2026-05-17T01:24:17Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/187332024-09-21T21:40:56Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927
Repisalud
author
Barturen, Guillermo
author
Carnero-Montoro, Elena
author
Martínez-Bueno, Manuel
author
Rojo-Rello, Silvia
author
Sobrino, Beatriz
author
Porras-Perales, Óscar
author
Alcántara-Domínguez, Clara
author
Bernardo, David
author
Alarcón-Riquelme, Marta E
2024-02-27T15:10:13Z
2024-02-27T15:10:13Z
2022-08-06
10.1038/s41467-022-32357-2
2041-1723
Nature communications
http://hdl.handle.net/10668/19543
35933486
http://hdl.handle.net/20.500.12105/18733
SARS-CoV-2 infection can cause an inflammatory syndrome (COVID-19) leading, in many cases, to bilateral pneumonia, severe dyspnea, and in ~5% of these, death. DNA methylation is known to play an important role in the regulation of the immune processes behind COVID-19 progression, however it has not been studied in depth. In this study, we aim to evaluate the implication of DNA methylation in COVID-19 progression by means of a genome-wide DNA methylation analysis combined with DNA genotyping. The results reveal the existence of epigenomic regulation of functional pathways associated with COVID-19 progression and mediated by genetic loci. We find an environmental trait-related signature that discriminates mild from severe cases and regulates, among other cytokines, IL-6 expression via the transcription factor CEBP. The analyses suggest that an interaction between environmental contribution, genetics, and epigenetics might be playing a role in triggering the cytokine storm described in the most severe cases.
eng
Whole blood DNA methylation analysis reveals respiratory environmental traits involved in COVID-19 severity following SARS-CoV-2 infection.
research article