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#covidcompetent

2 posts2 participants0 posts today
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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
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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.
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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.

"Post Covid Syndrome and Cognitive Dysfunction – Aetiology and Possible Treatment" - I think figure 1, the arrows going towards "cognitive dysfunction" should be bidirectional - but otherwise, yet another lay of the land paper implicitly but strongly suggesting that there is a pressing need for research focus on LC and ME/CFS treatments: cdn.fortunejournals.com/articl

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"SARS-CoV-2 spike RNA- and SARS-CoV-2-related inflammation persist in the epipharynx for more than six months post infection. Although no expression of the SARS-CoV-2 spike protein in the epipharynx was evident in these patients with long COVID, genetic analysis revealed activation of [...] the SARS-CoV-2 signalling pathway in epithelial cells, B cells, and pDCs. This aligns with theories that even nonactive viral fragments may possess biological significance. This persistence of inflammation, identified for the first time at the genetic level, highlights the epipharynx as a critical site for continual immune responses in long COVID patients, suggesting that residual viral antigens may contribute to the chronic symptoms experienced"

"After the administration of EAT [epipharyngeal abrasive therapy] once a week for 3 months, the expression of viral RNA disappeared in patients 1 and 2. Patient 3 presented a substantial reduction in viral RNA expression; although complete clearance was not achieved, a marked decrease was observed."

"observed dysregulation of immune and ciliary pathways" - might explain the chronic nonsmoker cough that seems more common now

"These findings suggest that T cells still play a subtle role in the immune dysregulation observed in patients with long COVID. Collectively, these findings indicate that interactions among pDCs, B cells, plasma cells, and T cells contribute to the chronic inflammation and immune dysregulation characteristic of patients with long COVID"

"In the pre-EAT state of long COVID Patient 2, the tissue surface was predominantly covered by ciliated epithelium (Cluster 7). In contrast, following treatment, the ciliated epithelium was no longer observed, and a new cluster of squamous epithelial cells (Cluster 12) emerged"

"EAT effectively eliminates the inflamed ciliated epithelium in patients with long COVID and induces the formation of squamous cells with high barrier function"

nature.com/articles/s41598-025

thanks @MEActNOW

NatureSpatial transcriptomics of the epipharynx in long COVID identifies SARS-CoV-2 signalling pathways and the therapeutic potential of epipharyngeal abrasive therapy - Scientific ReportsIn this study, the critical role of the epipharynx in managing long-term coronavirus disease 2019 (COVID-19), and in particular, how residual SARS-CoV-2 RNA affects signalling pathways in the epipharynx were investigated via spatial gene expression analysis (Visium HD). Moreover, we hypothesize that epipharyngeal abrasive therapy (EAT) targeting the epipharynx could improve long COVID symptoms by modulating local inflammation and gene expression. We conducted a comparative analysis of the gene expression profiles of three patients with long COVID and two control individuals without COVID-19. Residual SARS-CoV-2 RNA was detected in the epipharynx of patients with long COVID, along with the activation of signalling pathways in epithelial and immune cells. After EAT, the viral RNA was either completely cleared or significantly reduced. T-cell receptor signalling pathways were suppressed; the levels of proinflammatory cytokines, such as interleukin-6 and tumour necrosis factor-α, were reduced; and excessive antibody production was mitigated. Histology showed that EAT effectively eliminated the inflamed, dysfunctional ciliated epithelium. This study clarifies that SARS-CoV-2 has long-term effects on the immune response in the epipharynx, emphasizing the need to focus on chronic epipharyngitis as a potential cause of long COVID. Furthermore, EAT may offer a promising approach to alleviating persistent long COVID symptoms.

Hey men who enjoy sex! MASK UP TO KEEP IT UP! :mastorespirator: 🍆

If taking a soccer ball ⚽ to the crotch had 1/5 odds of long term erectile dysfunction (ED) would you wear a cup when you play soccer?

nature.com/articles/s41598-025

20% of men in this study got NEW ED - and only 1/4 "got their mojo back" after two years.

