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@ZdenekVrozina Yes, superoxide dismutase, a marker of oxidative stress responsible for destroying free superoxide radicals was persistently upregulated two years after the acute infection.

@DiscMedNews And some oxidative stress related proteins remained persistently altered as well.

A new Scientific Reports study adds an important nuance to the long COVID conversation. The biggest difference was not between people with PCC and without PCC, but between uninfected people and everyone who had recovered from SARS2🧵

@ZdenekVrozina _Yes, some neuron-related signaling pathways, such as the generation and differentiation of neurons and neuron projection development had a slow recovery rate after one year and were persistently suppressed over two years after the SARS-CoV-2 infection.

@DiscMedNews Neuron related signaling recovered more slowly and remained suppressed even after 2 years.

@ZdenekVrozina Importantly, tropomyosin chain proteins involved in cardiomyopathy signaling pathways did not recover at the six-month follow-up and remained significantly upregulated in COVID-19 survivors.

@ZdenekVrozina In this paper, in COVID-19 survivors, most immune response pathways, such as complement and coagulation cascade, and cholesterol metabolism, were comparable to those of the healthy controls before the two-year follow-up.

@Parsifaler SARS-CoV-2 S1 protein activates human cardiac fibroblasts by priming NLRP3 inflammasomes through NF-κB signaling in an ACE2-dependent way and promotes cardiac fibrosis. discovermednews.com/sars-cov-2-spi…

Spike Protein (mRNA) Myocarditis Shows Evidence of Persistent Fibrosis: Further Understanding Sudden Cardiac Deaths: Dangers of Reexposures Myocarditis induced by the Spike Protein has been shown to induce mid to epicardial lateral wall fibrosis – an arrhythmogenic zone.

@DrDenDunnen @CellRepMed @amsterdamumc @UMCUtrecht And preprint of this paper is from May 2024. Why did the paper wait so long for publication? discovermednews.com/transfer-of-ig…

Our paper is (finally) out in @CellRepMed: antibodies from #LongCOVID patients transfer symptoms to mice, pointing to a potential causal role for autoimmunity: cell.com/cell-reports-m… @amsterdamumc @UMCUtrecht 1/12

@ZdenekVrozina And preprint of this paper is from May 2024. Why did the paper wait so long for publication? discovermednews.com/transfer-of-ig…

Patient-derived IgG in Long COVID appears functionally pathogenic - and in some cases, this autoreactivity persists for years🧵

@ZdenekVrozina 7 antigenic sites of the SARSCoV2 S protein RBD show molecular similarity with 54 antigenic determinants of 15 pathogenic bacteria, parasites, and viruses, including the enterotoxin A from Staphylococcus aureus, and M protein from Streptococcus pyogenes. discovermednews.com/molecular-simi…

The real headline here is simple - this preprint study set immunity debt against SARS-CoV-2 as rival explanations for rising invasive strep - and only one of them held up in the data🧵

@Yash25571056 Phosphorylated tau Thr181 and Thr217, and hyperphosphorylated tau AT8+ (all associated with Alzheimer’s disease) were unexpectedly up-regulated in the hippocampus and medial entorhinal cortex of people who died within 4-13 months of acute COVID-19. discovermednews.com/alzheimers-dis…

FYI, "In ICU-Cv (those with ICU admission due to COVID-19), ERC (entorhinal cortex) volume was significantly reduced compared to HC (healthy controls).. ERC, a key gateway for neocortical input to the hippocampus, is particularly susceptible in the early stages of AD (Alzheimer's disease), contributing to deficits in episodic memory and spatial navigation.. This finding (selective atrophy of the ERC in ICU-Cv patients) suggests that severe COVID-19 may lead to targeted neurodegeneration through mechanisms distinct from AD but potentially overlapping in terms of hypoperfusion, inflammation, and metabolic stress." Remember this. 'Long-Term Effects of Severe COVID-19 on the Hippocampus: A 7T MRI Comparison with Alzheimer’s Disease' alz-journals.onlinelibrary.wiley.com/doi/pdf/10.100…

