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RTHM is a secure health platform that makes it easy to gather your records, connect the dots with AI, and affordably access treatments.

SARS-CoV-2 Omicron variant spike protein maintains the ability to bind and activate human platelets: Comparison with the wild-type This study found that both wild-type and Omicron SARS-CoV-2 spike proteins significantly increase platelet binding and ADP-induced P-selectin expression compared to controls. The Omicron spike protein uniquely increased platelet aggregation under SFLLRN stimulation, suggesting a persistent prothrombotic risk across viral mutations.
Acute COVID-19 is associated with altered CD8 T-cells indicative of impaired ability to control Epstein–Barr virus reactivation The study found significant reactivation of Epstein-Barr Virus (EBV) in 72.7% of patients with critical COVID-19 and 67.9% with moderate COVID-19 at hospitalization, suggesting a link between EBV reactivation and the development of Long COVID symptoms. Notably, patients with EBV reactivation displayed altered CD8 T-cell activation profiles characterized indicating impaired viral control.
Endovascular profiles linked to neutrophil activation in children and young adults with long COVID This research highlights that children and young adults with long COVID exhibit significant endovascular profiles, characterized by elevated microclots and markers of endothelial injury, underlying their debilitating cardiovascular symptoms. Increased neutrophil activation, evidenced by elevated cell-free DNA and altered cytokine levels, suggests that intravascular NETosis may drive endovascular pathology.
On the Correspondence of Diseases Showing Microparticles, Fibrinaloid Microclots and Disorders of the Microcirculation doi: 10.20944/preprints202604.1728.v1 The research highlights a significant relationship between cell-derived microparticles and fibrinaloid microclots in various chronic inflammatory diseases, indicating that their co-occurrence reflects underlying endothelial damage and protein misfolding processes. Both microparticles and microclots are consistently associated with microcirculatory disturbances across multiple conditions, suggesting they may serve as interconnected biomarkers for diagnosing and understanding the pathophysiology of these disorders.
Impaired peripheral oxygen delivery during submaximal exercise in adults with long COVID PMID: 42026739 This study on Long COVID (LC) reveals that individuals exhibit impaired muscle oxygenation and recovery during repeated exercise. Specifically, LC participants showed compromised peripheral oxygen extraction, and their physical performance declined significantly on a second exercise day compared to controls. The findings suggest that tissue hypoxia may contribute to the exacerbation of symptoms in LC.
About the Long COVID Treatment Guide The Long COVID Treatment Guide is meant to spark meaningful conversations with patients and their clinicians about potential treatment options that could become part of a personalized care plan. It offers thoughtfully selected options clinicians and patients can explore together, based on the unique symptoms, needs, and goals of each patient. The focus is primarily on 24 prescription medications, but also includes select supplements and over the counter medications, procedures, and lifestyle strategies. References PMID: 33536023, 36969241, 38813984, 40627388, 37793728, 37419575 A Collaboration between Patient-Led Research Collaborative and RTHM PLRC x RTHM Long COVID Treatment Guide 03
The Harvard/Stanford TREATME Study 22% of individuals with Long COVID or ME/CFS who tried rapamycin (n=18) reported “moderate to much better” symptom improvement. References 40627388, DOI: 10.21203/rs.3.rs-6596158/v1; Trial ID: NCT06960928 A Collaboration between Patient-Led Research Collaborative and RTHM PLRC x RTHM Long COVID Treatment Guide 03
Summary Findings from a phase one trial on ME/CFS patients found that weekly rapamycin doses of up to 6 mg significantly improved fatigue, sleep, and orthostatic intolerance over three months. These findings suggest rapamycin’s potential as a treatment, likely due to its autophagy-promoting and mTOR-inhibiting properties, with further analyses expected to provide deeper insights. A clinical trial studying low dose rapamycin in people with ME/CFS and people with Long COVID is also currently underway. A Collaboration between Patient-Led Research Collaborative and RTHM PLRC x RTHM Long COVID Treatment Guide 03
Especially Helpful For Myalgic encephalomyelitis chronic fatigue syndrome (ME/CFS) cognitive impairment fatigue post-exertional malaise (PEM) Notes Titrate from 1mg 1x weekly up to 6mg 1x weekly. Good to get baseline markers of CMP, CBC, lipids, fasting glucose, A1C and fasting insulin before starting. Not all markers are required, but it can cause some insulin resistance and elevated lipids and LFTs in some people, particularly early on. A Collaboration between Patient-Led Research Collaborative and RTHM PLRC x RTHM Long COVID Treatment Guide 03
