PSA: COVID-19 isn’t “just a cold,” isn’t “a respiratory virus,” and “mild” doesn’t mean what you think it does.
If you “aren’t scared of COVID”, this thread is for you.
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Please R/T if it opens your eyes.
This thread is long, and hard to read - not just because of the technical language, but because “it’s just a cold,” “the vaccine protects me,” and “at least our children are safe” are comforting fairy tales.
I wish they were true.
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This virus is like measles and polio: a virus with long-term impact.
Even a “mild” case in a vaccinated individual can lead to long-term issues which cause a measurable uptick in all-cause mortality in the first 6 months, and get progressively worse with time.
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SARS-CoV-2 is a systemic disease which has multiple avenues to induce long-term impairment, attacking the brain, heart, lungs, blood, testes, colon, liver, and lymph nodes, causing persistent symptoms in more than half of patients by six months out.
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The CoVHORT study, limited to non-hospitalized patients in Arizona - “mild” cases - found a 68% prevalence of 1 or more Covid symptom after 30 days, rising to 77% after 60 days. (We will explore an explanation later).
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Bell et al, journals.plos.org/plosone/articl…
Despite a different definition of “symptoms”, the Bergen study in Norway found that 61% of patients had symptoms after six months, including 52% of patients aged 16-30 years who had not been hospitalized.
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Blomberg et al, nature.com/articles/s4159…
To prevent panic, @CDCgov has been using the term “mild” to describe any case of COVID-19 which does not require hospitalization.
#LongCOVID, however, is anything but “mild”, as the replies to @ahandvanish's thread make heartbreakingly clear.
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Davis
A University of Washington study found that 30% of Covid patients had reduced Health Related Quality of Life, with 8% of the patients limited in routine daily activities.
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Logue et al jamanetwork.com/journals/jaman…
These patients are struggling with real physical issues.
This Yale study demonstrated reduced aerobic capacity, oxygen extraction. and ventilatory efficiency in “mild” COVID patients even after recovery from their acute infection.
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Singh, et al journal.chestnet.org/article/S0012-…
It’s also a vascular disease. A Columbia study found "significantly altered lipid metabolism" during acute disease, which "suggests a significant impact of SARS-CoV-2 infection on red blood cell structural membrane homeostasis."
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Thomas, et al pubs.acs.org/doi/10.1021/ac…
Oregon Health & Science University found that “symptomatic or asymptomatic SARS-CoV-2 infection is associated with increased risk of [fatal] cardiovascular outcomes and has causal effect on all-cause mortality.”
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Tereschenko et al medrxiv.org/content/10.110…
Let’s review: SARS-CoV-2 causes an increase in mortality and reduced aerobic capacity even after asymptomatic cases, and remains in the body months after the initial infection.
No, it’s not “just a cold.”
But we’re just getting started. It gets worse. Way worse.
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The virus appears to be able to cross the blood-brain barrier and cause significant neurological damage.
The ability of the spike protein to cross the blood-brain barrier was demonstrated in mice at the University of Washington.
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Rhea, et al pubmed.ncbi.nlm.nih.gov/33328624/
A joint study by Stanford and Germany’s Saarland University found inflammation in the brain, and “show[ed] that peripheral T cells infiltrate the parenchyma.”
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Yang, et al nature.com/articles/s4158…
For context, the parenchyma is the functional tissue of the brain - your neurons and glial cells. It isn’t normally where T cells are:
“In the brain of healthy individuals, T cells are only present sporadically in the parenchyma.”
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Evans, et al ncbi.nlm.nih.gov/pmc/articles/P…
The Stanford study also discovered microglia and astrocytes which displayed “features .. that have previously been reported in human neurodegenerative disease.”
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Yang, et al, above
Post-mortem neuropathology in Hamburg, Germany found “Infiltration by cytotoxic T lymphocytes .. in the brainstem and cerebellum, [with] meningeal cytotoxic T lymphocyte infiltration seen in 79% [of] patients.”
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Matschke, et al sciencedirect.com/science/articl…!
An autopsy of a 14-month-old at Brazil’s Federal University of Rio de Janeiro found that “The brain exhibited severe atrophy and neuronal loss.”
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Gomes, et al thelancet.com/journals/lanam…
The UK Biobank COVID-19 re-imaging study compared before and after images of “mild” cases, and found “pronounced reduction in grey matter” and an “increase of diffusion indices, a marker of tissue damage” in specific regions of the brain.
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Douaud ++ medrxiv.org/content/10.110…
That seems to explain why there is evidence of persistent cognitive deficits in people who have recovered from SARS-CoV2 infection in Great Britain.
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Hampshire et al thelancet.com/journals/eclin…
Also worrisome are syncytia, where an infected cell extrudes its own spike protein and takes over its neighbors, fusing together to create a large multi-nucleus cell.
