TTOR

(FR) Anti #LongCovidKids #LongCovid #PACS #MECFS #ChronicLyme #PAIS #MS

[Carmen Scheibenbogen @C_Scheibenbogen]

Diese Immunadsorptions-Studie hat ein methodisches Problem: Der Tryptophan-Adsorber hat die Autoantikörper nur unzureichend abgesenkt (siehe Supplementary Fig. 3). Auch war der Nachweis von Autoantikörpern kein Einschlusskriterium. Long COVID und ME/CFS sind heterogene Erkrankungen, nur ein Teil ist autoantikörpervermittelt.

https://t.co/bOnZ9smnXZ

[Tom Kindlon @TomKindlon]

"The predominance of cerebral hypometabolism in [Long covid] patients with PEM draws important corollaries to similar changes seen in patients with FM & ME/CFS in prior neuroimaging studies"

https://t.co/c9Dd2Eij1p

Screenshot from Science for ME update

#LongCovid #MEcfs

[Hiroshi Yasuda (保田浩志) @Yash25571056]

FYI, "The reactivation of latent herpesviruses has been associated with sustained immune dysregulation for long periods of COVID-19.
The reactivation process refers to the mechanism by which the latent viruses [(e.g. EBV and Varicella Zoster Virus (VZV)], which remain dormant in B lymphocytes and epithelial cells following initial infection, become active and enter their replication cycle.
The reactivation of these dormant viruses can be triggered by concurrent infections, physical or psychological stress or immunosuppression..
For instance, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) has been linked to LC..
Furthermore, dysautonomia, a condition observed in several post-viral infections, has also been reported in LC patients..
these viruses (EBV and VZV) can remain latent within the host and can be reactivated by a stressor such as another serious viral infection (e.g. SARS-CoV-2), leading to chronic inflammation and neurological disorders..
EBV infects B lymphocytes and epithelial cells, potentially triggering autoimmune disorders such as multiple sclerosis, Systemic Lupus Erythematosus (SLE), and rheumatoid arthritis.. Association between EBV reactivation and SARS-CoV-2 infection has been demonstrated by several studies.."

Stay relaxed in clean air.

'Mechanisms and impact of long COVID: pathophysiology, neuropsychiatric effects and vaccination'
https://t.co/wsoj2Jg0NF

[Harry Spoelstra @HarrySpoelstra]

🚨Long COVID is linked to lasting sleep problems, including unhealthy sleep duration, poor sleep quality, and sleep disturbance, nearly 3 years after initial infection.

So, Covid-19 can add an extra #HealthRisk for multiple chronic conditions and mortality!

Thanks, David!

[Manuel Ruiz @manruipa]

⚠️💊 Long COVID and ME/CFS: a layered strategy, not a single treatment for everyone

One of the mistakes when talking about Long COVID and ME/CFS is looking for “the treatment”, as if all patients had exactly the same mechanism.

They do not.

But that does not mean there is no common logic.

The model I propose is to think of these diseases as post-infectious processes maintained by layers:

A persistent pathogen or a sustained antigenic source.
Chronic immune hyperactivation.
Immune exhaustion and poorer control of latent pathogens.
Secondary reactivations that add more antigenic load.
Systemic consequences: inflammation, mast cells/histamine, oxidative stress, barrier dysfunction, autoimmunity, dysautonomia, neuroinflammation, endocrine alterations or vascular involvement.
Baseline treatments and then treatments directed according to the dominant mechanism.

The key is not to place all layers at the same level.

Not everything is a primary cause.

Some things are consequences.

And some consequences, once they appear, can become amplifiers that maintain the vicious cycle.

Long COVID and ME/CFS: same model, different degree of classification

For me, Long COVID and ME/CFS are not opposite processes.

They may follow the same post-infectious model.

The main difference is that Long COVID is better classified by its initial pathogen: SARS-CoV-2.

By contrast, ME/CFS is a more heterogeneous label where post-infectious patients initiated or maintained by different pathogens may be grouped together: EBV, HHV-6, CMV, enteroviruses, parvovirus B19, Borrelia, Toxoplasma or other persistent, latent or intracellular pathogens.

In other words:

Long COVID would be a post-infectious disease defined by SARS-CoV-2.

ME/CFS could include several similar post-infectious subtypes, but initiated by different pathogens.

