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#CovidIsNotOver

64 posts54 participants8 posts today
Public
Tom Kindlon

New from Germany:

Brainstem Reduction and Deformation in the 4th Ventricle Cerebellar Peduncles in Long COVID Patients: Insights into Neuroinflammatory Sequelae and “Broken Bridge Syndrome”

medrxiv.org/content/10.1101/20

@longcovid
#LongCovid #PASC #PwLC #postcovid #postcovid19 #LC #Covidlonghaulers #PostCovidSyndrome #longhaulers #COVIDBrain #NeuroPASC
@covid19 #Coronavirus
#COVID19 #COVID #COVID_19 #COVIDー19 #SARSCoV2 @novid@chirp.social #novid @novid@a.gup.pe #CovidIsNotOver
@auscovid19 #auscovid19

1/

medRxiv · Brainstem Reduction and Deformation in the 4th Ventricle Cerebellar Peduncles in Long COVID Patients: Insights into Neuroinflammatory Sequelae and "Broken Bridge Syndrome"Post-COVID Syndrome (PCS), also known as Long COVID, is characterized by persistent and often debilitating neurological sequelae, including fatigue, cognitive dysfunction, motor deficits, and autonomic dysregulation (Dani et al., 2021). This study investigates structural and functional alterations in the brainstem and cerebellar peduncles of individuals with PCS using diffusion tensor imaging (DTI) and volumetric analysis. Forty-four PCS patients (15 bedridden) and 14 healthy controls underwent neuroimaging. Volumetric analysis focused on 22 brainstem regions, including the superior cerebellar peduncle (SCP), middle cerebellar peduncle (MCP), periaqueductal gray (PAG), and midbrain reticular formation (mRt). Significant volume reductions were observed in the SCP (p < .001, Hedges' g = 3.31) and MCP (p < .001, Hedges' g = 1.77), alongside decreased fractional anisotropy (FA) in the MCP, indicative of impaired white matter integrity. FA_Avg fractional anisotropy average tested by FreeSurfer Tracula, is an index of white matter integrity, reflecting axonal fiber density, axonal diameter and myelination. These neuroimaging findings correlated with clinical manifestations of motor incoordination, proprioceptive deficits, and autonomic instability. Furthermore, volume loss in the dorsal raphe (DR) and midbrain reticular formation suggests disruption of pain modulation and sleep-wake cycles, consistent with patient-reported symptoms. Post-mortem studies provide supporting evidence for brainstem involvement in COVID-19. Radtke et al. (2024) reported activation of intracellular signaling pathways and release of immune mediators in brainstem regions of deceased COVID-19 patients, suggesting an attempt to inhibit viral spread. While viral genetic material was detectable, infected neurons were not observed. Matschke et al. (2020) found that microglial activation and cytotoxic T lymphocyte infiltration were predominantly localized to the brainstem and cerebellum, with limited involvement of the frontal lobe. This aligns with clinical observations implicating the brainstem in PCS pathophysiology. Cell specific expression analysis of genes contributing to viral entry (ACE2, TMPRSS2, TPCN2, TMPRSS4, NRP1, CTSL) in the cerebral cortex showed their presence in neurons, glial cells, and endothelial cells, indicating the potential for SARS-CoV-2 infection of these cell types. Associations with autoimmune diseases with specific autoantibodies, including beta 2 and M 2 against G protein coupled alpha 1, beta 1, beta 2 adrenoceptors against angiotensin II type 1 receptor or M1,2,3 mAChR, among others, voltage-gated calcium channels (VGCC) are known (Blitshteyn et al. 2015 and Wallukat and Schminke et al. 2014). These findings support the "Broken Bridge Syndrome" hypothesis, positing that structural disconnections between the brainstem and cerebellum contribute to PCS symptomatology. Furthermore, we propose that chronic activation of the Extended Autonomic System (EAS), encompassing the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system, may perpetuate these symptoms (Goldstein, 2020). Perturbations in this system may relate to the elevation of toxic autoantibodies AABs (Beta 2 and M 2), specific epitopes of the COVID virus's SPIKE protein and Cytokine storm of IL-1, IL-6, and IL-8 in their increased numbers (1,000->10,000) Further research is warranted to elucidate the underlying neuroinflammatory mechanisms, EAS dysregulation, and potential therapeutic interventions for PCS. Keywords: Long COVID, Brainstem, Cerebellar Peduncles, Diffusion Tensor Imaging, Neuroinflammation, Broken Bridge Syndrome, Extended Autonomic System (EAS) ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This study was funded by OTTO Research Group ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: 2022-100867-BO-ff 1. Ethics approval was granted by the Ethics Committee of the Hamburg Medical Association, Germany, on September 5, 2022, under the title "MRI Biomarkers in Chronic Fatigue," by Prof. Dr. Rolf Stahl. 2. The project complies with the ethical and professional requirements. The Ethics Committee approves the project. The Ethics Committee operates on the basis of German law and professional regulations, as well as in accordance with ICH-GCP. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes All data produced in the present study are available upon reasonable request to the authors All data produced in the present work are contained in the manuscript
Continued thread
Public
meduz'