@vipintukur Something different: Azithromycin is in vitro superior to other macrolides in the respiratory epithelial barrier enhancement, phospholipid retention, vesicle build-up, and its effect on gene sets related to keratinocyte differentiation. discovermednews.com/azithromycin-i…

A study of hospitalized COVID-19 patients found that azithromycin quickly alters the respiratory microbiome and increases antibiotic resistance genes, with effects lasting over a week. ➡️ Importantly, it did not provide clear anti-inflammatory benefits. ➡️ These findings suggest that routine use of azithromycin in viral infections may promote antimicrobial resistance without significant clinical advantage. nature.com/articles/s4156…

@vipintukur Individuals with post-COVID vaccination syndrome were found to have a specific immunological profile, serological evidence of recent Epstein-Barr virus reactivation, and circulating SARS-CoV-2 S1 protein up to 700 days after vaccination. discovermednews.com/immunological-…

Post-COVID syndrome may involve problems with blood clotting and reactivation of latent Epstein–Barr virus (EBV). ➡️ Researchers identified circulating blood microaggregates that could impair capillary blood flow and found increased immune responses to EBV in affected patients. ➡️ Retrospective observations suggest that some patients improved with antithrombotic therapy and antiviral treatment targeting EBV, indicating potential therapeutic avenues. nature.com/articles/s4159…

@ZdenekVrozina Individuals with post-COVID vaccination syndrome were found to have a specific immunological profile, serological evidence of recent Epstein-Barr virus reactivation, and circulating SARS-CoV-2 S1 protein up to 700 days after vaccination discovermednews.com/immunological-…

A new long COVID paper suggests that, in a subset of patients, the picture may involve circulating microaggregates, impaired capillary flow, and - EBV-related immune activation🧵

@vipintukur Correlation between increased [11C]PBR28 PET/MR brain binding (as an indicator of neuroinflammation) and parameters of vascular health could partially reflect variations in vascular anatomy and perivascular immune infiltration in postacute COVID-19. discovermednews.com/brain-pet-sign…

A NEW review examines how COVID-19 may affect memory and cognitive function. ➡️ Evidence suggests that inflammation in the brain, activation of immune cells called microglia, and possible vascular injury can disrupt normal brain signaling. ➡️ These changes may contribute to symptoms such as brain fog and memory problems seen in some people after COVID-19. ➡️ Further research is needed to better understand these mechanisms and develop effective treatments. mdpi.com/2571-6980/7/1/…

@Parsifaler In 2021, Yapici-Eser et al. found a mimicry of SARS-CoV-2 proteins (spike protein, NSP7, and papain-like protease, which is responsible for viral replication) with ferritin light chain protein. frontiersin.org/journals/human…

The Spike Protein, Ferritin and Long COVID: Additional Damage to the Microvasculature The Spike Protein appears to induce massive release of iron from Ferritin, damaging the microvasculature much like after mini strokes.

@Parsifaler Long COVID patients who developed ME/CFS based on all 3 internationally standardized criteria, had elevated serum ferritin levels, identifying serum ferritin as a possible biomarker for detecting the transition to ME/CFS, especially in female patients. discovermednews.com/ferritin-in-lo…

@ZdenekVrozina CD56+CD3- NK cell numbers were significantly lower in unvaccinated COVID-19 convalescents ten months after initial infection with the Wuhan Hu-1 strain of SARS-CoV-2 than in uninfected control group negative for SARS-CoV-2. discovermednews.com/immune-paramet…

Rather than framing long COVID as a simple state of persistent systemic inflammation, this new study points toward a model of chronically dysregulated immunity in which NK-cell dysfunction may occupy a central mechanistic role🧵

@HarrySpoelstra CD56+CD3- NK cell numbers were significantly lower in unvaccinated COVID-19 convalescents ten months after initial infection with the Wuhan Hu-1 strain of SARS-CoV-2 than in uninfected control group negative for SARS-CoV-2. discovermednews.com/immune-paramet…

