR. FSC received funding [grant no. PID2022-141527OB-I00] by the MCIN/AEI/10.13039/501100011033/ and by FEDER Una manera de hacer Europa. This work was supported by Fundación Amancio Ortega Gaona, Banco de Santander S.A. and Instituto de Salud Carlos III (COV20/00622) and the European Regional Development Fund. Genotyping service was carried out at CEGEN-PRB3-ISCIII, supported by grant PT17/0019, of the PE I+D+i 2013-2016, funded by ISCIII and ERDF. The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia e Innovación (MCIN) and the Pro CNIC Foundation) and is a Severo Ochoa Center of Excellence (grant CEX2020-001041-S funded by MICIN/AEI/10.13039/501100011033).
dc.identifier.citationCommun Biol. 2025 Jan 9;8(1):33.
dc.identifier.journalCommunications Biology
dc.identifier.pubmedID39789223
dc.identifier.urihttps://hdl.handle.net/20.500.12105/26754
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RTI2018-099357-B-I00
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PID2021-1279880B
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/TED2021-131611B-I00
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/MCIN/AEI/10.13039/501100011033
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PID2022-141527OB-I00
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/COV20/00622
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PT17/0019
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/MICIN/AEI/10.13039/501100011033/CEX2020-001041-S
dc.relation.publisherversionhttps://doi.org/10.1038/s42003-024-07314-y
dc.repisalud.institucionCNIC
dc.repisalud.orgCNICCNIC::Grupos de investigación::Genética Funcional del Sistema de Fosforilación Oxidativa
dc.rights.accessRightsopen access
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.titleShaping current European mitochondrial haplogroup frequency in response to infection: the case of SARS-CoV-2 severity.
dc.typejournal article
dc.type.hasVersionVoR
dspace.entity.typePublication

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