Mij
Senior Member (Voting Rights)
Abstract
Long COVID is characterized by persistent symptoms following acute SARS-CoV-2 infection, yet its biological mechanisms remain incompletely understood. Emerging evidence suggests that immune dysregulation, mitochondrial dysfunction, and altered cell survival pathways may contribute to prolonged symptomatology.
In this cross-sectional study, peripheral blood mononuclear cells were collected from individuals with Long COVID approximately 10 months post-infection and from recovered individuals without Long COVID symptoms.
Symptom burden was assessed using a composite domain-based score. mRNA expression of immune and antiviral genes (IL-6, IL-1β, IL-10, SOCS3, HIF-1α, OAS1, MAVS, IFN-α, IFN-γ), anti-apoptotic markers (MCL1, BCL-2, XIAP, LIVIN), cell cycle kinases (CDK4, CDK6), mitochondrial biogenesis and dynamics markers (NRF1, TFAM, PGC-1α, DRP1, MFN1/2, OPA1), and mitophagy regulators (PARKIN, PINK1) were quantified using quantitative real-time PCR. Data was analyzed by SPSS and GraphPad Prism. Individuals with Long COVID demonstrated significantly higher expressions of IL-6, IL-1β, IL-10, SOCS3, HIF-1α, OAS1, MAVS, NRF1, DRP1, PARKIN, MCL1, and LIVIN compared with recovered controls after using the Benjamini–Hochberg False Discovery Rate (FDR) method.
Several transcriptional markers, particularly HIF-1α, IL-1β, IL-10, and NRF1, remained independently associated with symptom burden after adjustment for age and sex. Correlation analysis demonstrated coordinated transcriptional co-expression patterns across immune, antiviral, mitochondrial, and apoptosis-related genes.
Long COVID at 10 months post-infection is associated with coordinated transcriptional alterations across multiple biological pathways. The association of these changes with symptom burden suggests a potential link between persistent immunometabolic activation and clinical manifestations.
These findings are exploratory and highlight the need for longitudinal and functional studies to further elucidate underlying mechanisms.
LINK
Long COVID is characterized by persistent symptoms following acute SARS-CoV-2 infection, yet its biological mechanisms remain incompletely understood. Emerging evidence suggests that immune dysregulation, mitochondrial dysfunction, and altered cell survival pathways may contribute to prolonged symptomatology.
In this cross-sectional study, peripheral blood mononuclear cells were collected from individuals with Long COVID approximately 10 months post-infection and from recovered individuals without Long COVID symptoms.
Symptom burden was assessed using a composite domain-based score. mRNA expression of immune and antiviral genes (IL-6, IL-1β, IL-10, SOCS3, HIF-1α, OAS1, MAVS, IFN-α, IFN-γ), anti-apoptotic markers (MCL1, BCL-2, XIAP, LIVIN), cell cycle kinases (CDK4, CDK6), mitochondrial biogenesis and dynamics markers (NRF1, TFAM, PGC-1α, DRP1, MFN1/2, OPA1), and mitophagy regulators (PARKIN, PINK1) were quantified using quantitative real-time PCR. Data was analyzed by SPSS and GraphPad Prism. Individuals with Long COVID demonstrated significantly higher expressions of IL-6, IL-1β, IL-10, SOCS3, HIF-1α, OAS1, MAVS, NRF1, DRP1, PARKIN, MCL1, and LIVIN compared with recovered controls after using the Benjamini–Hochberg False Discovery Rate (FDR) method.
Several transcriptional markers, particularly HIF-1α, IL-1β, IL-10, and NRF1, remained independently associated with symptom burden after adjustment for age and sex. Correlation analysis demonstrated coordinated transcriptional co-expression patterns across immune, antiviral, mitochondrial, and apoptosis-related genes.
Long COVID at 10 months post-infection is associated with coordinated transcriptional alterations across multiple biological pathways. The association of these changes with symptom burden suggests a potential link between persistent immunometabolic activation and clinical manifestations.
These findings are exploratory and highlight the need for longitudinal and functional studies to further elucidate underlying mechanisms.
LINK