We have 2 more days left on our survey! You can fill out at the link below docs.google.com/forms/d/e/1F… #LongCovid #LongCovidScotland

Progress in mast cell activation syndrome: the global consensus-2 diagnostic criteria at six years degruyterbrill.com/document/…

😷 BREAKING🚨 Canada launches a new National Advisory Committee on Preventive Health Services. It will be chaired by Dr. David Keegan, a leading advocate for masks in healthcare and on airplanes who filed human rights litigation on both fronts.

Research progress on the association between viruses and cardiac diseases 🚨Your heart’s deadliest serial offender just got named: SarsCoV2 Interesting Chinees review just mapped how six viruses attack the heart. One stands out! Not because the authors scream “worst ever,” but because the science does. →Direct heart-cell invasion long-term damage cumulative hits from regular reinfections = a unique threat! Vaccines help. But the data is sobering. Let’s break it down virus by virus(review): 1. SARSCoV2: - Enters cardiomyocytes and pericytes via ACE2 receptor (membrane fusion/endocytosis). - Direct infection triggers myocarditis, pericarditis, arrhythmias, heart failure (de novo or exacerbation), microclots, thromboembolic events and myocardial infarction, - Long-term: persistent cardiac inflammation, dysautonomia and long-COVID cardiovascular symptoms, - Possible viral persistence in tissue, - Vaccination reduces myocarditis risk/CV complications compared with natural infection, -Regular reinfections! 2.Influenza (A/B): - Direct replication in cardiomyocytes, Purkinje cells and endothelial cells (independent of lung titers), - Causes myocarditis, pericarditis, arrhythmias, heart-failure flares and myocardial infarction via both cytopathic effects and cytokine-driven systemic inflammation/endothelial dysfunction. - Long-term: myocardial fibrosis and remodelling, - Vaccines lower infection-related cardiovascular complications, 3. HIV: - No productive cardiomyocyte infection, - Indirect damage from chronic immune activation, endothelial dysfunction, metabolic changes and antiretroviral toxicity, - Drives cardiomyopathy (myocarditis in advanced cases), heart failure, myocardial infarction and stroke, - Long-term: premature cardiovascular aging, fibrosis and remodelling even on suppressive therapy, 4. CVB3 (Coxsackievirus B3): - Enters via CAR receptor, - Direct cytopathic necrosis, oedema and impaired contractility in cardiomyocytes, - Rapid progression to myocarditis, dilated cardiomyopathy, arrhythmias (QTc prolongation) and heart failure, - Chronic inflammatory cardiomyopathy is a hallmark sequela, 5. Human cytomegalovirus(HCMV): - Lifelong latency with reactivation (especially in immunocompromised), - Induces myocarditis, heart failure, transplant vasculopathy and atherosclerosis through sustained inflammation and vascular injury, - Long-term myocardial remodelling, 6. Arthropod-borne viruses(Arboviruses = DENV, CHIKV, ZIKV): - Direct cardiac invasion (some models) plus immune-mediated injury, - Associated with myocarditis, arrhythmias, heart failure, shock and (CHIKV) dilated cardiomyopathy or long-term ischemic heart disease/cerebrovascular risk. ‼️So, this minireview examines six cardiotropic viruses side-by-side, yet SARS-CoV-2 receives the most space because of its proven direct cardiomyocyte invasion, explosive multi-pathway damage, and documented long-term cardiac persistence, risks that broader population data show accumulate relentlessly with every regular reinfection, creating an immediate and chronic cardiovascular burden on a global scale that no other virus in this review matches. →Your heart’s deadliest serial offender just got named: SarsCoV2! #PREVENTION #COVIDHeart #RepeatInfectionKills #AvoidSars2 #AvoidReinfections #YouOnlyHaveOneHeart journals.asm.org/doi/10.1128…

Covid is just one of thousands of viruses that spread through the air & are inhaled like smoke. Workplaces can be major sites of transmission. What action can trades unionists push for to keep workers safer from airborne illnesses? Register here: tinyurl.com/y4b29jkw x.com/covidactionuk/status/2…