The underlying logic would be the same:

persistent pathogen or antigenic reservoir
→ continuous immune stimulation
→ chronic immune hyperactivation
→ sustained inflammation
→ T/NK cell exhaustion
→ poorer control of latent pathogens
→ new reactivations
→ more antigenic load
→ more inflammation.

Therefore, the problem would not be that Long COVID and ME/CFS have nothing to do with each other.

The problem is that ME/CFS probably mixes post-infectious patients of different origins under the same clinical label.

▪️Long COVID: SARS-CoV-2 as the initial persistent source

In Long COVID, the initial axis would be the persistence of SARS-CoV-2 in tissue or cellular reservoirs, with sustained or intermittent production of viral antigens.

There does not necessarily have to be detectable viremia in blood.

But if the immune system keeps seeing viral antigens months or years later, those antigens are not well explained as simple passive “remnants” from the initial infection.

The body degrades proteins and RNA through proteases, nucleases, autophagy, the proteasome, cellular turnover and immune clearance.

For this reason, prolonged presence of viral antigen points to a sustained source:

tissue reservoirs;
infected cells;
low-level persistent infection;
abortive or incomplete infection;
intermittent production of viral material;
local reactivation;
or cellular persistence in tissues where the immune system does not properly eliminate the stimulus.

In other words:

if there is persistent antigen for months or years, we need to think of some type of reservoir or biological source that renews it.

That stimulus keeps the immune system chronically activated.

And that chronic activation can lead to persistent inflammation, immune exhaustion and poorer control of other latent pathogens.

[Evelio González Prieto @evelio_prieto]

🟡💀🟡"Autopsy studies confirmed viral replication predominantly in the brainstem, with potential invasion via neurotropic pathways (e.g., olfactory or trigeminal nerves) or ACE2-mediated transcellular entry across the Blood-Brain Barrier".

[SARS‑CoV‑2 (COVID-19) @COVID19_disease]

🚨 BREAKTHROUGH: Scientists Develop Sugar-Coated Nanoparticle That Blocks COVID-19 Virus From Binding to Human Cells Reduces Infection by ~99% in Lab Experiments

[Secretary Kennedy @SecKennedy]

I visited Fort Carson to see firsthand how the Army is transforming military nutrition through its Campus-Style Dining Venue modernization program, with the help of celebrity chef @RobertIrvine.

The results speak for themselves: healthier meals, higher morale, and lower costs. Fort Carson is proving that real, nutritious food can strengthen military readiness while saving taxpayer dollars.

[Long COVID Labs @longcovidlabs]

WOW- Huge news to see discussion of a tangible biomarker - with a known treatment- on the @nih website! ✨

The LC community has been waiting for too long, but sometimes there are moments where you see real leaps and jumps forward.

This feels like one of these moments @PutrinoLab

[Billy Hanlon @bhanlon15]

NIH: Immune system may attack nervous system in some Long COVID patients

“Our study now shows that if you are in a subgroup of Long COVID patients who have autoantibodies circulating...a quantifiable sign that you may be a good candidate for these drugs"

https://t.co/utBz7Mmxp6

[RTHM @RTHM_Health]

The FDA has approved ensitrelvir, sold as Xocova, as the first oral antiviral for post-exposure prevention of COVID-19 in people aged 12 years and older after close contact with someone who has COVID-19.

The approval was based on a phase 3 study (linked below) published in The New England Journal of Medicine, which tested a 5-day course of ensitrelvir in household contacts enrolled within 72 hours of exposure to SARS-CoV-2.

The study found that ensitrelvir significantly reduced symptomatic COVID-19 compared with placebo: 2.4% vs 9.9%. It also reduced overall SARS-CoV-2 infections, including asymptomatic infections, and showed evidence of suppressing viral replication. Side effects were similar between groups, and serious adverse events were uncommon.

Ensitrelvir is already approved in Japan for treating mild-to-moderate COVID-19, but in the U.S., it is only FDA-approved for post-exposure prevention, not acute COVID-19 treatment.

Read the full study: https://t.co/XNbpLnPBIT

[Tedros Adhanom Ghebreyesus @DrTedros]

Lenacapavir is one of the most exciting innovations in the history of #HIV.

My congratulations to #SouthAfrica for being among the first countries to launch the national lenacapavir programme.