NaturePrevalence of erectile dysfunction as long-COVID symptom in hospitalized Japanese patients - Scientific ReportsCoronavirus disease-2019 (COVID-19) is associated with a wide range of post-acute sequelae. The prevalence of erectile dysfunction (ED) that developed after COVID-19 and the associated underlying factors were analyzed based on a questionnaire survey, COVID-19 Recovery Study II in Japan. A case–control study was conducted with those with or without ED one and two years hospitalized with COVID-19 between March and September 2021. Six hundred and nine Japanese men, with a median age of 48 years, were analyzed. During the study period, 116 subjects (19.0%) had erectile dysfunction. The patients with ED responded with less subjective awareness of recovery and high breathless and fatigue scores compared to those without ED. The patients with ED also showed higher Hospital Anxiety and Depression Scale-D (depression) and the EuroQol 5-dimensions 5-level scores for pain/discomfort and anxiety/depression scores compared before COVID-19 infection. Sleep disturbance was suggested to be associated with erectile dysfunction using an exploratory clustering analysis in the one-year survey. There were no associations of COVID-19 severity, reinfection, vaccination frequency, antiviral treatment for COVID-19 with the presence of erectile dysfunction. It was considered that mental support for the subject with erectile dysfunction as a long-COVID symptom is warranted.

The person - the man - who spends the most on anti-aging in the world, whose physiology is the most measured in the world?

Lost 15% of lung capacity to "mild" acute COVID-19.

donotpanic.news/p/the-billiona

To be clear, 15% is not "you take an extra 6th breath for every 5." It is worse in ways that you can investigate for yourself. It is Not Good.

¡Do Not Panic! · The Billionaire Who Wants To Live Forever Has Long CovidBy Nate Bear

If we were to see immune damage manifesting at a population level, it would look like what we’re seeing today: big waves of common illnesses. Unusual spikes of uncommon illnesses. Course reversal for previously declining and eliminated illnesses. An unexplained, global wave of sickness.

How much more denial can the bodies of our children take? Are we going to force them to find out?

lots of citations demonstrating that damage and more at thegauntlet.news/p/kids-keep-g

The Gauntlet · Kids keep getting sicker as evidence for COVID immune damage buildsBy Julia Doubleday

"57% decreased odds of 1 or more PCC symptoms and a 73% decreased odds of 2 or more PCC symptoms" - that's dramatically lower odds of a child suffering:

➡️ unable to remember
➡️ unable to focus
➡️ unable to exercise
➡️ headache
➡️ insomnia
➡️ lightheadedness, fainting
➡️ extreme fatigue
➡️ loss of vivacity, joie de vivre
➡️ personality changes
➡️ hospitalization and death

Protect your children.

Otherwise, if they survive, they will wonder why you didn't protect them, when it costs only the time to get vaccinated, and a few pennies a day N95s and HEPA filters.

Otherwise, you might find yourself mourning the potential you KNEW your child had, and desperately hoping for treatments.

Treatments may never come. Neurons don't come back. Developmental windows close.

Don't be the ghoul that condemns your children, don't strip their future because it's not cool to mask. It might not be cool to wear a bike helmet either. Concussions can't be undone, either. Don't usher your children willingly into suffering and disability.

DON'T FUCKING STACK THE ODDS AGAINST YOUR KIDS.

