It's about the tipping point where mass vaccination becomes harmful for the population's health. Vaccines cant't stop viral replication in airways, so vaccinated are becoming asymptomatic carriers. But unlike unvaccinated, they are excluded from mask wearing, travel restrictions, regular testing etc. and thus will spread more virus to more potential hosts. Also, their suboptimal immunity will push viral evolution towards immune escape variants. In the worst case, thess variants will be able to escape from immunity in previously infected, in that case we're back to square 1 of this pandemic.
glowniggers helped me write my scriptI take this with a grain of salt, but Chris Carter the creator of X-Files has apparently said he used to get fed info from someone in the CIA. Okay, so within a year we get a worldwide pandemic, a pretty fast vaccine without clinical trials, and suddenly the government is finally acknowledging these Unidentified Aerial Phenomenons after 70 years of quiet.
This whole thing is reminding of the X-Files movie, and this scene. (best clip I could find)
Last year, Trump puts FEMA in charge as per protocol.
Trump puts FEMA in charge after Emergency Declaration.
I take this with a grain of salt, but Chris Carter the creator of X-Files has apparently said he used to get fed info from someone in the CIA. Okay, so within a year we get a worldwide pandemic, a pretty fast vaccine without clinical trials, and suddenly the government is finally acknowledging these Unidentified Aerial Phenomenons after 70 years of quiet.
Here's the data setIt did. I saw it earlier, still had the 12,313 version on my open CDC tab. I hadn't though to archive.md it, but someone else did:
Here is my personal screenshot, just to glaze this donut:
View attachment 2368755
Incredibly sinister of them to release one amount with a death percentage and everything done up and suppress it within hours. But love and trust your government overlords, right? If it were just a typo, you wouldn't think they would have had the percentage calculated as well... plus they would vet their information before they published it. What kind of typo would be a number twice as high?
When I saw someone else mention it the data was claiming to be only up to 7/13 instead of this update as of 7/19. It's possible that they rolled back the update completely. Maybe they let more out of the floodgate at once than they intended, since we already knew they were backlogged on VAERS and sprinkle in events from months ago with each update.
Louis Philippe II, Duke of Orleans was the next in line if the royal household all died. He also was the head of all French Freemasons who's salons and committees started the "revolution." It wasn't a revolution. Just a rich guy civil war, until the chaos turned on Louis Philippe and everything went to hell.What the fuck is wrong with the french.
Literally being stopped from living unless they submit.
So much for the people of the revolution (unless of course they prove me wrong)
Covid is the Zoomer 9/11, much like after 9/11 a change in political, social and overall tone took hold on society.The coof scare happened about 20 years after 9/11...
Unless you are protesting systematic racism then you are not a super-spreader. Do you even science, bro?Covid is the Zoomer 9/11, much like after 9/11 a change in political, social and overall tone took hold on society.
Now instead of Arabs being treated as possible terrorists, everyone is to be treated as a bio-terrorist. Allahu ak-cough.
It seems that long covid isn't infection. According to Bruce Patterson's research, there is no virus in long COVID patients. He thinks that long COVID is caused by spike protein fragments that are stuck in monocytes which leads to their activation and causes long COVID symptoms. https://www.biorxiv.org/content/10.1101/2021.06.25.449905v2.full
- Envelope (E) and spike (S) proteins have a triple cysteine structural motif located directly after the E protein’s transmembrane domain (NH2- … L-Cys-A-Y-Cys-Cys-N … -COOH) and a similar motif located in the carboxy terminus of the S protein (NH2- … S-Cys-G-S-Cys-Cys-K … -COOH). The position, orientation, and composition of these two motifs may serve as a center for the structural link between the E and S proteins which is mediated by the formation of disulfide bonds between the corresponding cysteine residues.36 Previous studies have indicated that the entry of viral glycoprotein is affected by thiol-disulfide balance within the viral surface and the cell-surface of the host.37,38 Any perturbations in the thiol-disulfide interchange equilibrium would deter the entry of the virus into host cells.39,40Cleavage of disulfide bridges by N-acetylcysteine disrupts the structural components of the interacting proteins, thereby impairing receptor binding affinity and infectivity.
- N-acetylcysteine is a chemical reducer of disulfide bonds via its free sulfhydryl groups may interact with the extracellular disulfide bridges of angiotensin II receptor, alter its tertiary structure, and inhibit the binding of angiotensin II to its surface receptors (AT1a receptors) with subsequent attenuation of signal transduction and cell action. The AT1a receptors possess two sets of disulfide bridges at the extracellular domain of the receptors: C18-C274 and C101-C180. N-acetylcysteine can reduce the disulfide bonds in a dose-dependent manner,41,42 decreasing angiotensin II and increasing angiotensin 1–7 (a biologically active peptide exerting many opposing actions to angiotensin II), thus protecting against lung inflammation and fibrosis.43
- The sulfhydryl group of N-acetylcysteine inhibits angiotensin converting enzyme, reducing production of angiotensin II.44 In human lungs, angiotensin converting enzyme is expressed in lower lungs on type I and II alveolar epithelial cells. Following infection, viral entry begins with the attachment of spike (S) protein expressed on the viral envelope to angiotensin converting enzyme on the alveolar surface. Hence, N-acetylcysteine may prevent viral entry by limiting viral protein angiotensin converting enzyme interaction and internalization of the receptor-ligand complex.45 It also protects against oxidative stress and prevents glycosylation of proteins which may confer protection against respiratory disease syndrome and lung failure.
- The antioxidant effect of N-acetylcysteine ameliorates oxidative stress and inflammatory response in COVID-19.46 It amplifies the signaling functions of toll-like receptor 7 protein and mitochondrial antiviral-signaling protein for boosting type 1 interferon production.47 Type I interferon functions to induce expression of various interferon-stimulated genes that exert antiviral activities to host cells.48
- The receptor for advanced glycation end products (RAGE) and its ligands have a crucial role in the pathogenesis of COVID-19 pneumonia and acute respiratory distress syndrome as well as lung inflammation. Circulating levels of soluble RAGE (sRAGE, a decoy receptor) are positively associated with acute respiratory distress syndrome severity and mortality risk, whereas reduction in circulating levels of sRAGE drop results in disease resolution.49 Advanced glycation end products are formed by a reaction of the dicarbonyl compounds methylglyoxal and glyoxal with amino acids in proteins during glycolysis. Methylglyoxal and methylglyoxal-derived AGE can further activate inflammatory cells by binding to RAGE.50 N-acetylcysteine induces endogenous glutathione and hydrogen sulfide synthesis, thus attenuating methylglyoxal-induced protein glycation and additional glycosylation events in SARS-CoV-2 which may then inhibit the virus’s infectivity and associated pathologies.51
- N-acetylcysteine inhibits NF-κB activation by suppressing TNF-induced IκB kinases, followed by impediment of proteasome-dependent degradation.52 This prevents translocation of NF-κB from cytoplasm to the nucleus and block expression of pro-inflammatory cytokines and chemokines which have been correlated with severity and lethality in various acute respiratory viral infections, including Influenza A H5N1, highly pathogenic H1N1, SARS-CoV, MERS-CoV, and SARS-CoV-2.53