DO NOT BELIEVE THE HYDROXYCHLOROQUINE HYPE. THIS DRUG DOES *NOT* CURE OR PREVENT YOU FROM GETTING Covid-19.

HCQ does NOT increase PO2 with your red blood cells. Post-Mortem on Covid-19 infected lungs show these lungs filled with fluid and mucus as indicated on CT scans. CONT’D
2) There is a conspiracy theory about heme cleavage from red blood cells and HCQ is supposed to stop that. The conspiracy theory says people shouldn’t be ventilated and that low PO2 is not from ARDS but in a process involving red blood cells losing its hemoglobin.
3) Covid-19 is notable for the way the X-ray looks: The entire lung is basically whited out from fluid. Patients with ARDS are extremely difficult to oxygenate. ARDS is something that happens over time as the lungs get inflamed...”

https://www.healthleadersmedia.com/clinical-care/medical-worker-describes-terrifying-lung-failure-covid-19
4) NOTE IN POST-MORTEM — “...the lungs of both patients exhibited edema, proteinaceous exudate, focal reactive hyperplasia of pneumocytes with patchy inflammatory cellular infiltration, and multinucleated giant cells. Fibroblastic plugs were noted in airspaces.” —
5) Another article stating PNEUMONIA findings post-mortem... “Histopathologic examination of lung biopsy tissues revealed diffuse alveolar damage, organizing phase. Denuded alveolar lining cells (Figure 2, A-1, arrow 1), with reactive type II pneumocyte hyperplasia, were noted...
5a) ...(Figure 2, A-1, arrow 2). Intra-alveolar fibrinous exudates were present (Figure 2, A-2, arrow 3), along with loose interstitial fibrosis and chronic inflammatory infiltrates (Figure 2, A-2, arrow 4). Intra-alveolar loose fibrous plugs of organizing pneumonia were noted...
5b) ... (Figure 2, A-3, arrow 5), with presence of intra-alveolar organizing fibrin seen in most foci (Figure 2, A-4, arrow 6).”

https://annals.org/aim/fullarticle/2763174/histopathologic-changes-sars-cov-2-immunostaining-lung-patient-covid-19
6) Looking for the histopathology reports that would support this heme theory. This specious Hgb conspiracy theory supports hydroxychlororquine as a cure. THERE IS NO CURE. THERE IS ONLY ALLEVIATION OF SYMPTOMS. And if the application of hydroxychlroquine were correct in this
6A) ...Hgb theory, we would see an immediate uptick of PO2 on a pulse oximeter. And basically, this has never been observed... and HCQ is not part of any protocol FOR GOOD REASON. Short of any health pro having done this protocol, we’re squarely in conspiracy theory.
8) BUT NOTE THE SCIENCE... Looking at the biokinetic mechanisms of this drug —
“Chloroquine and hydroxychloroquine increase pH within intracellular vacuoles and alter processes such as protein degradation by acidic hydrolases in the lysosome, assembly of macromolecules in the...
8a) Looking at the biokinetic mechanisms of this drug —
“Chloroquine and hydroxychloroquine increase pH within intracellular vacuoles and alter processes such as protein degradation by acidic hydrolases in the lysosome, assembly of macromolecules in the endosomes, and...
8b) ...posttranslation modification of proteins in the Golgi apparatus. It is proposed that the antirheumatic properties of these compounds results from their interference with "antigen processing" in macrophages and other antigen-presenting cells. Acidic cytoplasmic...
8c) compartments are required for the antigenic protein to be digested and for the peptides to assemble with the alpha and beta chains of MHC class II proteins. As a result, antimalarials diminish the formation of peptide-MHC protein complexes required to stimulate CD4+T cells...
8d) and result in down-regulation of the immune response against autoantigenic peptides.”

^^^This indicates it may have an effect with slowing down the drowning process that happens with inflammation and your lungs filling up with fluid.