One thing I’ve never heard about wearing a mask: I’m used to it when not ill (e.g. in the subway), but having to wear it while ill is way harder. I quickly get hot flashes, it’s harder to breathe when the nose is stuffed, and on day 3 I almost fainted while waiting in the waiting room at the practitioner.

So that’s what happen if you want to protect others because someone else did not protect you.

#COVID#CovidIsNotOver
Public *
Shaula Evans

People complain to me about "skin hunger".

People with spouses, children, pets, sexual partners & access to human touch. They just aren't getting the quantity or quality of touch they want from the people they want.

That's not what skin hunger means.

I have not been touched by another human being in 5+ years.

*That* is #SkinHunger.

For the love of all that's holy, don't use this phrase in your normie life with people in isolation. 1/n

@lonelinesscorps #TouchDeprivation #CovidIsNotOver

Public
Broadwaybabyto

I understand wanting to go 'back to normal'. Pandemics are traumatizing and scary. Of course people want to forget them.

But they don't end when we decide we've had enough. The threat doesn't go away because we have 'Covid fatigue' or because we’re sick of masking.

We must stop denying the reality that Covid is still with us, still killing and still disabling people.

We must work on our collective trauma and push for common sense measures like masks in healthcare, free respirators and tests and clean air in public spaces.

“Back to normal” isn’t working. It’s a mirage. The comfortable lie.

But we can move towards a new normal together. One where everyone is safer and healthier. It’s not too late.

#covidisnotover#covidisairborne#longcovid
Public *
Trenton Hoshiko | Filmmaker

There were roughly 2.7 million covid cases THIS WEEK! Roughly 1/120 in the US infected.

Covid really is not over.

It's as important now as it was in March 2020 to protect yourself, your family, your friends, your colleagues, & your community! Wearing an n95 mask in public spaces is the most efficient and effective way to protect yourself day to day especially when combined w/ vaccines!

#CovidIsNotOver#wearamask
Public
VeeRat

I went to my doctor's office this morning (for vertigo and a tick bite). Just wanted to post about my experiences in regards to masking.

Last week, I had gone to the same office, but my doctor was out so I saw someone else. That doctor had told me, "you know that you don't have to wear a mask, right?" And she was not masked.

I saw my own doctor today, and she continues to double-mask. She wears an N95 (3M Aura head strap), and over that she wears a surgical mask. The healthcare staff who are not doctors were all wearing surgical masks, semi-decent face-hugging ones, not the really baggy blue ones. Receptionists were not masked.

None of the other patients that I saw were masked. I had an ear-loop KN95. I knew I would have to remove it briefly for the exam, or else I would have worn my Flo-Mask. That mask takes me a while to get sealed, while I can get a quick decent seal on the KN95, and I wanted it to seal as quickly as possible when re-donning. (My doctor gave me the option to remove it; she would have accepted it if I had refused. I didn't refuse because frankly I'm nervous about having vertigo for two weeks ongoing and wanted to have all available tests done.)

