Revisiting Snopes Fact Check from March 2021 - Will mRNA COVID-19 Vaccines Wreak ‘Havoc on The Lungs’ in 4 to 14 Months

Why a severe Covid disease often leads to a secondary organizing pneumonia while receiving mRNA "vaccines" does not? What gives (and takes)?

Potential mechanisms of lung damage in COVID-19 patients: IFNs, interferons; AT2, alveolar epithelial type 2.“

We all love Snopes for their objective, balanced fact checking of all things Covid.

Kidding aside, we need getting to the bottom of things in cases where dire predictions of mRNA “vaccine” doubters do not pan out, as much or more than in the cases where they do. For the sake of our credibility and integrity, and to maintain upper hand in the ongoing Covid infowars. Or for a goodnight story to your children or grandchildren. Or to your cat or dog, as the case may be.

Case at hand - the mentioned in the title Snopes fact check “Will mRNA COVID-19 Vaccines Wreak ‘Havoc on The Lungs’ in 4 to 14 Months?“ (Mar. 1, 2021). In it, they mock Sherri Tenpenny for her statement in particular that mRNA “vaccines” would cause a massive damage to the lungs 4-14 months post jab, although I did not spot her saying that in the video and the post they quote (a Bigchute video from Feb. 2021, “DR. TENPENNY AND REINETTE SENUM - MRNA SHOTS TICKING TIME BOMB” and a blog post from Dec. 2020, “Coronavirus Pt. 6: The COVID Vaccines – part 2“, let me know if you spot her saying exactly that anywhere):

Not only could these antibodies enhance infection through ADE, Tenpenny alleges, but their presence — in the absence of the immune system’s anti-inflammatory cells — could directly harm lung tissue through inflammation and indirectly by creating an unchecked army of pro-inflammatory immune system cells. For these reasons, Tenpenny implies, a vaccine that creates COVID-19 spike proteins will generate massive immunopathologic damage to the lungs after someone vaccinated to COVID-19 is exposed to the virus.

As we now know for a fact, Snopes was right and Tenpenny was wrong (if she really said that) on this one. Did you ever wonder why would that be:

Why does the Covid disease often result in an organizing pneumonia, but the “vaccination” with the “safe and effective” SARS-CoV-2 mRNA “vaccine”, introducing much larger quantities of the S spike into the vaccinee bodies, does not?

(!!! Spoiler alert: mRNA !!!)

Are we wrong about the whole S spike thing, sitting in the echo chambers of the Covid misinformation and rejecting the $cience, and the jabs are actually good for those that take them? Let’s dig in to find out!

First of all, the secondary organizing pneumonia is a proven fact, first vocally exposed by none other than Dr. Pierre Kory in “Has there been a widespread failure to identify and treat this prevalent condition in COVID-19?’” (2020.09.22):

With SARS, OP and its histological variant, acute fibrinous and organising pneumonia (AFOP), were reported in 30%–60% of intensive care unit patients.7 The reported CT findings of COVID-19 suggest that secondary OP, AFOP or both may be occurring even more frequently.8–10

…However, the CT findings in this cohort were all consistent with OP and not diffuse alveolar damage (DAD), thus suggesting that OP was likely the initial response to injury, with DAD then occurring later perhaps as a result of a thrombotic microangiopathy, cytopathic effect or the subsequent ventilator-induced lung injury, of which DAD is the hallmark. This progression is further supported by the fact that OP is known to present with radiographic abnormalities despite minimal or no symptoms.

…Ultimately, the exact sequence of progression is currently unknown due to the lack of early, antemortem tissue biopsy in patients with COVID-19 along with the inherent bias that results from classifying COVID-19 lung injury only among those most severely affected given that the majority of autopsies were performed in patients after prolonged mechanical ventilation which unsurprisingly demonstrated DAD. Thus, in the early phases of the disease, the radiological findings and clinical assessment should be weighed more heavily in determining the type of lung injury occurring. The exact prevalence of OP or AFOP will ultimately be determined over time as the body of postmortem (and potentially antemortem) pathological studies accumulate.

Later on, Dr. Kory became a vocal advocate for a hugely successful therapy of applying large doses of corticosteroids to treat the OP, which of course, has been suppressed and caused the death of hundreds of thousands, in not millions, of people around the world. “Dr Pierre Kory: Hospitalized COVID-19 Patients are Systematically Dying from Under-Treatment with Corticosteroids?“ (January 02, 2022):

Let’s start at the beginning when COVID-19 began to roll across the world. Every doctor caring for a COVID-19 patient was looking for guidance on how to treat the disease. The below table summarizes the inital guidance they recieved on the use of corticosteroids, coming from the worlds major national and international health care societies:

And so was born the FLCCC’s first mission: advocating for effective treatment of COVID-19 by trying to get the world to understand that it was a “corticosteroid responsive disease.”

