期刊
METABOLITES
卷 12, 期 12, 页码 -出版社
MDPI
DOI: 10.3390/metabo12121206
关键词
COVID-19; atherosclerotic risk; metabolomics; lipidomics; inflammation; long COVID
资金
- SPRI I + D COVID-19 fund (Basque Government)
- BIOEF EITB Maratoia [BIO21/COV/037]
- European Research Council (ERC) [ERC-2018-StG 804236-NEXTGEN-IO]
- ISCiii [DTS21/00094, RYC2018-024183-I]
- Spinnaker Health Research Foundation, WA [PID2019-107956RA-I00]
- McCusker Foundation, WA
- UK MRC
- Department of Jobs, Tourism, Science and Innovation, Government of Western Australian Premier's Fellowship
- Ministerio de Ciencia, Tecnologia e Innovacion (Minciencias)
- Ministerio de Educacion Nacional, Ministerio de Industria, Comercio y Turismo e ICETEX 2a Convocatoria Ecosistema Cientifico - Colombia Cientifica para la Financiacion de Proyectos de I + D + i [792-2017]
- Vicerrectoria de Investigaciones, Pontificia Universidad Javeriana, Bogota, Colombia [FP44842-221-2018]
- Western Australian State Government
- ARC Laureate Fellowship
- MRFF [2014349]
This study investigated the natural history of COVID-19 disease at the molecular level and characterized the metabolic and immunological phenoreversion in hospitalized severe patients and non-hospitalized recovered patients. The findings suggest that acute patients experience metabolic and immunological dysregulation, resulting in a slower recovery time, while non-hospitalized recovered patients do not show any associated metabolic or immune alterations.
After SARS-CoV-2 infection, the molecular phenoreversion of the immunological response and its associated metabolic dysregulation are required for a full recovery of the patient. This process is patient-dependent due to the manifold possibilities induced by virus severity, its phylogenic evolution and the vaccination status of the population. We have here investigated the natural history of COVID-19 disease at the molecular level, characterizing the metabolic and immunological phenoreversion over time in large cohorts of hospitalized severe patients (n = 886) and non-hospitalized recovered patients that self-reported having passed the disease (n = 513). Non-hospitalized recovered patients do not show any metabolic fingerprint associated with the disease or immune alterations. Acute patients are characterized by the metabolic and lipidomic dysregulation that accompanies the exacerbated immunological response, resulting in a slow recovery time with a maximum probability of around 62 days. As a manifestation of the heterogeneity in the metabolic phenoreversion, age and severity become factors that modulate their normalization time which, in turn, correlates with changes in the atherogenesis-associated chemokine MCP-1. Our results are consistent with a model where the slow metabolic normalization in acute patients results in enhanced atherosclerotic risk, in line with the recent observation of an elevated number of cardiovascular episodes found in post-COVID-19 cohorts.
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