When I took it off for the 30 seconds or so of the facial exam, I was overwhelmed by the scent of perfume. I can't believe a medical office allows that much fragrance. Even if Covid and other respiratory illnesses vanished, I would continue to mask just to block out that horrible overwhelming perfume (and other awful intrusive scents) in public places.

This place has a mask policy posted, but it just says if you are feeling sick or had a positive Covid test to wear a mask. It doesn't specify KN95+ and isn't sufficient to protect against asymptomatic and pre-symptomatic infections.

No one bothered me about my mask. I hope that continues.

#Covid#CovidIsNotOver#WearAMask
Public
Dennis

A surprise work lunch appears. You don't *have* to go, but it's awkward if you don't. You have been wearing an #N95 at work for over a year.

#COVID #CovidIsNotOver #WearAMask

Do you:

· 11 people · Closed
Continued thread
Public
Jeanine B. aus H.

mir diese Ignoranz nicht geben kann!

Wenn mein Vati aufgrund eines Infektes stirbt, weil so ein ignoranter Mensch 'Vulnerable nicht schützen' wollte, kann man dann eigentlich Krankenhauskosten, etc. als Schadensersatz einklagen? Frage für ne Freundin

Was ich die Schnauze voll hab, glaubt man mir erst, wenn ich M's werfe

#Corona#SARSCoV2#Influenza
Public *
datum (n=1)

This preprint seems so good! [edit: pre-proof not pre-print, it has been peer reviewed and the data passed muster, but might have formatting, grammar, and spelling tweaks]

goals were: a) to detect viral load in indoor air in different areas and floors of a separate COVID building in a hospital [...], b) to evaluate the effect of an air-cleaner in the reduction of viral load in the presence of patients, and c) to examine the correlation between viral presence in the air and particle matter burden.

their methodology is making me happy!

Their system separated aerosols into > 2.5 μm, 1.0 to 2.5 μm, 0.5 to 1.0 μm, 0.25 to 0.50 μm, and < 0.25 μm, and found

SARS-CoV-2 was detected in all different fractions and the highest viral loads were detected at stages A (> 2.5 μm) and B (1 - 2.5 μm).

however this was in open-window conditions, ie. low CO2 and higher airflow; sampling with the same equipment in households, they found

the highest amount was detected in Stage 4 (0.25 - 0.5 μm)

The data is mostly PCR but they did do some sequencing, and positively confirmed the dominant variants were stable through the study, and not confounding.

Note the air cleaner was a "Airocide (APS GCS-25 model) air purifier" which uses "photocatalytic oxidation technology" as well as 254nm UV, with no HEPA or other mechanical filter.

Also, this is vindicating for those of us pleading with folks to not immediately de-mask in the hallway:

the highest concentration was detected in COVID clinic rooms displaying a high peak of 1123 copies/m3, whereas at the corridor area showed 481 copies/m3

Also highly of note, they could not detect any virus in the areas that were upstream of negative-pressure COVID-19 care. So yes, home isolation protocols that emphasize negative pressure zones absolutely are well founded!

sciencedirect.com/science/arti via aus.social/@Sidherian

www.sciencedirect.com“SARS-CoV-2 airborne detection within different departments of a COVID-19 hospital building and evaluation of air cleaners in air viral load reduction”The pandemic of COVID-19 has brought in light the necessity for the development of novel detection methods for airborne transmitted pathogens, and the…
#SARSCoV2#COVID#COVID19
Public *
datum (n=1)

These findings support the “Broken Bridge Syndrome” hypothesis, positing that structural disconnections between the brainstem and cerebellum contribute to PCS [Long COVID] symptomatology. Furthermore, we propose that chronic activation of the Extended Autonomic System (EAS), encompassing the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system, may perpetuate these symptoms

In this high quality brain volume data,

Significant volume loss was observed in the superior cerebellar peduncle (SCP) in LC patients compared to healthy controls (LC: 219.74 mm³ vs. controls: 347.03 mm³, p < .001, Hedges’ g = 3.31). Furthermore, reduced volumes were evident in the dorsal raphe (DR) and midbrain reticular formation (mRt) (p < .001)

It was not metabolism-marker scanning, but volumentric, so they were able to capture:

Three-dimensional reconstructions revealed deformities in the 4th ventricle and cerebellar peduncles, suggesting impaired cerebrospinal fluid dynamics [...] Importantly, these volume reductions and FA changes correlated with motor deficits,
proprioceptive dysfunction, and autonomic dysregulation

TLDR?