Looking ahead, South Africa has the opportunity not only to scale up access, but to contribute to regional production and supply, strengthening health security across the continent.

[Jon Douglas @atranscendedman]

An immunocompromised man with neuroinvasive West Nile virus received donor derived virus specific T cells.

West Nile targeted T cells appeared in blood and MRI lesions improved, suggesting immune therapy may help fight persistent infection.

https://t.co/CTGWTRP73N

[Heather C @Burning_mama47]

#1

I have another piece of arsenal to add to my case!!
🙌🙏🙌🙏🙌🙏🙌🙏🙌🙏

Biopsy confirmed Small Fiber Neuropathy! 🤛

But not the typical kind. Mine is NON LENGTH DEPENDENT, meaning the damage is not in my hands and feet. And that has always puzzled me!
Every person I ever heard describe burning described it in their hands and feet first. Mine has always been everywhere but there. That distinction just became one of the most validating pieces of scientific evidence I have ever received.😊

This is molecular mimicry. The spike protein from the vaccine is so similar to my own nerve tissue that my immune system cannot tell the difference between the invader and my own body. So it attacks both. It has been attacking both for 1,642 days.

Since day one I have told every doctor the same thing. It feels like Biofreeze running through my veins.
24/7. Its permanent.
Now it is confirmed under a microscope.

On June 2nd I begin treatment at Edogawa Hospital in Japan 🇯🇵

DFPA will filter my blood, removing the spike antibodies, microclots, and inflammatory burden that have been destroying my nerves and blood
vessels.💯

Then SHED, stem cell growth factors derived from children's baby teeth, will work to regenerate the nerve fibers and repair the damage left behind. 🧬

You cannot rebuild what is still being destroyed. That is why the sequence matters. Clean first. Rebuild second.

This is the science my own country cannot offer me.🤔

@SecKennedy @DrJBhattacharya @POTUS @VP @RonJohnsonWI @RandPaul @ThomasMassie @RepMTG @SenatorCassidy @SenTedCruz @Jim_Jordan @AaronSiriSG @SiriGlimstad @MaryBowdenMD @DrMargaretShow @DrJordanVaughn @MartyMakaryMD @DrPeterMcCullough @drmalone @DrJohnCampbell @VigilantFox @DietrichKlinghardt @BrianneDressen @IamJessicaSutta @KyleWarnerMTB @CatsRule2023 @React19org
#SFN #SmallFiberNeuropathy #VaccineInjury #SpikeProtein #LongVax #MolecularMimicry #DFPA #SHED #EdogawaHospital #BurningAlive

[TTOR @VPAV8]

@AnneliseBocquet Tellement intéressant ! Dans ce cas, comment éliminer les virions infectieux dans les corps apoptotiques ou bien les rendre inertes ? De façon à ce que les macrophages ne soient pas infectés à leur tour ? Anticorps monoclonaux ? Existe-t-il des antiviraux/antivirions ?

[Bocquet Annelise 🔬🧬📚🚜 @AnneliseBocquet]

L'efferocytose des corps apoptotiques mène l'infection par le SARS-CoV-2 et l'inflammation par les macrophages.
Très intéressante, l'étude...
https://t.co/i6mFlm3iiY

Les auteurs ont mis en évidence que les cellules infectées par le SARS-CoV-2 meurent par apoptose (mort cellulaire programmée). En mourant, elles emballent des virions infectieux vivants dans des corps apoptotiques (petites vésicules extracellulaires, ApoBDs). Puis, les macrophages (cellules immunitaires) avalent ces corps apoptotiques via un processus appelé efferocytose.

Du coup, le virus entre dans le macrophage sans passer par ACE2 (les macrophages expriment très peu ACE2). Cela déclenche une forte inflammation via l’inflammasome et la voie NF-κB = cytokine storm ou "tempête cytokinique".

C’est un nouveau mécanisme d’infection et d’amplification de l’inflammation dans les poumons sévères.

Pourquoi c’est important dans les Spikeopathies ? Ben... Cela explique pourquoi les macrophages sont infectés et très inflammatoires même quand ils n’expriment presque pas ACE2.
Cela renforce l’idée que la Spike (et le virus) peut persister ou circuler via des vésicules. Et l’étude identifie même une piste thérapeutique : les bloqueurs des canaux calciques T-type réduisent la formation de ces corps apoptotiques et limitent la transmission et l’inflammation.