Title: Medications in the Long COVID Treatment Guide RTHM Logo and PLRC Logo A collaboration between Patient-Led Research Collaborative and RTHM Image of an arrow to swipe forward
Low Dose Naltrexone (LDN) Pill image 57% of RTHM Platform users who had taken LDN reported that they saw overall improvements in their symptoms. 38% of those reported 
significant improvements. All data presented is based on 992 patient reports. Rthm logo at the bottom
RTHM’s Take: “The growing evidence surrounding the impact of Long COVID in school-age children stands in stark contrast to the dearth of public health information parents, teachers and educators are receiving about the condition. Chronic absenteeism remains high in the United States compared to pre-pandemic levels, and this study makes a compelling case for Long COVID playing a significant role in driving this sustained change. Long COVID urgently needs to be a priority for discussion and action between our education institutions and public health institutions.” “— Jennifer Curtin, MD, RTHM Co-Founder
Study Author Conclusions: “Together, our findings suggest that long COVID has a potentially large impact on US school-aged children. Parents, caregivers, teachers, and schools may consider that children with long COVID disproportionately experience both functional limitations and sick days off from school.” “From 2018–19 to 2021–22 enrollment-weighted prevalence of chronic absenteeism in the United States increased from 14.8% to 28.3%, a 91% increase relative to the prepandemic timeframe… Schools might consider health-related factors in their ongoing efforts to improve school attendance and could collaborate with healthcare systems to provide integrated systems of support to address complex needs for children with disabilities and health concerns.” (Arrow pointing right) Small Citation
What This Suggests Long COVID in children may have meaningful downstream impacts on learning and social development because it’s linked to both functional limitations and higher illness-related absenteeism. Authors propose considering school accommodations (e.g., reduced workload, rest periods), analogous to supports used for conditions like concussion or ADHD. (Arrow pointing right) Small Citation
Key finding: long COVID is linked to much more illness-related school absence Missing >30 days for illness/injury in the past year: 10.7% with Long COVID vs. 1.5% without Long COVID. Illness-related chronic absence (>18 days): 13.9% with Long COVID vs 3.5% without Long COVID To reduce confounding from acute COVID-related school absences, the authors also analyzed a subset of 4,587 children with prior COVID-19. In this prior-COVID subsample, illness-related chronic absence was 13.9% (ever long COVID) vs 4.9% (never long COVID, but prior COVID). Having Long COVID at some point was associated with 2.5x the odds of illness-related chronic absenteeism compared with never having had Long COVID. (Arrow pointing right) Small Citation
Key finding: Long COVID is linked to higher rates of functional limitations Compared with children who never had Long COVID, those who ever had Long COVID showed higher prevalence in multiple domains, including: Learning difficulty: 19.8% vs 10.4% Difficulty concentrating: 14.3% vs 7.7% Difficulty with memory: 18.3% vs 8.6% Weekly/daily depression: 18.9% vs 6.2% (Arrow pointing right) Small Citation
Description of the Study: Using a nationally representative US survey of 11,057 US children aged 5–17 years, the authors asked whether children with Long COVID report more functional limitations and more illness-related chronic school absenteeism than peers without Long COVID. Authors classified illness-related chronic absenteeism, according to the US Department of Education, as missing 18 or more school days in the past 12 months due to illness or injury. The authors used the Washington Group/UNICEF Child Functioning Module (24 questions) for ages 5–17 years, covering multiple functional domains. Long COVID was defined as children having any symptoms lasting >3 months that they did not have before having COVID-19. (Arrow pointing right) Small Citation
Recent Study: Long COVID among school-aged children associated with chronic absenteeism. Authors: Nicole D. Ford, Regina M. Simeone, Caroline Pratt, and Sharon Saydah (Arrow pointing right) Small Citation
RTHM’s Take: “This is a concerning study that shows Long COVID (and any COVID infection) may heighten the risk of ADRD, and in some cases accelerate disease progression. This study should sound a public health alarm that without effective treatments and better infection prevention, we may experience a worsening wave of neurodegenerative conditions and cognitive decline in the years to come.” “— Jennifer Curtin, MD, RTHM Co-Founder
