Post/Long-Covid seit Sommer 2021, Soziale Projekte, Ehrenamt und Zivilcourage, Parteien in Deutschland, Umwelt, Regionalnachrichten, Westdeutsche in Sachsen
@BBMB_bund@ADS_Bund Es gibt über 200 Symptome bei #PostCovid / #LongCovid - u.a. #MECFS WO SIND DIE ZUGESICHERTEN GELDER 2023 - 100 Millionen ?🖤🇩🇪🖤Forschung und Therapie wie TMS, die TPS und tDCS jetzt auch in 🇩🇪Frau @starkwatzinger - Rente, Behinderungsgrad, Pflegegrad ? 🆘wann möglich ? 🖤🇩🇪❤️🔥
#USDA reports a big jump in #H5N1#BirdFlu in dairy cows in Idaho. 25 new herds have tested positive, bringing the state's total to 156 herds. Since this outbreak in cows was first detected in March 2024, 1,134 herd in 19 states have tested positive. https://t.co/2BioBG0wUw
Europe: low surveillance, high BA.3.2?
SARS-CoV-2 sequences collected between May 15 and July 10 and submitted to GISAID:
• Asia: 281 total, 31 BA.3.2 (11%)
• North America: 50 total, 6 BA.3.2 (12%)
• Australia: 145 total, 25 BA.3.2 (17%)
• Europe: 18 total, 8 BA.3.2 (44%)
BA.3.2 frequencies appear highest in Europe, but the estimate is based on only 18 sequences, highlighting how limited genomic surveillance has become in many European countries.
🇹🇼Taiwan: COVID-19 cases rise for 3rd straight week.
🔹ER visits hit 1,000 for May 31–June 6, up 4.1% from the previous week.
🔹The main circulating variants are currently BA.3.2 and XFG, followed closely by NB.1.8.1.
H/T: @interPARASect24
https://t.co/KN5BWKnDjN
😷 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.
🇦🇺Australia: Starting in mid-2026, a new national program will test wastewater across Australia to track diseases like COVID-19 and the flu. This will help health officials spot outbreaks early and stay ready for future threats.
Source: https://t.co/0WUKg7EiLs
Long-Term Outcomes of Multisystem Inflammatory Syndrome in Children up to 4.5 Years After COVID-19
🚨IMPORTANT new study just dropped: MIS-C in kids is NOT a temporary illness!!
🚨It raises cardiovascular disease risk 14×, hypertension 9×, and gut/lung/brain problems for up to 4.5 years later(=LC)
Earlier “kids recover fine” claims are now officially challenged! Study:👇
➡️ A retrospective cohort study from New York’s Montefiore Health System examined 173 children under 21 with MIS-C versus 346 propensity score-matched controls without MIS-C, all following documented COVID-19 infection.
➡️Follow-up extended up to 4.5 years (March 2020–August 2024) using electronic health records, with MIS-C confirmed by ICD-10 code M35.81 plus CDC/WHO criteria.
➡️Results:
1. MIS-C patients faced markedly elevated risks compared to controls:
- Cardiovascular disorders (aHR 13.88, 95% CI 4.69–41.07),
- Hypertension (aHR 8.86),
- Gastrointestinal disorders (aHR 9.48),
- Respiratory disorders (aHR 3.46), and
- Neurological disorders (aHR 2.02),
- Shock and chronic kidney disease (CKD) occurred almost exclusively in the MIS-C group,
2. Kaplan-Meier analysis showed persistent cumulative incidence in the MIS-C cohort ranging from 6.8% (CKD) to 35.2% (respiratory disorders), with risks diverging and accumulating over years rather than resolving,
3. Preexisting hypertension strongly predicted cardiovascular, neurological, respiratory, and gastrointestinal outcomes,
4. Preexisting diabetes increased CKD risk 49-fold,
5. Older age modestly raised risks of shock and CKD.
6. Sensitivity analyses using stricter MIS-C definitions and alternative respiratory coding confirmed the main results.
7. No mention or data on vaccination and/or reinfection impact.
➡️The study directly challenges earlier reports portraying MIS-C as a transient, self-limited condition with minimal long-term sequelae.
‼️So, MIS-C is not a temporary inflammatory storm that children outgrow. It inflicts severe, lasting multisystem damage that multiplies the lifetime risk of serious cardiovascular disease, hypertension, gastrointestinal, respiratory, and neurological disorders by several-fold to more than ten-fold, while introducing rare but devastating conditions like shock and CKD that almost never occur in peers.
‼️Sadly enough risks continue to accumulate years later.
‼️Earlier short-term “excellent recovery” narratives are contradicted by this longer, rigorous evidence.
‼️Affected children now carry a heavy, potentially permanent burden of chronic illness that will require lifelong medical surveillance and coordinated care or face accelerated morbidity and reduced quality of life!
‼️Of course we need further confirmation, but this does fit the ongoing concerns within the LC science community!
