ArticleRevista do Instituto de Medicina Tropical de Sao Paulo2026
Circulating cell-free mitochondrial DNA as a candidate marker of hyperinflammation and immune activation in pre-adolescents, adolescents and young adults with COVID-19 and comorbidities.
Article in Revista do Instituto de Medicina Tropical de Sao Paulo, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Phase-dependent dynamics of circulating cell-free mitochondrial DNA reflect distinct immunometabolic states.Revista do Instituto de Medicina Tropical de Sao Paulo · 2026Article
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9 authors.
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Abstract
Youth encompasses pre-adolescence (10-14 years), adolescence (15-17 years), and young adulthood (18-24 years). Adolescents in general, particularly those with comorbidities, appear more susceptible to severe COVID-19, a vulnerability also observed in newborns and young infants. The mechanisms underlying this increased risk remain unclear, highlighting the need for early disease biomarkers. Circulating cell-free mitochondrial DNA (ccf-mtDNA), a damage-associated molecular pattern (DAMP), has been linked to systemic inflammation and immune activation during viral infections. This study evaluated plasma ccf-mtDNA levels in pre-adolescents, adolescents, and young adults with and without COVID-19, all presenting respiratory symptoms and predominantly harboring comorbidities, some with coinfections by other respiratory viruses. In this prospective study of 88 participants aged 12-21 years, half tested positive and half negative for SARS-CoV-2 by Reverse-Transcribed Polymerase Chain Reaction (RT-PCR). Comorbidities were present in 75% of COVID-19-positive and 54.5% of COVID-19-negative participants. Coinfections were detected in 52.3% and 25% of tested participants, respectively. Plasma ccf-mtDNA was quantified by a quantitative Real Time PCR (qPCR) targeting the mitochondrial NADH dehydrogenase 2 (ND2) gene or MT-ND2. COVID-19-positive participants exhibited significantly higher ccf-mtDNA levels than both symptomatic COVID-19-negative individuals and healthy controls (p<0.001). Although median levels were numerically higher in severe/critical compared with mild/moderate cases (7,769 vs. 4,649 ccf-mtDNA/mL), the difference was not statistically significant, likely due to limited sample size. In conclusion, elevated ccf-mtDNA distinguishes young individuals with COVID-19 and comorbidities from non-COVID-19 symptomatic participants and healthy controls. Although not linked to disease severity in this preliminary study, ccf-mtDNA may serve as an early biomarker of SARS-CoV-2-induced hyperinflammation and immune activation, supporting further targeted clinical investigations.
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