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#covidcompetent

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@ducky 's weekly roundup is out! covidbc.webfoot.com/2025/04/18

"95% of flu and herpes infection neutralized by [a specific] chewing gum [made with lablab beans]" newatlas.com/infectious-diseas which also links to sciencedirect.com/science/arti

"On 2022-09-27, Singapore stopped requiring full PPE for healthcare workers (HCW) when attending to patients with suspected or confirmed COVID-19. Instead of gowns, face shields, gloves, and N95 masks, they only required N95 masks after that. Good news: the change did not make more HCWs sick." but Ducky didn't link the source on that one.

covidbc.webfoot.com2025-04-18 General – Pandemics in British Columbia
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.

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

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
Replied in thread

@sfwrtr Metformin for Long COVID prevention in your spouse? (I am not a doctor! But "those who took metformin for early-stage COVID-19 were 41% less likely to later develop long COVID (6.3% of people) than the people who received placebo (10.4% of people)." ncats.nih.gov/news-events/news among other sources)

Negative air pressure in the spouse's recovery rooms? (Fan pulling air out the windows - ensuite bathroom fan for example, or window mounted) combined with rags under doors to minimize air exchange between their air compartment and yours?

There is some evidence that iota-carrageenan and xylitol nasal sprays might reduce upper airway viral load in infected people, and reduce risk of infection in exposed peole, also. Since the upper airways can transmit aerosolized (or cilia-driven?) virus to the nasal bulb which directly grants brain access, I'd particularly guess those might reduce risk of brain fog sequelae.

As @surfingreg said diluted air helps! Not just because it flushes aerosols out, but also a less obvious way: lower CO2 makes aerosolized virus degrade much faster

Best of luck to your spouse for a healthy recovery, and to you to retain your novid status

ncats.nih.govCan Metformin Treat COVID-19 and Prevent Long COVID? NCATS and Partners Pursue Answers | National Center for Advancing Translational Sciences
Replied in thread

@Ashedryden sure:

  • be well rested and less stressed. Really! Immune systems perform better when the organism is well-rested, and worse when under stress conditions. Literally calm your system beforehand with meditation if you can?
  • have your vitamins. Results for vitamins D and C vary from "no effect" to "protective" (pmc.ncbi.nlm.nih.gov/articles/ for example), with clear evidence that low vitamin D can down-modulate immunity. Especially important for PoC in northern climes, folks who don't work outdoors, and similar. Maybe start supplementing vitamin D (through sun exposure or pills) a week+ ahead?
  • nasal sprays and mouthwashes. There is evidence for both xylitol and iota-carrageenan giving protection against SARS-CoV-2. A nice review with links to actual research from this past summer: integrativewomenshealthinstitu
  • UV light disinfection, aka Germicidal Ultraviolet. This is harder to access as most installations are for industry, but if you have time and energy perhaps you can DIY it or find a supplier.
  • explicitly say "And if you want to come but are feeling sick, let us know, and we'll drop off a get-better goodie basket and a little gift!" or similar, so folks who are ill have motivation to not come.

You've already said you will ventilate and filter. Add more filters? HEPA is great but Corsi-Rosenthal boxes with MERV-13 filters are also highly effective, relatively inexpensive, and if made with computer fans, very very quiet. They can be totally DIY - there's even a song about it youtube.com/watch?v=5XS-7vgThf !!! - , and various sellers have them available as kits or prefabbed, too.

Less likely to be useful:

  • vaccinate 2-3 weeks prior to be at peak vax-induced immunity before waning
  • PlusLife or RAT testing at the door
  • free mask basket at the door. You sound perhaps willing to use an N95 but you indicated your guests wouldn't.

I hope some of those help! None of them will guarantee no infection, but when one must face such situations, the odds can be improved.

PubMed Central (PMC)Protective Effect of Vitamin D Supplementation on COVID-19-Related Intensive Care Hospitalization and Mortality: Definitive Evidence from Meta-Analysis and Trial Sequential AnalysisBackground: The COVID-19 pandemic represents one of the world’s most important challenges for global public healthcare. Various studies have found an association between severe vitamin D deficiency and COVID-19-related outcomes. Vitamin D plays a ...
Replied in thread

Some highlights from @ducky 's weekly roundup at covidbc.webfoot.com/2025/03/28

SARS-CoV-2 can interact with / activate the CD147 receptor to get into lymphocytes (T-cells and B-cells). (sciencedirect.com/science/arti)

women are 13.4 times more likely to get Long COVID if they are 🤰pregnant than if they are 🚫🤰not, with the danger highest if they catch COVID-19 in the third trimester. (sciencedirect.com/science/arti)

the rate of cases of postural orthostatic tachycardia syndrome (POTS) has gone up more than fourteen times compared to pre-pandemic (academic.oup.com/ehjqcco/advan)

covidbc.webfoot.com2025-03-28 General – Pandemics in British Columbia
Replied in thread