😡So much for paediatric minimalizations!
#AvoidSars2 #AvoidReinfections #ProtectChildren
https://t.co/xXJFs0bFSH
“The reasonable man adapts himself to the world: the unreasonable one persists in trying to adapt the world to himself. Therefore all progress depends on the unreasonable man.”
– George Bernard Shaw
Ich begrüße ausdrücklich die Arbeit eines Mannes, der VW Käfer zu Elektroautos umbaut.
Aus wissenschaftlicher Sicht handelt es sich um doppelte Nachhaltigkeit: Ein bestehendes Fahrzeug wird weiter genutzt und gleichzeitig lokal emissionsärmer betrieben.
Man könnte sagen: Kreislaufwirtschaft trifft Energiewende. Der Käfer bekommt ein zweites Leben – diesmal ohne Auspuffgeräusche, aber mit gutem Gewissen.
1) 🇧🇪 Researchers from Leuven and Hasselt university published a protocol for an extensive ME/CFS study.
It includes cytokine measurements, MRI and PET scans, gut microbiome analysis, and salivary cortisol following a stress test.
“If the cells are frequently turning over and they are still detecting viral persistence, what other plausible explanations are there for this other than replication?”
That's a very good question, and it's one of the central puzzles in the field of viral persistence. Let’s see why:
If a tissue contains cells that turn over relatively quickly (intestinal epithelium, immune cells, etc.), and viral RNA or proteins are still being detected months or years after an infection, then ongoing replication is the most intuitive explanation, but it is not the only one. Other reasonable options are:
1. Persistence in long-lived reservoir cells.
The tissue as a whole may turn over, but a subset of cells may not. We know this happens for neurons, some endothelial cells, tissue macrophages, lymphocytes, and others. In this case, the virus isn't replicating continuously, but instead, a long-lived infected cell survives for months or years and continues to produce low levels of viral RNA or protein. This is essentially how the HIV reservoir works, for example.
2. Defective viral genomes.
A cell can also contain incomplete viral genomes incapable of producing infectious viruses, so the genome may still produce RNA transcripts and some proteins. While this stimulates innate immunity (so enough to cause symptoms and pathology), it doesn’t generate new infectious virions.
3. Protein persistence without viral persistence.
The virus itself may be gone but you can have lingering viral remnants like spike protein and nucleocapsid fragments that can persist inside phagocytic cells or in extracellular compartments. In this case, what is being detected is essentially debris rather than an active infection, but their presence is enough to induce immunological responses (and again, enough to produce symptoms/pathology).
4. Continuous release from another hidden reservoir.
The tissue where detection occurs may not be the reservoir. Hidden reservoir can include gut, bone marrow and lymphoid tissue, while the released is being detected in blood or peripheral immune cells. In this model, the virus replicates (or persists) in one location, while viral products continually seed other compartments.
5. Cell-to-cell transfer without productive infection.
Macrophages and other immune cells can acquire viral material from neighboring cells. These cells may test positive for viral RNA or viral proteins like spike, despite never being truly infected. So a positive signal does not necessarily mean productive viral replication.
From a scientific perspective, the most reasonable model may actually be a combination of different situations, like a small reservoir that exists in a long-lived cell, which can induce low-level or intermittent replication. This can induce viral proteins and RNA to be continuously released. These products can then be captured by immune cells and distributed through the body.
That model can explain why viral material remains detectable despite turnover, and why it is so hard for scientists to recover large amounts of infectious virus years later.
One of the key unresolved question is whether the reservoir is producing new virus, or merely old viral products that are being recycled and retained. That's one of the areas where the field is still struggling to obtain definitive evidence.
#LongCovid #MECFS
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
https://t.co/BPKRV7nwbA
Frage an die #MECFS, #LongCovid und #PostVac Betroffenen:
Ist bei euch eine Penicillin-Allergie bekannt? Oder habt ihr zumindest den Verdacht, dass da was sein könnte?
“ME can be invisible, it can be unpredictable, and it can be isolating. So we should do our best as public and professionals to support those people as much as we can.”
Dr Ranj on how to help people with ME/CFS
Clip from BBC Morning Live.
Die Menge an Abfall hat 2024 in Deutschland erneut abgenommen und ist auf dem tiefsten Stand seit 2009. Seit dem Höchststand 2018 hat das Müllaufkommen kontinuierlich abgenommen.
🗑️🗑️🗑️
Es gibt zu viele negative News, deswegen poste ich jeden Tag eine #guteNewsdesTages.
Termine kosten immer viel mit ME.
Aber trotzdem hat es oft ein bisschen was schönes.
Nette Begegnungen im "echten Leben"
Die Welt ein bisschen durchs Autofenster sehen können.
Und das schöne Gefühl, dass wieder was erledigt ist.
Preis dafür ist klar: PEM.
(Tav*r, do your magic)