Our findings reveal significant structural and functional alterations in the brainstem and cerebellar peduncles of LC patients

medrxiv.org/content/10.1101/20

via zeroes.ca/explore/links

medRxiv · Brainstem Reduction and Deformation in the 4th Ventricle Cerebellar Peduncles in Long COVID Patients: Insights into Neuroinflammatory Sequelae and "Broken Bridge Syndrome"Post-COVID Syndrome (PCS), also known as Long COVID, is characterized by persistent and often debilitating neurological sequelae, including fatigue, cognitive dysfunction, motor deficits, and autonomic dysregulation (Dani et al., 2021). This study investigates structural and functional alterations in the brainstem and cerebellar peduncles of individuals with PCS using diffusion tensor imaging (DTI) and volumetric analysis. Forty-four PCS patients (15 bedridden) and 14 healthy controls underwent neuroimaging. Volumetric analysis focused on 22 brainstem regions, including the superior cerebellar peduncle (SCP), middle cerebellar peduncle (MCP), periaqueductal gray (PAG), and midbrain reticular formation (mRt). Significant volume reductions were observed in the SCP (p < .001, Hedges' g = 3.31) and MCP (p < .001, Hedges' g = 1.77), alongside decreased fractional anisotropy (FA) in the MCP, indicative of impaired white matter integrity. FA_Avg fractional anisotropy average tested by FreeSurfer Tracula, is an index of white matter integrity, reflecting axonal fiber density, axonal diameter and myelination. These neuroimaging findings correlated with clinical manifestations of motor incoordination, proprioceptive deficits, and autonomic instability. Furthermore, volume loss in the dorsal raphe (DR) and midbrain reticular formation suggests disruption of pain modulation and sleep-wake cycles, consistent with patient-reported symptoms. Post-mortem studies provide supporting evidence for brainstem involvement in COVID-19. Radtke et al. (2024) reported activation of intracellular signaling pathways and release of immune mediators in brainstem regions of deceased COVID-19 patients, suggesting an attempt to inhibit viral spread. While viral genetic material was detectable, infected neurons were not observed. Matschke et al. (2020) found that microglial activation and cytotoxic T lymphocyte infiltration were predominantly localized to the brainstem and cerebellum, with limited involvement of the frontal lobe. This aligns with clinical observations implicating the brainstem in PCS pathophysiology. Cell specific expression analysis of genes contributing to viral entry (ACE2, TMPRSS2, TPCN2, TMPRSS4, NRP1, CTSL) in the cerebral cortex showed their presence in neurons, glial cells, and endothelial cells, indicating the potential for SARS-CoV-2 infection of these cell types. Associations with autoimmune diseases with specific autoantibodies, including beta 2 and M 2 against G protein coupled alpha 1, beta 1, beta 2 adrenoceptors against angiotensin II type 1 receptor or M1,2,3 mAChR, among others, voltage-gated calcium channels (VGCC) are known (Blitshteyn et al. 2015 and Wallukat and Schminke et al. 2014). These findings support the "Broken Bridge Syndrome" hypothesis, positing that structural disconnections between the brainstem and cerebellum contribute to PCS symptomatology. Furthermore, we propose that chronic activation of the Extended Autonomic System (EAS), encompassing the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system, may perpetuate these symptoms (Goldstein, 2020). Perturbations in this system may relate to the elevation of toxic autoantibodies AABs (Beta 2 and M 2), specific epitopes of the COVID virus's SPIKE protein and Cytokine storm of IL-1, IL-6, and IL-8 in their increased numbers (1,000->10,000) Further research is warranted to elucidate the underlying neuroinflammatory mechanisms, EAS dysregulation, and potential therapeutic interventions for PCS. Keywords: Long COVID, Brainstem, Cerebellar Peduncles, Diffusion Tensor Imaging, Neuroinflammation, Broken Bridge Syndrome, Extended Autonomic System (EAS) ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This study was funded by OTTO Research Group ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: 2022-100867-BO-ff 1. Ethics approval was granted by the Ethics Committee of the Hamburg Medical Association, Germany, on September 5, 2022, under the title "MRI Biomarkers in Chronic Fatigue," by Prof. Dr. Rolf Stahl. 2. The project complies with the ethical and professional requirements. The Ethics Committee approves the project. The Ethics Committee operates on the basis of German law and professional regulations, as well as in accordance with ICH-GCP. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes All data produced in the present study are available upon reasonable request to the authors All data produced in the present work are contained in the manuscript
#SARSCoV2#COVID#COVID19
Public
trendless 🇨🇦 :flag_AB:

Dear Editor,

With recent cuts to funding linked to COVID-19 and pandemic readiness, the US Department of Health and Human Services (HHS) has proclaimed it “will no longer waste billions of taxpayer dollars responding to a non-existent pandemic that Americans moved on from years ago”. While devastating for researchers and the many who continue to suffer from COVID-19, including long COVID, this move should perhaps be unsurprising in a world where “after COVID” and “post COVID” are common parlance, including within our public health community. This language is confounding not only because COVID-19 straightforwardly remains a threat, but also because one would be hard-pressed to find anyone similarly willing to say “post AIDS”, for example, despite AIDS being first recognized nearly half a century ago, or “post Ebola”, despite the two Ebola public health emergencies of international concern (PHEIC) ending years ago.

Even the language of “post pandemic” confuses the end of the COVID-19 public health emergency of international concern in May 2023 with the end of the pandemic, the latter being something that is not formally declared and remains contestable. Irrespective of where one stands on this point, the metaphysical questions of what constitutes a pandemic and exactly when one ends is less important than the risk communication question of whether using the language of “post COVID”, “post pandemic”, or even “back during COVID” obscures risk perception and contributes to an unwitting shift in research priorities. Unless we wish to move on from COVID in research, we must not imply we have moved on from COVID through our language.

🔗 bmj.com/content/388/bmj.r636/r

The BMJSuggesting the world is “post COVID” contributes to an unwitting shift in research priorities
#CovidIsNotOver
Public
Tom Kindlon

From Australia:

"WEHI researchers have developed a drug compound that can protect mice from contracting long COVID symptoms.

The world-first study also found the compound can treat acute #COVID with better efficacy than Paxlovid"

eurekalert.org/news-releases/1

@longcovid
#LongCovid #PASC #PwLC #postcovid #postcovid19 #LC #Covidlonghaulers #PostCovidSyndrome #longhaulers #COVIDBrain #NeuroPASC

@covid19 #Coronavirus
#COVID19 #COVID_19 #COVIDー19 #SARSCoV2 #CovidIsNotOver
@auscovid19 #auscovid19

News Release 8-Apr-2025 Tackling the ‘silent pandemic’: breakthrough study puts first long COVID treatment on horizon Peer-Reviewed Publication Walter and Eliza Hall Institute Covid Front image: COVID-19 is caused by the SARS-CoV-2 virus. This image shows antibodies (shown in orange and purple) binding to ‘spike proteins’ on the surface of SARS-CoV-2 virus (shown in teal and yellow). Spike proteins are critical for SARS-CoV-2 to enter human cells, and this can be blocked by specific antibodies – breaking the infection cycle. Credit: WEHI Researchers have shown a new drug compound can prevent long COVID symptoms in mice – a landmark finding that could lead to a future treatment for the debilitating condition. The world-first study found mice treated with the antiviral compound, developed by a multidisciplinary research team at WEHI, were protected from long term brain and lung dysfunction – key symptoms of long COVID. Researchers hope the unprecedented results could lead to clinical trials and the first treatment for the disease in the future. At a glance WEHI researchers have developed a drug compound that can protect mice from contracting long COVID symptoms. The world-first study also found the compound can treat acute COVID with better efficacy than Paxlovid – the leading treatment currently approved for COVID-19. It’s hoped the results could lead to clinical trials and an oral treatment for long COVID in the future.
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