Là où c'est aussi intéressant, c'est le lien potentiel avec mTOR...
https://t.co/Etg4ptatIB
https://t.co/zwugJ6tTCN
https://t.co/N3794dEBO4
https://t.co/uKIWYqfUfh

Accrochez-vous... je vais tenter de faire simple...

Pour expliquer simplement, l’efferocytose, c'est le travail normal des éboueurs... les Pacmans de l'immunité ou macrophages.
Quand une cellule est infectée et qu'elle meurt (apoptose), elle envoie un signal "je suis morte, ramassez-moi". Les macrophages la mangent tranquillement, sans déclencher d’alarme (production de TGF-β et IL-10 = anti-inflammatoire). C’est la "résolution" normale de l’inflammation.

Qu'est-ce que fait le SARS-CoV-2 et sa Spike ?
Le virus transforme les cellules mortes en petits paquets piégés (corps apoptotiques) qui contiennent encore du virus vivant. Les macrophages les mangent... mais au lieu d’éteindre l’incendie, ils s’enflamment violemment (tempête cytokinique). C’est aussi un cheval de Troie : le virus entre dans le macrophage sans passer par la porte habituelle (ACE2).

Maintenant, on sait que AXL est comme un "bouton" sur les éboueurs qui leur dit "mange doucement, sans faire de bruit".
La Spike du virus utilise ou dérègle ce bouton... du coup, les éboueurs deviennent fous : ils mangent le paquet piégé, s’infectent, et déclenchent une énorme inflammation au lieu de calmer les choses.
On assistera aussi à une boucle vicieuse avec une inflammation chronique et une tolérance immunitaire (IgG4, IL-10 élevé).

Oui oui... j'ai toujours la tolérance immunitaire en marotte. 😅

On sait aussi que si mTOR est inhibé, cela favorise l'efferocytose...
Oula... oupsy oups.

La Spike a un effet sur mTOR : Parfois l'active...
Parfois l'inhibe...

Le hic : cela dépend du type de cellule concernée.
Pour les macrophages, on a plutôt une activation de mTOR par la Spike, ce qui favorise la survie... la survie de quoi ? De macrophages ayant "ingurgité" le virus via les corps apoptotiques.

Dans les cellules épithéliales infectées (poumons, etc.), la Spike inhibe souvent la voie mTOR... Cela favorise l’autophagie (nettoyage cellulaire) mais aussi l’apoptose (mort cellulaire).
Résultat : plus de cellules mortes qui libèrent des corps apoptotiques contenant du virus vivant. Qui seront "gobés" par les macrophages... utilisés en cheval de Troie.

C'est du génie. Un génie diabolique... mais du génie...
La Spike favorise indirectement l’expansion du virus en créant plus de « paquets piégés » (via inhibition mTOR dans les cellules infectées) et en transformant les macrophages en cellules inflammatoires persistantes (via activation mTOR dans les macrophages).

[Vipin M. Vashishtha @vipintukur]

What if viruses don’t need to infect the brain to damage it?

➡️ A growing body of evidence suggests that viral proteins themselves can act as neurotoxins, triggering long-lasting neurological symptoms even when little or no virus is present in the CNS. 1/

[Nick Norwitz MD PhD @nicknorwitz]

Peptides for Long-COVID?

One ongoing theory about long COVID is that viral reservoirs and spike protein may persist in the gut, then leak into circulation because of increased intestinal permeability.

Along these lines, the specific peptide, larazotide, is being explored for long COVID at Harvard and elsewhere.

The idea is that by improving tight junction function and reducing “leaky gut,” larazotide may help prevent spike protein and other viral antigens from escaping into the bloodstream and perpetuating inflammation.

More details in yesterday’s letter on larazotide and leaky gut, linked below.

#larazotide #peptides #staycurious

[Vipin M. Vashishtha @vipintukur]

What if #LongCOVID is an immune system stuck in the wrong gear?

➡️ Single-cell profiling of 156,000+ immune cells revealed chronically activated B cells, inflammatory monocytes, exhausted T cells, and dysfunctional NK cells in Long COVID patients.

➡️ The more severe the symptoms, the stronger the inflammatory immune signature. 1/

H/T: @CatchTheBaby