NOTHING on heme properties and...
9) HCQ — “Recent studies have elucidated the steps involved in the association of antigenic peptides with major histocompatibility complex (MHC) encoded proteins and have suggested how antimalarial compounds might influence this important site of immune activation. These steps of
9A) ...antigen presentation in the macrophage (or other antigen-presenting cells) include: (a) the partial proteolytic degradation of endogenous and exogenous proteins into peptides within the lysosome; (b) the synthesis of MHC class II (i.e. HLA-D associated) alpha, beta, and...
9B) invariant (Ii) chains in the endoplasmic reticulum; (c) the initial association of alpha-Ii and beta-Ii chains in the endoplasmic reticulum and the transport of these complexes to the primary endosome; (d) the fusion of lysosomal vacuoles and endosomal vacuoles, allowing the
9C) mixtures of lysosomal enzymes, peptides, alpha-Ii and beta-Ii; (e) the displacement of Ii chains by peptides to form alpha-beta-peptide complexes in the endosome; and ****NOTE THIS MECHANIC (f) the migration of alpha-beta-peptide complexes to the macrophage cell surface where
9D) they can stimulate CD4 T cells, resulting in release of cytokines. A low pH is required for digestion of the protein by acidic hydrolases in the lysosome, for assembly of the alpha-beta-peptide complex and for its transport to the cell surface. Chloroquine and...
9E) hydroxychloroquine are weak diprotic bases that can diffuse across the cell membrane and raise the pH within cell vesicles.****This background provides the underlying basis for the theory that antimalarials may act to prevent autoimmunity by the following putative mechanism.”
10) From @Jennifer L. Kasten, MD — https://www.facebook.com/100553591597588/posts/119316446387969/?d=n

“COVID-19 4/8: 1) Debunking the "COVID had us all fooled" hemoglobin theory. — Firstly, many have read an alternative physiologic mechanism of the coronavirus which has been circulating. The theory was originally...
10a) published on Medium by a non-MD, non-physiologist; a self-titled "professional disrupter" called Andrew Gaiziunas (AKA "libertymavenstock"), who predominantly is on the internet as a cryptocurrency enthusiast but who happened to read a single non-peer reviewed journal...
10b) article about SARS-CoV-2 inhibiting human heme synthesis, an education which he felt was sufficient to permit him to comment.

Let's start with the original paper. It involved computer analysis of the predicted structure of the virus' proteins, in three dimensions. (Computer
10c) simulation is a common technique in the field of proteomics). The authors noticed, wow, it looks like the structure of a couple of the surface proteins could "dock" with the heme synthesis mechanism human red blood cells employ. "Could" being the operative word- this has...
10d) never been observed, as the virus is not found in human blood except rarely in ultra-highly-infected people. The authors quite inappropriately titled their paper "COVID-19 Attacks the 1-Beta Chain..." instead of "A couple of proteins in this virus could theoretically bind...
10e) with the 1-beta chain.. based on our structural simulation."

So, the Gaiziunas piece started from the assumption that this was scientific fact instead of an extremely theoretical, unproven, unlikely assertion. He was then off to the races. His main premise is that basically
10f) COVID-19 isn't a primary respiratory disease, it's a blood disease. It causes organ failure of all organs, not just the lungs, at the same time, and that's what kills people. He asserts they don't have ARDS, but instead red blood cells release maverick, rogue radical oxygen
10g) species which causes unmitigated tissue damage.

There is no evidence for any of this, and if anyone took it seriously (treating COVID with blood transfusions instead of respiratory support) it would be extremely dangerous. Let's start: we pathologists can visualize the..,
10h) virus, with our eyes and our light & electron microscopes, infecting the Type 2 pneumocytes of the lungs, along with the cells lining the respiratory tree and associated mucinous glands. We know the virus enters these cells via its spike protein and the ACE receptor. And we
10j) also know the virus is generally never found in blood. Unlike the lung cells, we cannot see it in human red blood cells, though we've looked (out of interest in this theory a few people have tried hemoglobin electrophoresis and looked carefully at peripheral smears, and came
10k) up with nothing).

We can also see ARDS- there is a specific cascade of visible changes, including the filling of the airspaces with fluid which eventually coalesce into sticky coatings called hyaline membranes. I will attach a nice photo from Xiao et al of the lung...
10l) pathology in COVID patients to this post, which include virus in the cells. The hyaline membranes coat the gas-exchange part of the lungs, making gas exchange difficult and sending the infected patient teetering off into respiratory failure. That being said- apart from him,
10m) there is some interest generated in alternative ventilatory strategies for COVID, because the patients do seem to tolerate hypoxemia (lower blood oxygen saturation) better than other respiratory failure patients, so some critical care doctors are letting them "go lower" to
10n) avoid intubation than they would usually be comfortable with.

I want to stress that anyone can come up with a good idea. The fact that Andrew Gaiziunas doesn't have a relevant background doesn't mean that his idea, if reasonable or interesting, shouldn't be considered.
You can follow @CelesteWolfe.
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