And, yes, syncytia formation can happen in neurons. For our visual learners, here is video of syncytia and apoptosis (cell death) in a (bat) brain:
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Aicher et al
Luckily, the University of Glasgow found that “Whilst Delta is optimised for fusion at the cell surface, Omicron .. achieves entry through endosomal fusion. This switch .. offers [an] explanation for [its] reduced syncytia formation.”
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Willet et al gla.ac.uk/media/Media_82…
If you’re interested in further understanding the host of neurological symptoms and the mechanisms underlying them, this Nature article is an excellent primer:
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Marshall nature.com/articles/d4158…
Let’s review: SARS-CoV-2 can cross the blood-brain barrier, and even “mild” or asymptomatic cases can cause loss of neurons and persistent cognitive defects?
That doesn’t sound “mild” to me; I like my brain.
But it keeps getting worse.
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The brain isn’t the only organ affected: Testicular pathology has found evidence of “SARS-Cov-2 antigen in Leydig cells, Sertoli cells, spermatogonia, and fibroblasts” in post-morten examination.
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Duarte-Neto onlinelibrary.wiley.com/doi/10.1111/an…
A Duke pathology study in Singapore “detected SARS-CoV-2 .. in the colon, appendix, ileum, haemorrhoid, liver, gallbladder and lymph nodes .. suggesting widespread multiorgan involvement of the viral infection.”
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Cheung, et al gut.bmj.com/content/gutjnl…
The same study found “evidence of residual virus in .. tissues during the convalescent phase, up to 6 months after recovery, in a non-postmortem setting,” suggesting that “a negative swab result might not necessarily indicate complete viral clearance from the body.”
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ibid
It also causes microclots: “Fibrin(ogen) amyloid microclots and platelet hyperactivation [were] observed in [Long COVID] patients,” in this work by Stellenbosch University of South Africa, which also explored potential treatments.
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Pretorius et al researchsquare.com/article/rs-120…
Johns Hopkins' @fitterhappierAJ found that “CD95-mediated [T cell] differentiation and death may be advancing T cells to greater effector acquisition, fewer numbers, and immune dysregulation.”
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Leonardi et al frontiersin.org/articles/10.33…
This Chinese military study of the initial Wuhan outbreak concluded that “T cell counts are reduced significantly in COVID-19 patients, and the surviving T cells appear functionally exhausted.”
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Diao et al frontiersin.org/articles/10.33…
The study authors went on to warn, “Non-ICU patients with total T cells counts lower than 800/μL may still require urgent intervention, even in the immediate absence of more severe symptoms due to a high risk for further deterioration in condition.”
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ibid
Those warnings have since been proven by discovery of autoimmune features.
This study of 177 Los Angeles healthcare workers found that all had persistent self-attacking antibodies at least 6 months after infection, regardless of illness severity.
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In the words of T-cell immunologist Dr. Leonardi (@fitterhappierAJ)
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This Kaiser Permanente S.California study found that, although natural immunity provided substantial protection against reinfection, “Hospitalization was more common at suspected reinfection (11.4%) than initial infection (5.4%).”
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Slezak et al clinicalmicrobiologyandinfection.com/article/S1198-…
In fact, remember those cytokine storms? It turns out that even that even severe COVID-19 may not be a viral pneumonia, but an autoimmune attack of the lung.
Let’s review - it’s autoimmune: SARS-CoV2 convinces our body to attack itself.
That might explain why the Arizona study saw more symptoms after 60 days than at 30 days.
It also means “natural immunity” isn’t something to count on.
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But if you’re counting on vaccination to feel safe, there’s even more bad news.
A study of Israel healthcare workers found that “Most breakthrough cases were mild or asymptomatic, although 19% had persistent symptoms (>6 weeks).”
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Bergwerk et al nejm.org/doi/full/10.10…
Perhaps the most terrifying study is from Oxford University, which examined the effects of vaccination on long COVID symptoms, because not only did it find that vaccination does not protect against Long Covid, but that Long Covid symptoms become more likely over time:
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Please consider re-reading my thread on what "De-Nazify" meant -- written March 13th -- and consider it in light of what we have learned since then about the horrors of Bucha and Irpin.
It continues to happen in Kherson, Melitopol, Berdyans'k, Mariupol, and more:
Did you ever wonder how the world stood by and watched the #Holocaust unfold?
The gas chambers didn’t start until 1942, but the #genocide started in 1939.
Pour yourself a relaxing tea, or coffee - or perhaps, for tonight's article, something a little stronger.
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This article will look at Adolf Hitler’s plan for the invasion of #Poland in 1939 - discussing only the events of 1939.
However, rather than provide supporting links - it’s all well documented - I will link to contemporary articles about Russia’s #genocide in #Ukraine.
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Hitler's grand plan, as described in Mein Kampf, was to acquire "living space" for German colonists to settle in Eastern Europe, expanding the German borders by conquest. The problem? Those lands were already settled - by Poles, Ukrainians, and more.
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At 14:01, Israeli account @ignus_fatu, with 753 followers, broke the story to Twitter, correctly crediting Ukrainian journalist Yuri Butusov, and accurately summarizing a translation, calling the plane a "fighter jet".