Long-term mitochondrial and metabolic impairment in lymphocytes of subjects who recovered after severe COVID-19.

Long-term mitochondrial and metabolic impairment in lymphocytes of subjects who recovered after severe COVID-19.

Publication date: Jan 10, 2025

The underlying mechanisms explaining the differential course of SARS-CoV-2 infection and the potential clinical consequences after COVID-19 resolution have not been fully elucidated. As a dysregulated mitochondrial activity could impair the immune response, we explored long-lasting changes in mitochondrial functionality, circulating cytokine levels, and metabolomic profiles of infected individuals after symptoms resolution, to evaluate whether a complete recovery could be achieved. Results of this pilot study evidenced that different parameters of aerobic respiration in lymphocytes of individuals recuperated from a severe course lagged behind those shown upon mild COVID-19 recovery, in basal conditions and after simulated reinfection, and they also showed altered glycolytic capacity. The severe groups showed trends to enhanced superoxide production in parallel to lower OPA1-S levels. Unbalance of pivotal mitochondrial fusion (MFN2, OPA1) and fission (DRP1, FIS1) proteins was detected, suggesting a disruption in mitochondrial dynamics, as well as a lack of structural integrity in the electron transport chain. In serum, altered cytokine levels of IL-1β, IFN-α2, and IL-27 persisted long after clinical recovery, and growing amounts of the latter after severe infection correlated with lower basal and maximal respiration, ATP production, and glycolytic capacity. Finally, a trend for higher circulating levels of 3-hydroxybutyrate was found in individuals recovered after severe compared to mild course. In summary, long after acute infection, mitochondrial and metabolic changes seem to differ in a situation of full recovery after mild infection versus the one evolving from severe infection.

Concepts Keywords
Atp Adult
Lymphocytes COVID-19
Mitochondrial COVID-19
Pilot Cytokines
Recovery Cytokines
Cytokines
Disease severity
Female
Glycolysis
Humans
Immune system
Lymphocytes
Male
Metabolomics
Middle Aged
Mitochondria
Mitochondria
Mitochondrial Dynamics
Pilot Projects
SARS-CoV-2
SARS-CoV-2

Semantics

Type Source Name
disease MESH COVID-19
pathway REACTOME SARS-CoV-2 Infection
disease IDO immune response
disease MESH reinfection
disease IDO production
disease MESH infection
drug DRUGBANK ATP
disease IDO acute infection
disease MESH Long Covid
pathway REACTOME Glycolysis
pathway REACTOME Immune System

Original Article

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