Study Author Conclusions: “Results are consistent with the view that changes in pTau-181 inconsistent with normal ageing may be common among participants with N-PASC. Indeed, more than half of participants with N-PASC experienced a ≥20% increase in absolute levels of pTau-181 relative to pre-COVID-19 levels… Among participants with N-PASC who exhibited pTau-181 increases ≥20% relative to pre-COVID levels, 45.1% expressed pTau-181 levels above an established cutoff to identify ADRD (Alzheimer’s Disease and Related Dementias) “Intriguingly, in this study we found that evidence of increased pTau-181 was associated with increases in AB40/42 ratios consistent with a pTau-mediated ADRD. These findings support pTau-181 as a valuable longitudinal biomarker for N-PASC and highlight the potential need for early, tau-targeted interventions to mitigate progressive cognitive decline.” (Arrow pointing right) Small Citation
What This Suggests The authors connect findings to a broader hypothesis that COVID-related neuroinflammation/microglial activation could contribute to tau phosphorylation/spread, potentially accelerating latent vulnerability. Patients who develop N-PASC after COVID-19 might share certain clinicopathological features with Alzheimer's Disease, however the authors explicitly caution that replication with neuroimaging/brain measures is needed to know whether plasma pTau‑181 elevations reflect cerebral tauopathy in N‑PASC. The authors suggest pTau‑181 could potentially help prognosticate neurological Long COVID—especially for symptoms persisting beyond ~1.5 years—but emphasize the need for long-term follow-up to see whether pTau‑181 continues rising or predicts later cognitive impairment. (Arrow pointing right) Small Citation
Amyloid Signals Moved With pTau‑181 in a Subset Among people with N‑PASC, ≥20% pTau‑181 increases were linked to a much higher chance of a ≥20% increase in Aβ40/42 ratio and higher risk of a ≥20% rise in IAB. Authors frame this as potentially concerning because pTau‑181 + amyloid ratio changes are a pattern often discussed in Alzheimer’s disease biology—though this study does not diagnose dementia or measure brain pathology directly. Time Course Matters: pTau‑181 Elevation Bigger After 1.5 years of Symptoms Average pTau‑181 elevation was reported as ~14.6% within ≤1.5 years since infection, but ~56.5% among those assessed >1.5 years after symptom onset (suggesting a possible lag or progression). GFAP decreases were more pronounced earlier (≤1.5 years) than later.
Symptom cluster tracked with pTau‑181 rises A ≥20% pTau‑181 increase was associated with higher risk of: “Any central nervous system” symptoms (aRR ~1.31) Loss of taste/smell (aRR ~1.30) Anxiety/depression (aRR ~1.26) Brain fog (aRR ~1.22) Muscle weakness (aRR ~1.30 (Arrow pointing right) Small Citation
Before COVID: Evidence of Higher Amyloid Burden Helped Predict N‑PASC Individuals who developed N-PASC had higher Aβ40/42 ratios, NfL, and IAB values, before developing COVID-19. Interpretation offered by authors: this pattern could reflect pre-existing vulnerability (amyloid-related biology) that may make some individuals more susceptible to neurologic sequelae. Amyloidosis often requires a secondary neuropathology to elicit the most severe symptomatology Authors note that if these findings indicate that cerebral amyloidosis is present, even in its mildest forms, then the post-COVID-19 increase in pTau-181 may correspond to the onset of pathological Alzheimer's disease. (Arrow pointing right) Small Citation
Key Finding: After COVID, pTau‑181 rose sharply in N‑PASC, but not in controls Main longitudinal result: pTau‑181 increased ~59% after COVID-19 onset in the N‑PASC group, relative to matched controls. About 58.6% of N‑PASC participants had more than 20% increase in pTau‑181 from their own pre‑COVID levels. N-PASC was associated with changes in pTau-181 that exceeded cutoffs used in studies of ADRD (Alzheimer’s Disease and Related Dementias). In contrast, GFAP and NfL showed post‑COVID decreases in the N‑PASC group versus never‑COVID controls. (Paradoxical finding that could be from neuroimmune system repairing itself, or from neuroinflammation restricting glymphatic clearance.) Among participants infected with COVID-19, there was an increase in IAB (biomarker for Alzheimer's risk) when compared to never-infected controls (Arrow pointing right) Small Citation