May 2020 - I left the University of Wisconsin to help my former hospital in New York City - Mount Sinai Beth Israel. They were inundated with severe hospital cases and all my former colleagues and trainees were exhausted. Upon resuming the care of my old ICU, I became quickly intrigued by how all these COVID patients were presenting early on with “happy hypoxia” - a description meant to convey the combination of low oxygen levels with a lack of breathlessness or discomfort. I had definitely seen patients present in similar fashions but they were rare in my mind.. I couldn’t put my finger on the connection until one night, I was obsessing about this familiarity as I was trying to fall asleep, when it suddenly hit me that these patients reminded me of patients with a rare-ish disease called “organizing pneumonia (OP).” The name is actually a confusing one becuase OP is not an infectious illness but instead a reaction to a lung injury, typically from an unknown source or most commonly a drug reaction. In some cases, it can be “associated with” or “caused by” a viral infection but it is not a true infection itself.. in that, the treatment is as follows: 1) remove offending agent/drug and/or 2)treat with... corticosteroids (and use high, “pulse doses” in fulminant cases). These patients were notoriously in need of oxygen, often for prolonged periods, and often in high fractions despite being fully conversant and not in overt respiratory distress while resting in their hospital beds. “Happy Hypoxia” solved! SARS-CoV2 was causing an “organizing pneumonia”.. in almost everybody?

Why does this Covid-induced organizing pneumonia is so effectively treated with corticosteroids? Because it is being the result of a runaway inflammatory immune reaction (the ill-famed cytokine storm). “The type I interferon response in COVID-19: implications for treatment“ (Nature, 2020.08.12):

Despite early reports to the contrary, there is increasing evidence that patients with severe COVID-19 have a robust type I interferon response, which contrasts with the delayed, possibly suppressed, interferon response seen early in infection. A robust type I interferon response could exacerbate hyperinflammation in the progression to severe COVID-19 through diverse mechanisms.

To be even more specific, “Cellular and Molecular Effects of SARS-CoV-2 Linking Lung Infection to the Brain” (2021.08.13):

A less prevalent route for the immune evasion of SARS-CoV-2 is the infection of alveolar macrophages. While the “conventional” way of the entry of viral particles to the host cells is ACE2-mediated, in some cases, macrophages can be infected, and this happens via an antibody/Fcγ-mediated route. In this situation, SARS−CoV−2 virions are recognized by cross reactive neutralizing antibodies against seasonal coronaviruses (48); and then are taken up by the macrophage cells via Fcγ-receptors in a mechanism termed antibody directed enhancement (ADE) (49) (Figure 2B). Once taken up via Fcγ receptors, the virus particles inhibit the signaling of IFN-I in infected macrophages (14), leading to an increased expression of pro-inflammatory factors (IL-1β, IL-6 and TNF-α), which might result in hyperinflammation (14, 41). Besides this, the number of alveolar macrophages present during SARS-CoV-2 infection correlates well with disease severity (50) The increased pulmonary expression of significant amounts of pro-inflammatory cytokines, NF-κB and hypoxia-inducible factor-1 α (HIF-1α) help uninfected, activated macrophages to invade into the alveoli, which recruit other immune cells such as CD8+ T effectors, and this produces more clones and causes tissue damage (50, 52, 53).

Capish? This is the case of ADE, where the SARS-CoV-2 antibodies serve as the helpers for the virions to invade the macrophages, which causes the cytokine storm, which, in turn, can be doused off with the corticosteroids. This is also why the lungs get affected a week or so after the initial symptoms - only after the robust antibody response by the immune system.

In addition, as has already been observed in the case of SARS-CoV-2 progenitor plain-vanilla SARS, “SARS Coronavirus and Lung Fibrosis”(2009.07.22):

According to the data from autopsy of fatal cases, the major pathological characteristic in SARS patients is diffuse alveolar damage (DAD) (Chan et al. 2003). The mechanism of DAD is believed to be endothelial and alveolar epithelial injury due to both direct viral effects and other indirect factors (Nicholls et al. 2003). During the early phase of SARS development (7–10 days), the lungs demonstrate the features of DAD including extensive edema, hyaline membrane formation, fluid and cellular exudation, collapse of alveoli, and desquamation of alveolar epithelial cells. At the same time, fibrous tissue could be detected in alveolar spaces. This phase is referred as the acute stage. In the medium phase of SARS development (10–14 days), the lungs display fibrous organization including interstitial and airspace fibrosis, reparative fibroblastic proliferation and type II pneumocytic hyperplasia. The fibrous organization becomes more extensive with time. This phase is referred as the proliferative organizing stage. In the late phase of SARS (2–3 weeks), referred as the fibrotic stage, the lungs exhibit dense septal and alveolar fibrosis. The time duration is counted from onset of the symptoms, and the pathological process does not always evolve through all the three stages, but may cease or recover at any phase.