Dysregulated NK-cell gene expression defines the enduring symptoms of long COVID-19 🚨Long COVID's crippling fatigue, lost smell & brain fog now traced to profoundly exhausted & depleted NK cells, maybe unlocking a precise immune target for real treatments at last. A further IMPORTANT confirmation! #LEONARDI_EFFECT ➡️This German study on long-term COVID-19 syndrome (LTCS, or long COVID) identifies immune dysregulation, centred on natural killer (NK) cells, as a driver of persistent symptoms like fatigue, pulmonary issues, and cognitive impairment in 2%–8% of SARS-CoV-2 survivors. ➡️IMPORTANT FINDINGS: 1. LC patients show sustained high anti-SARS-CoV-2 IgG titers (S1/RBD/N proteins) up to 500 days post-infection, similar to convalescents, but with markedly reduced systemic cytokines (e.g, IFN-γ, TNF-α, IL-6, IL-10, IL-8), signalling immune suppression rather than hyperinflammation, 2. Flow cytometry reveals depletion of CD56+ CD16+ NK cells and CD56+ CD3+ NKT cells in LTCS compared to healthy controls and convalescents, alongside altered T-cell activation states, 3. Single-cell RNA sequencing confirms NK cell loss and profound transcriptional changes (455 differentially expressed genes: 115 upregulated like PDCD4 and CXCR4, 340 downregulated like TGFBR3 and MBNL1), 4. Single-cell RNA-seq reveals NK-cell exhaustion and impaired neuronal/sensory pathways and links immune dysfunction to hallmark symptoms such as fatigue, loss of smell, and cognitive impairment, 5. Enriched NK pathways include circadian rhythm regulation and translational programs. 6. Suppressed ones involve olfactory perception, neurotransmitter/GABA signalling, and sensory smell, linking to neuroimmune dysfunction. 7. Functional validation shows impaired NK cell inflammation (reduced TNF-α), mirroring chronic viral exhaustion and contributing to symptoms via a neuroimmune axis, 8. Vaccination and reinfection are not discussed as factors influencing NK-cell dysregulation or long COVID persistence, 9. Some valid limitations mentioned. ‼️This groundbreaking study reveals that dysregulated, exhausted natural killer (NK) cells, with profound depletion, transcriptional rewiring, and impaired function, directly drive the debilitating, persistent symptoms of long COVID, linking immune exhaustion to neuro-sensory and fatigue pathways! ‼️So, according to this study, dysregulated NK cells fundamentally underpin long COVID's enduring pathology, calling for urgent NK-targeted interventions to avoid lifelong suffering for millions. #LongCOVID #NKcells #Immunology #AVOIDSARS2 frontiersin.org/journals/immun… FYI: @fitterhappierAJ

@ZdenekVrozina Highly expressed markers of vascular impairment and autophagy are co-localized with SARS-CoV-2 spike protein in placenta samples of unvaccinated women positive for SARS-CoV-2. discovermednews.com/colocalization…

This new Nature Communications study is the most comprehensive look we’ve ever had at SARS-CoV-2 inside the human fetus. And the message is straightforward. Vertical transmission is real, and the virus can reach multiple fetal organs - even early in pregnancy🧵

@vipintukur From 2024: Sensory trigeminal neurons with axonal projections to the oronasal epithelium and brainstem, or superior cervical ganglia neurons with synaptic connections to the salivary glands and brainstem could serve as alternative route for CNS invasion. discovermednews.com/susceptibility…

A recent study suggests that SARS-CoV-2 may affect the trigeminal nerve and brainstem, which are involved in facial sensation and pain. ➡️ The virus and related inflammation were found in nerve cells in animal studies, which may increase nerve sensitivity. ➡️ These changes could help explain symptoms such as headache, migraine, and facial pain seen in some COVID-19 patients. link.springer.com/article/10.118…