pmc.ncbi.nlm.nih.gov/articles/

ht/ @augieray mastodon.social/@augieray/1141

PubMed Central (PMC)COVID-19 Vaccination and Odds of Post–COVID-19 Condition Symptoms in Children Aged 5 to 17 YearsDoes COVID-19 mRNA vaccination reduce the occurrence of post–COVID-19 condition (PCC) following SARS-CoV-2 infection in children aged 5 to 17 years? In this case-control study with 622 participants, vaccination was associated with a 57% decreased ...
AJ's got a new blog post! Some highlights:
"a Nature Immunology study from January 2024 "Long COVID manifests with T cell dysregulation, inflammation and an uncoordinated adaptive immune response to SARS-CoV-2" reveals further harm through T cell dysregulation in long COVID patients. The research identified increased frequencies of exhausted SARS-CoV-2-specific CD8+ T cells, alongside CD4+ T cells primed for inflammation, and a lack of coordination between T and B cell responses."
"a paper in JCI insight showing T cell exhaustion to other infections following a covid infection"
"a Nature Immunology study from January 2022 "Immunological dysfunction persists for 8 months following initial mild-to-moderate SARS-CoV-2 infection" shows that COVID-19 leads to a prolonged reduction in naive T cells (both CD4+ and CD8+) in individuals with long COVID, persisting up to eight months post-infection."
"Such a long-term impact on the naive T cell pool is not a standard feature of recovery from other acute viral infections like influenza, [...] This effect may not completely persist, however, what it represents is sloughing of the T cells."
A study published in Immunity found "Even after vaccination, those with a history of COVID-19 showed weaker and less functional CD8+ T cell responses, a phenomenon likened to the immune damage seen in chronic viral infections like hepatitis C or HIV. This attenuation indicates that SARS-CoV-2 inflicts a lasting impairment on CD8+ T cell effector function"
from https://www.easychair.info/p/5-years-later-covid-still-harms-t #AirborneAware #CovidCompetent #COVIDIsNotOver #COVID #COVID19 #SARSCoV2 #immunology #LongCOVID
Easy Chair · 5 Years later, Covid still Harms T cellsBy Anthony J Leonardi, MBBS, PhD

@Westcoastmaven I hear you, and regret to inform you that neither the official narrative nor the corporate media narrative are aligned with scientific results. The risk of acute death was always low in relatively healthy people. The risk of long term damage per single infection was and remains high, with Statistics Canada estimating that half of people don't fully recover from Long COVID, and that more than 1/3 of people experience Long COVID symptoms by their 3rd COVID-19 infection.

And that 1/3 risk of Long COVID symptoms by a third infection IS if the person is vaccinated.

And numerically, cases are not low right now:

"Canadian COVID Forecast Mar 1-14, 2025

About 1 in every 52 people infected

Compared to lowest point of pandemic in Canada:
-Infections ~14X higher
-Long COVID ~13X higher
-Hospitalizations ~12X higher
-Deaths ~11X higher"

from fed.brid.gy/r/https://bsky.app who are still doing COVID-19 modelling at UofT

Bluesky Social · Tara Moriarty (@moriartylab.bsky.social)Canadian COVID Forecast Mar 1-14, 2025 CANADA VERY HIGH (no change) About 1 in every 52 people infected Compared to lowest point of pandemic in Canada: -Infections ~14X higher -Long COVID ~13X higher -Hospitalizations ~12X higher -Deaths ~11X higher

"We know that infection and reinfection, even when mild, is linked to cell and organ damage that may harm their future health. More needs to be done to protect our children, and the first step is ensuring that our schools are safe"

"The briefing also says Long Covid can also lead to a 'substantially increased' risk of sudden death and 'silent' damage to cells and organs which can lead to later illness.

"Certainly the silent organ damage is a real problem, we think, for future development of disease."

rnz.co.nz/news/national/543885

RNZ · Long Covid warning: 'Silent organ damage is a real problem'By RNZ News
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@augieray @elliek I think Ellie is in Canada

we have slower but cleaned results from:
@MoriartyLab at covid19resources.ca/covid-haza

we have @ratnegative posting wastewater data, with some careful hand cleaning to remove artefacts

we have lots of bots like @wastewater @covid19ab_wastewater @OntarioWasteWater_GTA and more - you can search zeroes.ca for "wastewater bot" and click on "Profiles", I'm not sure if there's a graphic map or a list of known wastewater bots in Canada, but now I kinda want to compile one.