Exploring DNA methylation, telomere length, mitochondrial DNA, and immune function in patients with Long-COVID, 2025, Polli et al

Exploring DNA methylation, telomere length, mitochondrial DNA, and immune function in patients with Long-COVID

Andrea Polli, Lode Godderis, Dries S. Martens, Madhura Shekhar Patil, Jolien Hendrix, Arne Wyns, Jente Van Campenhout, Emma Richter, Lara Fanning, Olivia Vandekerckhove, Eveline Claeys, Wim Janssens, Natalie Lorent

Background
Long-COVID is defined as the persistency or development of new symptoms 3 months after the initial SARS-CoV-2 infection, with these symptoms lasting for at least 2 months with no other explanation. Common persistent symptoms are fatigue, sleep disturbances, post-exertional malaise (PEM), pain, and cognitive problems. Long-COVID is estimated to be present in about 65 million people. We aimed to explore clinical and biological factors that might contribute to Long-COVID.

Methods
Prospective longitudinal cohort study including patients infected with SARS-CoV-2 between March 2020 and March 2022. Patients were assessed between 4 and 12 months after infection at the COVID follow-up clinic at UZ Leuven. We performed a comprehensive clinical assessment (including questionnaires and the 6-min walking test) and biological measures (global DNA methylation, telomere length, mitochondrial DNA copy number, inflammatory cytokines, and serological markers such as C-reactive protein, D-dimer, troponin T).

Results
Of the 358 participants, 328 were hospitalised, of which 130 had severe symptoms requiring intensive care admission; 30 patients were ambulatory referrals. Based on their clinical presentation, we could identify 6 main clusters. One-hundred and twenty-seven patients (35.4%) belonged to at least one cluster. The bigger cluster included PEM, fatigue, sleep disturbances, and pain (n = 57). Troponin T and telomere shortening were the two main markers predicting Long-COVID and PEM-fatigue symptoms.

Conclusions
Long-COVID is not just one entity. Different clinical presentations can be identified. Cardiac involvement (as measured by troponin T levels) and telomere shortening might be a relevant risk factor for developing PEM-fatigue symptoms and deserve further exploring.

Link | PDF (BMC Medicine) [Open Access]

 

I would enjoy this "things we have known for years" research a lot more if it ever made any difference. The problem of course isn't with the research itself, it's that no amount of research matters unless it's a fully-packaged solution that explains everything and offers a solution. Dumb system.