Beyond brain fog: viral proteins as convergent drivers of neuroinflammation and proteinopathy 🚨“COVID-19 never really leaves your brain.” New science review proposes SARSCoV2 viral proteins stay behind as long-lived toxins, triggering chronic neuroinflammation and planting the seeds of Alzheimer’s and Parkinson’s, even after mild infection. This very interesting and eye-catching GERMAN review reframes post-viral neurological syndromes( L0ngC0vid) as driven by persistent viral proteins acting as long-term toxins ("protein-as-pathogen" model), not just the active infection! ➡️Core mechanisms: - SARSCoV2 Spike and OTHER viral proteins activate glial TLR4/TLR2 receptors, triggering chronic neuroinflammatory cascades via NLRP3 inflammasome, - They also disrupt autophagy, allowing toxic protein aggregates (tau, amyloid-beta, α-synuclein) to accumulate and seed neurodegeneration, ➡️SARSCoV2 specific evidence: - Animal studies show Spike protein alone (without live virus) induces TLR4-mediated cognitive deficits, memory impairment, synaptic loss, and sustained neuroinflammation, recapitulating post-COVID syndrome, - Spike binds α-synuclein, accelerating Parkinson-like clumps, ➡️Human data evidence: - Millions experience "brain fog," - Post-COVID patients exhibit measurable brain damage: cortical thinning, hippocampal iron accumulation, and biomarkers of ongoing neuronal injury, ➡️Broader risks: - Even mild infections leave lingering proteins that promote Alzheimer’s and Parkinson’s-like pathology via shared pathways, - Same pathways seen in influenza, dengue, West Nile etc, - Mild infection = no protection, ‼️So, according to this review, the “protein-as-pathogen” model makes it crystal clear: every new SARSCoV2 infection (even mild or asymptomatic) deposits more of these long-lived toxic viral proteins into the brain. They don’t fully clear. They accumulate. Each reinfection reloads the TLR4/TLR2 → NLRP3 inflammasome trigger and further collapses autophagy, speeding up the tau/amyloid/α-synuclein proteinopathy and neurodegeneration. SARS-CoV-2 does not just infect. It weaponizes its own proteins as long-lived intracellular saboteurs. Millions are probably already carrying this hidden payload. This is not brain fog. This is a silent, population-scale reprogramming of human brains toward dementia-like decline. The long-term neurological cost will probably dwarf the acute pandemic itself! #AvoidSars2 #AvoidReinfections sciencedirect.com/science/ar…

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We did this. Well done, human species for destroying the conditions necessary for its own health 🤦

In this large multicenter real-world cohort study, patients who developed long COVID had a substantially higher risk of major adverse cardiovascular events (MACE) and death compared with COVID-19 patients who did not develop #LongCOVID. ➡️ The overall risk of MACE was increased more than fourfold (HR 4.48), with particularly high risks for coronary artery disease (HR 6.48) and stroke (HR 3.46). 1/

Children with Long COVID had measurable retinal microvascular changes. buff.ly/fPSg320 In 74 kids ages 7–17, scans found wider arterioles, wider venules, and a higher A/V ratio, consistent with endothelial dysfunction. The eye may help track pediatric Long COVID.

Don't forget Clean Air Day on 18th June. And please can we work together to make every day a clean air day 🙏🙏

Wonderful example of a worldwide phenomenon - how pandemic-disabled people have founded and come together in new kinds of communities, blending global and local, online and onsite👏

Prof. Klaus Wirth proposes that a substantial subset of Long COVID—the group that clinically resembles ME/CFS—is driven by a vicious cycle involving vascular dysfunction, impaired sodium handling, calcium overload, and ultimately mitochondrial injury. In his model, exertion does more than temporarily deplete energy reserves. Instead, exercise may trigger abnormal sodium accumulation within muscle cells. Excess sodium then promotes calcium influx, including into mitochondria. Calcium overload is a well-established mechanism of mitochondrial injury in other diseases, and Wirth argues that repeated episodes may progressively impair cellular energy production. This hypothesis attempts to unify several observations reported in Long COVID and ME/CFS research: orthostatic intolerance, impaired cerebral blood flow, elevated lactate during exercise, post-exertional malaise (PEM), cognitive dysfunction, autonomic abnormalities, and exercise intolerance. Importantly, this remains a hypothesis—not a proven mechanism—but it offers a biologically plausible framework linking many seemingly disconnected findings.

1/ Long COVID is one of the most complex post-infectious syndromes ever studied. A new review in Nature Communications Medicine attempts to unify the biology. Here’s what’s established, what’s emerging, and what’s still speculative. 🧵

“This new class of universal vaccines are future-proofed. They not only protect against many variants simultaneously, but potentially against related viruses that haven’t yet emerged...". Wow! Would be good to know more on the science but well done @UHSFT👏uhs.nhs.uk/whats-new/press-r…

Proud to be a signatory. Well done @LongCovidAdvoc for making this letter happen👏. Just hope the letter has an impact now.

Those of us who keep up with the science are about as unsurprised by this as it's possible to be. The only surprising thing is that a medical establishment noticed!

The PCR positivity map is out. Most areas are either not reporting or have stopped within the last 7 days, hence this week's national average is unlikely to have any meaning at all. I'll discuss known hotspots first, then the data shortage issue. jamestindall.info/skeuomorph… 1/8

Why do so many charts on different kinds of illness show soaring rises from 2020-21? Findings show approx 1 in 6 develop post acute Covid sequelae but diagnostic coding systems capture under half, so millions are invisible to health systems & policymakers jamanetwork.com/journals/jam…

It’s good to see the @resfoundation highlighting how the deterioration in young people’s health since 2019 is a significant driver of the NEET crisis. And yet, the official report does not even mention Long Covid once. Covid continues to be the elephant in the room. 🐘