As SARS-CoV-2 has ten times the affinity to ACE2 receptors in human lungs, so is also its potential for the organizing pneumonia.

For even more in-depth treatment of this subject, read “Mechanisms of Lung Injury Induced by SARS-CoV-2 Infection”(2021.10.26).

So, what about the mRNA jabs? Why aren’t they causing a similar effect, when they come with S spikes in 10-30 times higher quantities than during a natural SARS-CoV-2 infection, as we have established in the previous post?

• First of all, because the S spikes in the jab mostly come into contact with the endothelial cells of the lungs, being carried around in serum mostly by exosomes after have been generated via mRNA translations in various transfected tissues, whereas in the natural SARS-CoV-2 infection they come into contact with the epithelium in the upper airways, and then the lungs.

• Second, the ADE effect just described above, with the virus infecting macrophages in the lungs, usually does not come into play when the macrophages “swallow” an S spike rather than the whole replicating virus. And the macrophages do not raise the cytokine storm in the former case, at least this is a much rarer, although reported, occurrence.

• Third, the combination of LNPs and pseudouridinated mRNA in jabs severely suppresses one’s immune responses (hence the reactivation of latent viruses, for example), and this also affects the macrophages. Snopes actually boasts in their fact check: “The inactivation of type two macrophages is one of several outcomes that occur from vaccines that produce a large Th-2 biased response, Baylor’s Atmar told us. As discussed earlier, the defense against this outcome is a vaccine that does not produce a Th-2 response and instead creates a strong Th-1 response. Had Tenpenny researched the actual vaccines she maligns —  instead of sharing articles from Infowars —  she would have learned that both mRNA vaccines produce strong Th-1 biased responses with little to no Th-2 response.

  In an October 2020 report in the New England Journal of Medicine, researchers reported that, “The mRNA-1273 vaccine [i.e Moderna] induced [Th1] biased … responses and low or undetectable Th2 … responses.” As reported in Nature this month, data from the Pfizer/BioNTech vaccine indicate a “TH1-biased response.” In other words, the biochemical requirements for the scary reactions Tenpenny alleges to be looming in a few months are simply not created by the mRNA COVID-19 vaccines. This is by design.“

  Therefore, the pro-inflammatory responses to S spike are being suppress “by design”, we are being told. At least for the duration of the S spike production, which is upwards of four months on end - choose your poison, so to say.

What is Th1 and Th2? Glad you’ve asked! “Th1 and Th2 responses: what are they?“ (2000.08.12):

T lymphocytes are a major source of cytokines. These cells bear antigen specific receptors on their cell surface to allow recognition of foreign pathogens. They can also recognise normal tissue during episodes of autoimmune diseases. There are two main subsets of T lymphocytes, distinguished by the presence of cell surface molecules known as CD4 and CD8. T lymphocytes expressing CD4 are also known as helper T cells, and these are regarded as being the most prolific cytokine producers. This subset can be further subdivided into Th1 and Th2, and the cytokines they produce are known as Th1-type cytokines and Th2-type cytokines.

Th1-type cytokines tend to produce the proinflammatory responses responsible for killing intracellular parasites and for perpetuating autoimmune responses. Interferon gamma is the main Th1 cytokine. Excessive proinflammatory responses can lead to uncontrolled tissue damage, so there needs to be a mechanism to counteract this. The Th2-type cytokines include interleukins 4, 5, and 13, which are associated with the promotion of IgE and eosinophilic responses in atopy, and also interleukin-10, which has more of an anti-inflammatory response. In excess, Th2 responses will counteract the Th1 mediated microbicidal action. The optimal scenario would therefore seem to be that humans should produce a well balanced Th1 and Th2 response, suited to the immune challenge.

So, there you have it. The jabbed get their 10X dose of S spike and the suppressed immune response to go. On one hand, the immune suppression ameliorates the organizing pneumonia scenarios (hence the famed reduction in the severe outcomes, for 4-6 months, somehow less with every subsequent jab). On the other hand, they get all the consequences of being flooded with S spikes and LNPs.