Description of the Study: The authors studied a prospective cohort of essential workers with paired plasma samples (one collected before the pandemic and one after) to test whether neurological Long COVID (N‑PASC) tracks with changes in Alzheimer’s-linked blood biomarkers. Participants with N‑PASC (n=227) were matched 1:1 to controls (n=227) who either had COVID without N‑PASC (n=124) or had no COVID by follow-up (n=103) N‑PASC required ≥1 neurological symptom (e.g., loss of taste/smell, brain fog, dizziness/vertigo, tinnitus, headache, balance issues) emerging within 3 months of infection and persisting more than 3 months. N‑PASC was assessed on average ~2.7 years after symptom onset. They measured neurological biomarkers well-established to correlate with neurodegeneration: pTau‑181, GFAP, NfL, Aβ40, Aβ42; plus derived measures like Aβ40/42 ratio and an inverse mean amyloid burden (IAB) metric. (Arrow pointing right) Small Citation
New Study: Patients who develop Long COVID have increased amyloid biomarkers consistent with Alzheimer's Disease. Authors: Xiaohua Yang, Ashley Fontana, Sean A.P. Clouston, Benjamin J. Luft (Arrow pointing right) Small Citation
Study # 10 Title: Muscle tissue exposed to blood from ME/CFS & Long COVID patients leads to severe muscular and mitochondrial deterioration. Key Findings: Overall, skeletal muscle degeneration followed a multi-phasic progression from compensatory adaptation to structural and metabolic collapse driven by mitochondrial impairment and disrupted protein turnover. Author Conclusions “We propose that skeletal muscle tissue in ME/CFS and LC-19 progresses through a hypermetabolic state, leading to severe muscular and mitochondrial deterioration. This is the first study to suggest such transient metabolic adaptation.” doi.org/10.1088/1758-5090/adf66c
Blood vessels in the retinas of Long COVID patients show a significant reduction in density Description In the study, researchers used advanced imaging called optical coherence tomography angiography (OCT-A) to examine the retinas of Long COVID patients vs. healthy controls. 
 They found that patients with long COVID had a significant reduction in the density of small blood vessels in the back of the eye compared to healthy individuals, suggesting a reduction in the perfusion (blood flow) to the deep part of the retina. Author Conclusion: “In conclusion, our study identifies retinal perfusion changes in Neuro-PASC patients with a reduction in deep (DCP) capillary plexus and vessel length density (VLD), suggesting that the smallest capillary vessels are preferentially targeted.” Site Sourced: https://www.mdpi.com/2313-433X/11/2/62
AI model can identify ME/CFS patients with ~90% accuracy. A new artificial intelligence tool, BioMapAI, was developed by scientists at the Jackson Laboratory and Duke University School of Medicine, in collaboration with researchers at the Bateman Horne Center. The research team discovered that their AI tool could accurately estimate the severity of symptoms by analyzing immune cells and was able to predict gastrointestinal, emotional, and sleep problems by analyzing microbiome data. “Biologically, our study introduces a highly nuanced approach to link physiological changes in gut microbiome, plasma metabolome, and immune status, with host symptoms, moving beyond the initial causes of the disease… This study represents a substantial technical and biological advance over... other investigations of ME/CFS to date.” doi.org/10.1038/s41591-025-03788-3
Long COVID risk doubles in children after reinfection. Description A retrospective cohort study used data from 40 children's hospitals participating in the Researching COVID to Enhance Recovery (RECOVER) Initiative investigated reinfection in children and adolescents. This study was the first and largest investigation of its kind. The study included patients younger than 21 years with documented SARS-CoV-2 infection after Jan 1, 2022. The second SARS-CoV-2 infection was confirmed at least 60 days after the first infection. “Children and adolescents face a significantly higher risk of various PASC outcomes after reinfection with SARS-CoV-2… regardless of severity, and suggest that the risk of PASC might be cumulative with each successive infection” Author: doi.org/10.1016/S1473-3099(25)00476-1
Exercise Increases Microclots In Long COVID. 46 people living with Long COVID with a low risk of experiencing post exertional malaise (PEM) completed two submaximal cardiopulmonary exercise tests (CPET), separated by 24 hours. They had blood drawn before starting the exercise test (CPET) and after, to look for microclots and cytokines. Author Conclusions; “This study provides.. a biological basis that might explain exercise-induced symptom exacerbation in people with Long COVID.. “ Small at the bottom: doi.org/10.21203/rs.3.rs-6717727/v1
