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#COVID19

80 posts62 participants5 posts today
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@Sidherian My parents went to bars even though it was the primary place COVID was spreading and MN's DOH was telling people not to. They gave me COVID and then mocked me while I recovered. They then refused to believe me that I had long COVID and pretended it was all in my head until a few years ago. They never apologized for crippling me forever for a few bar drinks. They are pro vaccine liberals by the way. They are the upper end of American seriousness on COVID.

The CDC wrote its own elitaph by sneering, condescending at & ultimately dismissing #covid19 & airborne viral transmission advocates, letting Delta Airlines set public health policy, & ultimately being an agency captured & purposed to be subservient primarily to the ruling class.

Walensky et al can roast in hell.

This isnt a good thing of course -- millions will suffer.

But it was in large part because of their actions that it is so.

And yeah, I recall all those houses at Halloween in Atlanta mocking citizens for "doing their own research".

After tacitly suggesting we do just that -- "do your own risk assessment".

We can have cleaner air. We just need to demand it in healthcare, education, and the workplace.

“SARS-CoV-2 airborne detection within different departments of a COVID-19 hospital building and evaluation of air cleaners in air viral load reduction”

"air cleaners using TiO2-UV light technology can reduce up to 98,1% of viral load in the air of a COVID patient room with confirmed positive airborne viral RNA"

#Covid19 #CleanAir #Health

sciencedirect.com/science/arti

(Boston, Massachusetts)
Research study on the effectiveness of abrocitinib vs placebo for improving severe fatigue in adults with Long COVID

Image is from MassME April Newsletter

massmecfs.org/newsletters/922-

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

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

The CDC's vaccine advisory committee (ACIP) meeting's agenda for next week -- the one that was originally scheduled for this winter, but was abruptly canceled -- has been finalized: cdc.gov/acip/downloads/agendas. The discussion about the mRNA-1283 #covid #covid19 vaccine is still on the agenda.

The draft agenda from last month is here: cdc.gov/acip/downloads/agendas. I noticed that now some of the influenza presenters are now TBD, but otherwise I didn't see a lot of changes from the draft. Let me know if I've overlooked something. This meeting is scheduled to hold recommendation votes on Meningococcal, RSV, and Chikungunya vaccines.

In case anyone was feeling relief about this, Jeremy Faust has reported that because the CDC has no confirmed director or acting director, the final vaccine recommendation decision maker will be the HHS Secretary, RFKJr: insidemedicine.substack.com/p/. So it is not at all clear that the ACIP's recommendations will translate into actual policy decisions.

Another passage that speaks volumes for me since #covid19. Way before really, Iraq War probably; but never so explicitly conclusive.

"None of us got here overnight. There are stages to the process of being betrayed by your society. One is jolted from complacency by the discovery of difference, by hypocrisy, by inexplicable or incongruous ill treatment.

What follows is a time of confusion -- deconstructing & unlearning what one thought to be the truth. Immersing oneself in the new truth. And then a decision must be made.

Some accept their fate. Swallow their pride, forget the real truth, embrace the falsehood for all they're worth -- because, they decide, they cannot be worth much. If a whole society has dedicated itself to their subjugation after all, then surely they deserve it. Even if they dont, fighting back is too hard, too painful, too impossible. At least this way, there is peace of a sort. Fleetingly.

The alternative is to demand the impossible. To change society [& the prevailing unjust world order]. There can be peace this way too.

But not before conflict."

- NK Jemisin

Continued thread

that Blood Advances paper aligns with earlier autopsy results, and confirmed

SARS-CoV-2+ megakaryocytes are present in lung and brain autopsy tissues from deceased donors who had COVID-19

But heck! We already knew MKs were long-term impacted. This from 2024 ashpublications.org/bloodadvan - though in mice gives what I guess should be an obvious outcome, since the immune system isn't open-loop:

Megakaryocytes (MKs), integral to platelet production, predominantly reside in the bone marrow. [...] at peak SARS-CoV-2 viremia, when the disease primarily affected the lungs, MKs were not significantly different from those from healthy mice. Conversely, a significant divergence in the MK transcriptome was observed during systemic inflammation, although SARS-CoV-2 RNA was never detected in the BM, and it was no longer detectable in the lungs. Under these conditions, the MK transcriptional landscape was enriched in pathways associated with histone modifications, MK differentiation, NETosis, and autoimmunity

and autoimmunity

The breadcrumbs are everywhere.

fin/🧵

Continued thread

That aligns with results from 2022-2023 like ashpublications.org/bloodadvan which found

Using peripheral blood, we show that megakaryocytes are increased in the systemic circulation in COVID-19

peripheral blood - circulating!!

SARS-CoV-2–containing megakaryocytes are a strong risk factor for mortality and multiorgan injury

2/🧵

American Society of HematologyCirculating SARS-CoV-2+ megakaryocytes are associated with severe viral infection in COVID-19Key Points. To our knowledge, we provide the first evidence implicating SARS-CoV-2+ peripheral blood megakaryocytes in severe disease.Circulating megakaryo

So. How about this careful result demonstrating viral replication inside megakaryocyte immune cells?

transmission electron microscopy pointed to the presence of viral particles inside bone marrow MK. Immunolabeling confirmed the presence of two SARS-CoV-2 proteins, spike and Orf3a, as well as double-stranded RNA suggesting a potential viral replication cycle.

Note this study is from last month, but it's from hospitalized 2020-2021 patient data. It's existence proof, not population statistics.

That said:

bone marrow MK infection is not a strict determinant of mortality. However, all survivors experienced post-acute sequelae SARS-CoV-2 condition (PASC) diagnosed during post-intensive care follow-up

short 🧵

Replied in thread

@themaskerscomic this is really remarkably solid data

The cohort included 297,920 SARS-CoV-2-positive individuals and 915,402 SARS-CoV-2-negative controls. Every individual had at least a six-month follow-up after cohort entry

With a range of risk ratios from roughly +25% to +200%! That's up to triple the risk!

children and adolescents [...] infected with SARS-CoV-2 exhibited increased risks for a range of post-acute cardiovascular outcomes, with RR [risk ratio] between 1.26 and 2.92

and things have not gotten better with newer variants:

similar cardiovascular outcomes in children infected with the Delta and Omicron variants

nature.com/articles/s41467-025 also via @TRyanGregory

NatureCardiovascular post-acute sequelae of SARS-CoV-2 in children and adolescents: cohort study using electronic health records - Nature CommunicationsPost-acute sequelae of SARS-CoV-2 infection affecting the cardiovascular system have been reported, but evidence in young people is limited. Here, the authors quantify the incidence of a range of outcomes in children and adolescents using electronic health records from the United States.

"ME/CFS, ties to Long COVID are the focus of ongoing research studies"

accesspress.org/me-cfs-ties-to

Recent findings from NIH study show that COVID infection leads to more cases of ME/CFS (myalgic encephalomyelitis/chronic fatigue syndrome)

New incidence cases of ME/CFS were 15 times higher than pre-pandemic levels

@mecfs @longcovid

Access Press · ME/CFS, ties to Long COVID are the focus of ongoing research studies | Access PressUnderstanding the effects of Long COVID may also mean understanding what is called ME/CFS. ME/CFS is myalgic encephalomyelitis/chronic fatigue syndrome. […]
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