The review summarizes current findings on fibrinoid microclots that impair microcirculation in Long COVID and ME/CFS. TEG reveals increased clot strength and reduced fibrinolysis in Long COVID, suggesting a persistent hypercoagulable state. Therapeutic approaches such as apixaban and lumbrokinase are discussed but require further clinical validation.

The work directly addresses two central mechanisms in ME/CFS and Long COVID: microclots and impaired tissue perfusion. It proposes both a diagnostic method (TEG) and concrete treatment approaches (anticoagulants, fibrinolytics).

This long-term study tracked cytokines and biochemical parameters up to 9 months after COVID-19 hospitalization. Several inflammatory markers (IL-2, IL-6, IL-10, IL-17A, TNF-α, IFN-γ) remained persistently elevated, with IL-6 showing strong diagnostic value distinguishing patients from healthy controls. However, no stable associations were found between cytokine levels and symptoms such as fatigue, suggesting Long COVID involves multifactorial mechanisms beyond systemic inflammation.

The study confirms persistent immune dysregulation after COVID-19, a central mechanism also in ME/CFS. At the same time, it shows that cytokines alone cannot explain symptoms, highlighting the complexity of post-viral syndromes and motivating further research into other mechanisms (mitochondria, microthrombi, viral persistence).

The study analyzed 42 review articles covering over 150 devices and 17 different biometrics. Only heart rate measurement and atrial fibrillation detection showed reliably good accuracy, while other measurements varied substantially across devices and user populations. Clinical utility for patients remains limited in the evidence base.

Wearables are increasingly recommended for PEM detection and pacing in ME/CFS and Long COVID. This review helps patients and clinicians realistically assess which data they can trust – heart rate tracking in particular is well-validated and can support exertion management.

The study identifies HNRNPA2B1 as a key host factor that maintains Epstein-Barr virus in its dormant state. The protein recruits a chromatin-modifying enzyme (LSD1) to keep viral genes suppressed. Without HNRNPA2B1, the virus reactivates much more frequently.

EBV reactivation is discussed as a possible trigger or driver of ME/CFS and Long COVID. Understanding how the body keeps EBV latent could lead to new approaches for preventing harmful reactivations.

Six large language models from OpenAI, Anthropic and Google were evaluated on plasma cell-free RNA datasets, including an ME/CFS cohort vs. sedentary controls. Model-nominated gene panels recapitulated canonical immune pathways and outperformed random panels. However, end-to-end automated classification was weaker for ME/CFS than for other cohorts.

The study explicitly uses an ME/CFS cohort and explores AI-assisted biomarker discovery from blood—a potential path toward objective diagnostic tests urgently needed in ME/CFS research.

This review describes how various viruses (SARS-CoV-2, influenza, HIV, enteroviruses, etc.) can damage the heart directly and via immune responses. Mechanisms include endothelial dysfunction, prothrombotic states, and chronic inflammation, which can also lead to long-term sequelae such as post-acute cardiovascular symptoms in Long COVID.

The described mechanisms (endothelial dysfunction, microthrombi, viral persistence, chronic inflammation) strongly overlap with ME/CFS and Long COVID hypotheses and provide context for cardiovascular symptoms in patients.

The study identified diverse autoantibodies against brain and nervous system structures (e.g. locus coeruleus, thalamus, adrenal gland) in Long COVID patients with neurocognitive symptoms. Passive transfer of patient IgG into mice induced fatigue-like behavior, balance problems, hyperalgesia, and small fiber neuropathy. This provides the first causal evidence that autoantibodies can drive core Long COVID symptoms.

This is a landmark study establishing a causal mechanism for Long COVID (and potentially ME/CFS) and scientifically supports concrete therapeutic approaches such as antibody removal (plasmapheresis, immunoadsorption).

This commentary summarizes two landmark papers in Cell and Cell Reports Medicine showing that autoantibodies in a subset of long COVID patients directly drive disease symptoms. Transfer of these antibodies to animals reproduced typical symptoms including pain, fatigue, and neurocognitive problems. This provides a mechanistic foothold in a heterogeneous disease.

Autoantibodies (e.g., against adrenergic receptors) are considered a central mechanism in ME/CFS as well. These findings support the biological basis of long COVID and ME/CFS and open paths for diagnostics (antibody tests) and therapy (e.g., apheresis, B-cell depletion, IVIG).

The study shows Long COVID POTS patients have increased mitochondrial superoxide production in monocytes and decreased NRF2-dependent antioxidant enzymes. This leads to isolevuglandin-modified self-proteins that act as neoantigens activating T cells. Elevated circulating proinflammatory cytokines (IL-17A, IFN-γ, TNF-α) correlated with symptom severity, linking immune dysregulation to autonomic dysfunction.

POTS frequently occurs in ME/CFS and Long COVID. This study identifies specific molecular mechanisms (oxidative stress, neoantigens, T cell activation) that link several known ME/CFS mechanisms and open new therapeutic targets (e.g., NRF2 activators, IsoLG scavengers).

The authors analyzed 101 studies covering genomics, proteomics, metabolomics, and more in Long COVID. Despite methodological heterogeneity, consistent abnormalities emerged in the complement cascade, coagulation pathways, and sustained mitochondrial dysfunction lasting up to two years. Multiomics integration supports at least two endotypes (inflammatory vs. metabolic), enabling patient stratification and targeted therapy development.

The review identifies convergent biological signals in Long COVID that strongly overlap with ME/CFS mechanisms (mitochondrial dysfunction, immune dysregulation, microthrombi). The proposed endotypes could help explain patient heterogeneity in ME/CFS and point toward biomarkers and treatments.

In a study of 93 COVID-19 ARDS survivors, rotational thromboelastometry (ROTEM) was used 15 months after discharge to assess whether persistent symptoms correlate with coagulation abnormalities. Patients with PASC, post-exertional malaise (PEM), and fatigue showed significantly elevated FIBTEM values (fibrinogen contribution to clot strength), while brain fog did not. The findings suggest a long-lasting hypercoagulable state as a potential mechanism for physical Long COVID symptoms.

The study provides objective evidence of a measurable biomarker (FIBTEM) for PEM and fatigue—core symptoms of ME/CFS and Long COVID. It supports the microthrombi hypothesis and opens possibilities for anticoagulant therapeutic approaches.

The case report describes a patient who developed ME/CFS following SARS-CoV-2 infection and was successfully treated with therapeutic plasma exchange. The authors highlight the pathophysiological overlap between Long COVID and ME/CFS and emphasize the need to investigate novel therapeutic approaches such as plasma exchange.

Plasma exchange is a promising therapeutic approach for ME/CFS that may remove pathogenic autoantibodies (e.g., against adrenergic receptors). This case report supports the autoimmune hypothesis and provides evidence for a potential treatment.

In a prospective study, retinal vessels of children with Long COVID were examined and compared to healthy controls. Affected children showed significantly widened arterioles and venules and altered vessel responses to light – indicating endothelial dysregulation months after infection. Symptom improvement correlated with positive changes in vessel parameters.

Endothelial dysfunction is considered a central mechanism in ME/CFS and Long COVID. The study provides objective, non-invasive biomarkers in children and strengthens the biological basis of post-viral conditions – an important step for diagnostics and understanding.