Title at the Top: SARS-COV-2 infection in pregnant women is linked to developmental delays in toddlers This study aimed to evaluate the impact of maternal COVID infection on neurodevelopment of the child and investigate whether cytokine and chemokine profiles predict delays at 24 months. Author Conclusions “This study shows the long-term impact of maternal SARS-COV-2 infection on child development. Prenatal SARS-COV-2 infection in pregnant women is linked to developmental delays in toddlers, with cytokine and chemokine changes associated with neurodevelopmental outcomes at 24 months” Small at bottom: doi.org/10.1038/s41390-025-04192-w
Title at the top: Long COVID risk has not decreased over time As part of the National Institutes of Health (NIH)–funded Researching COVID to Enhance Recovery (RECOVER) Initiative, study authors leveraged electronic health record (EHR) data from three large clinical research networks to estimate Long COVID incidence over time. Author Conclusions: “We did not find evidence of Long COVID risk decreasing over time… Our findings indicate that preventing and mitigating Long COVID remains a public health priority.” Source: doi.org/10.1093/cid/ciaf046
Title at Top: 40% of Olympians experienced reduced sports performance for at least 4 months after COVID infection 37% reported symptoms lasting 
more than 4 weeks 25% had symptoms persisting for more than 8 weeks 20% were still symptomatic 16 weeks after initial infection. Author Conclusions “Our findings, which highlight the frequent occurrence of sport-limiting symptoms (e.g., fatigue) and performance impairments 16 weeks post-infection, underscore the need to revise current return-to-play (RTP) protocols for elite athletes.” Site: https://link.springer.com/article/10.1007/s12662-025-01024-1SOURCE
Title at Top: Infectious SARS-COV-2 particles detected in semen for up to 8 months after infections 45% had infectious viral particles confirmed via Vero cell culture. 55% had SARS-CoV-2 RNA detected in their semen (21 out of 38 patients). 91% detection in semen of patients with moderate acute COVID-19 severity. Author Conclusions: “This study confirms that SARS-CoV-2 can persist in the semen of patients who have recovered from COVID-19, indicating that the male genital tract may be a reservoir for the virus.” 

 Published 2024, observational cohort study (n=38)
Title at top: Long COVID may have surpassed Asthma as most common chronic condition in Children Among infants/toddlers (0-2 years) with SARS-CoV2 infection history, 40 of 278 (14%) were classified as having probable Long COVID. Among preschool-aged children (3-5 years), 61 of 399 (15%) were classified as having probable Long COVID. On average, infants and toddlers had symptoms that lingered for 10 months and preschool-aged children had symptoms that lingered nearly 17 months.
Title: 2025 End of Year Research Swipe to see the top research on Long COVID and ME/CFS ADD ARROW
“This is a remarkable study that presents a non-invasive in-vitro working model for the disease processes in muscle tissue to help understand the muscle pathophysiology in people with Long COVID and/or ME/CFS. And it is yet another study that counters the antiquated narrative that deconditioning is the primary driver of disease for these conditions.” “This study is also in agreement with findings from several other studies on ME/CFS and LC-19 that indicate factors in the blood of these patients are driving, or at least contributing to, these diseases. I am excited for additional, larger studies using this model to study ME/CFS and Long COVID and hope that use of this model may yield biomarkers and help identify treatments for ME/CFS and LC-19.” Image of Jennifer Curtin, MD RTHM Co-founder
Study Author Conclusions: “We propose that skeletal muscle tissue in ME/CFS and LC-19 progresses through a hypermetabolic state, leading to severe muscular and mitochondrial deterioration. This is the first study to suggest such transient metabolic adaptation.” “These findings provide strong evidence against the hypothesis that inactivity is the only cause of muscle wasting in ME/CFS and LC-19 patients. The contractile performance of a skeletal muscle can be diminished due to structural damage, lack of creatine reserves, local hypoxia or insufficient production of ATP due to disturbances in mitochondrial function.” “We speculate that at short exposures, there comes a point in which the biosystem attempts to resist against stress but when the stress is prolonged, the resistance gives in, allowing rapid deterioration. Our research presents the first 3D in vitro model to study performance profiles of ME/CFS and LC-19 patients without distressing them directly.” (Arrow pointing right) Small Citation