Here's another "literally brain responses are slower" result, a great one to pair with the reaction/response time slowdown, when trying to convince gamers and car drivers and sports players that COVID-19 is something to avoid:

This could suggest a form of accelerated central auditory aging in COVID-19

Our findings suggest that PASC may alter the central auditory pathway and lead to slower conduction and elevated auditory neurophysiology responses at the midbrain, a pattern associated with the typical aging process.

Notably, the younger and older groups did not differ on other dimensions of the ABR, including peak and inter-peak latencies, suggesting that heightened gain is not comorbid with deficient synaptic transmission

Delayed neural conduction time and increased central gain in the midbrain could give rise to functional cortical processing disparities in PASC

the V/I ratio increase in the PASC groups, particularly the younger subjects, potentially exceeds central changes that are expected to occur with natural aging. Indeed, in the PASC group, the younger subjects patterned similarly to the older subjects.

nature.com/articles/s41598-025

h/t the most admirable @tomkindlon

NatureAltered auditory brainstem responses are post-acute sequela of SARS-CoV-2 (PASC) - Scientific ReportsThe Post-acute Sequela of SARS-CoV-2 (PASC) syndrome, also known as Long-COVID, often presents with subjective symptoms such as brain fog and cognitive fatigue. Increased tinnitus, and decreased hearing in noise ability also occur with PASC, yet whether auditory manifestations of PASC are linked with the cognitive symptoms is not known. Electrophysiology, specifically the Auditory Brainstem Response (ABR), provides objective measures of auditory processing. We hypothesized that ABR findings would be linked to PASC and with subjective feelings of cognitive fatigue. Eighty-two individuals, 37 with PASC (mean age: 47.5, Female: 83%) and 45 healthy controls (mean age: 38.5, Female: 76%), were studied with an auditory test battery that included audiometry and ABR measures. Peripheral hearing thresholds did not differ between groups. The PASC group had a higher prevalence of tinnitus, anxiety, depression, and hearing handicap in addition to increased subjective cognitive fatigue. ABR latency findings showed a significantly greater increase in the wave V latency for PASC subjects when a fast (61.1 clicks/sec) compared to a slow click (21.1 clicks/sec) was used. The increase in latency correlated with cognitive fatigue scores and predicted PASC status. The ABR V/I amplitude ratio was examined as a measure of central gain. Although these ratios were not significantly elevated in the full PASC group, to minimize the cofounding effect of age, the cohort was median split on age. Elevated V/I amplitude ratios were significant predictors of both predicted PASC group classification and cognitive fatigue scores in the younger PASC subjects compared to age-matched controls providing evidence of elevated central gain in younger individuals with PASC. More frequent tinnitus also significantly predicted higher subjective cognitive fatigue scores. Our findings suggest that PASC may alter the central auditory pathway and lead to slower conduction and elevated auditory neurophysiology responses at the midbrain, a pattern associated with the typical aging process. This study marks a significant stride toward establishing an objective measure of subjective cognitive fatigue through assessment of the central auditory system.

Most interesting detail: "we detected the virus passing from one sinus at the peak of infection to the other a few days later"

Model animals: "cynomolgus macaques"

They also evaluated "two convalescent animals [...] exposed to the SARS-CoV-2 Delta variant three months prior" and found "no major uptake by the nasal cavity" but "detection of the PET signal for SARS-CoV-2 spike antigen up to three months post initial infection in the lungs and brains"

"local accumulation [...] in areas of the brain [...] consistent with previous findings of neuroinflammation in humans infected with SARS-CoV-2 and in rhesus macaques up to six weeks after SARS-CoV-2 infection. The localized crossing of the blood-brain barrier (BBB) by the radiotracer in convalescent animals can be explained by thrombo-inflammation previously reported in patients with active long-COVID."

nature.com/articles/s41467-025

h/t @EricCarroll

NatureWhole-body visualization of SARS-CoV-2 biodistribution in vivo by immunoPET imaging in non-human primates - Nature CommunicationsThere are limited approaches to monitor virus spread in vivo. Here, the authors report PET/CT-based in vivo imaging to track SARS-CoV-2 biodistribution in a COVID-19 non-human primate model using a radiolabeled human antibody revealing persistent detection in the lung and brain 3 months after infection.