What This Suggests Factors circulating in blood from ME/CFS and Long COVID may impair muscle contractility and drive mitochondrial stress in vitro. The team describes a multi‑phase pattern: short‑term compensation, followed by “structural and metabolic collapse driven by mitochondrial impairment and disrupted protein turnover” with longer exposure to patient serum. Patterns were noted as consistent with “push‑crash/PEM” dynamics seen in all patients with ME/CFS and many with LC-19, as patient sera not only lowered the overall ability of the muscle to execute work but post peak performance, the tissues experienced weakness and inability to reach the same performance again. This provides a non‑invasive lab model to test how serum factors affect muscle tissue—potentially helping screen for biomarkers and treatment candidates without triggering patient PEM. (Arrow pointing right) Small Citation
Gene Expression Shifted in Patients vs Controls The researchers further performed gene ontology (GO) enrichment analyses between both patient groups and controls, to identify dysregulated pathways and gene set enrichment analysis (GSEA) between ME/CFS and LC-19 to identify any underlying differential biological tendencies. ME/CFS: upregulation of protein translation, sarcomere/ECM programs; downregulation of several metabolic/organelle functions. This could indicate an environment characterized by chronic stress, impaired metabolic activity, and ongoing or maladaptive tissue remodeling. Long COVID: stronger upregulation of mitochondrial structure/function terms. These findings indicate a pronounced shift in LC-19 tissue toward enhanced mitochondrial fatty acid metabolism, electron transport, and protein synthesis processes. Markers suggested less fission (↓DNM1L), more fusion (↑MFN2), and activation of TCA/glycolytic genes in response to demand. This compensatory upregulation in the expression of mitochondrial genes evidenced the presence of a heavy energy burden which required a compensatory metabolic response. (Arrow pointing right) Small Citation
Longer Exposure (up to 6 days) With prolonged Long COVID serum exposure, tissues weakened more quickly, survival dropped, and muscle cell fibers atrophied. While muscles initially adapted by increasing glycolysis (glucose breakdown), prolonged exposure (96–144 H) caused muscle fragility and weakness, with mitochondria fragmenting into a toroidal conformation (indicating significant cellular stress). The results of prolonged exposure to patient sera (blood) signal progressive deterioration of muscle structure, function and mitochondrial energy production, mimicking the conditions observed in patients. (Arrow pointing right) Small Citation
Longer Exposure (up to 6 days) With prolonged Long COVID serum exposure, tissues weakened more quickly, survival dropped, and muscle cell fibers atrophied. While muscles initially adapted by increasing glycolysis (glucose breakdown), prolonged exposure (96–144 H) caused muscle fragility and weakness, with mitochondria fragmenting into a toroidal conformation (indicating significant cellular stress). The results of prolonged exposure to patient sera (blood) signal progressive deterioration of muscle structure, function and mitochondrial energy production, mimicking the conditions observed in patients. (Arrow pointing right) Small Citation
Key Findings Muscle Performance Fell & Energy Systems Stressed: Overall, skeletal muscle degeneration followed a multi-phasic progression from compensatory adaptation to structural and metabolic collapse driven by mitochondrial impairment and disrupted protein turnover. Short exposures (48 hours) to serum from ME/CFS and Long COVID (LC-19) patients led to a significant reduction in muscle contractile strength compared to exposure to serum from healthy controls. Compared to controls, ME/CFS and LC patient sera (blood) led to lower maximum force, slower contractions, shorter time at peak (the ability of a tissue to maintain peak performance during stimulation), and faster drop to 50% force during sustained activity.
Description of the Study Researchers exposed 3D healthy human skeletal muscle tissues to serum (a component of blood) from people with ME/CFS, Long COVID, or healthy donors and watched how the muscle tissue functioned/changed over the course of 48, 96, or 144 hours of exposure to the serum. Exposing tissues to patient serum allowed the researchers to see the impact of patient blood components on healthy muscle tissue in a controlled environment without potentially confounding factors such as physical deconditioning from reduced activity. The contractile profile (tissue health) of the muscle was recorded through electric pulse stimulation (EPS) and the transcriptome (which genes were being transcribed more vs. less) of treated tissues was analyzed through total RNA sequencing. They also quantified mitochondrial morphology and structural changes using bright field and confocal microscopy. ME/CFS n=4, Long COVID n=5, controls n=4; 3–7 tissues per serum. (Arrow pointing right) Small Citation
Recent Study: Muscle tissue exposed to blood from ME/CFS & Long COVID patients leads to severe muscular and mitochondrial deterioration Source citation and arrow pointing right Images of muscle tissue deteriorating in the background.