Published On: Wed, Jan 27th, 2021

New study acknowledges increased levels of ACE2 as factor in contracting Covid-19; who will take any notice?

In August of 2020, yours truly wrote the article, SARS-COV to ACE2 binding and the dangerous Covid-19 truth, and in it there appeared the statement “SARS-COV to ACE2 binding is a phenomenon so significant that it should be the central and permanent topic of debate”.

As it happens, and still all these months later, no one talks about it, of course, because it would create a huge problem for a government looking to inflict an economic blockade on a people by telling them that otherwise their activity would spread a disease. The ugly truth about Covid-19 is that it doesn’t matter how easy or difficult it is to pass a particular virus from one host to another. This is why, we must suppose, with an order having gone out, no one who can shape perception, or influence behaviour, ever talks about it.

The truth is that Covid-19 – or in fact SARS, as it should be called – is a lung condition which materialises when a particular pathogen is present at the lung – we’re calling it SARS-COV, because SARS-COV-2 appears to be an umbrella term for multiple variations of this coronavirus. If the host has or develops a level of presence of angiotensin-converting enzyme 2, or ACE2 , that makes him susceptible, then a complex will form between the pathogen and the ACE2, causing pulmonary fibroses, leading to pneumonia, and complications from it.

Therefore, the issue at the heart of Covid-19 is how to control the ACE2, not any virus. But, reader, you won’t be told that anywhere else on the internet but at FBEL – outside an academic research paper, that is.

As mentioned, people have no help from any of their corporate or alternative media, or their lockdown sceptic media influencers: “journalists”, politicians or scientists.

Take the site, for instance – which, by acknowledging the official narrative (and regurgitating its news),  is an operation to teach passivity to people who don’t like the economic blockade, but nevertheless a place where people can have their will to act purged by seeing their feelings manifested in headlines, and imagine that someone else is doing something about their problem. Now, the author has newly discovered a page on the site that pays lip service to the ICNARC reporting of ICU admissions. The article titled (in a typically misdirecting fashion), Is the Virus Becoming Less Deadly?, pays lip service because there is no point in talking about ICU admissions without also talking about pulmonary fibrosis, and the escalated nature of real Covid-19 that requires intervention in a critical care environment. So, the author’s regular complaint that alternative media won’t touch ICNARC reports with a barge pole is essentially upheld. The ICNARC reports give the best indicator of real numbers of death from Covid-19, so of course they would be ignored. Or, as it happens, just interpreted to suit: the piece wanted to argue that the data perhaps showed “the virus” had become less deadly. This is to pick an argument in itself, but it’s not why the example is being used; consider this extract:

Non-medical readers should note that these are the very sickest patients with Covid – the vast majority of Covid patients admitted to hospital never need intensive care and the vast majority of patients who contract Covid never need to go to hospital at all.

Here, joins in the mainstream deception that one can have a tickle of Covid-19, and never need to see a hospital bed. This, reader, is the fundamental lie used to prolong the economic blockade, being disseminated to people who should be being given reasons why the lockdown can end. If you sustain in its operation in any shape or form, you are a fool.

Here’s another example, for the sake of brevity, taken as is from a very recent FBEL article:

This truth [that Covid-19 is a pneumonia caused by SARS-COV to ACE2 binding at the lung] was not challenged by Michael Yeadon,  ex-Pfizer head of respiratory research, when it was put to him on Twitter. The author posted the following reply to a tweet in which Yeadon claimed to have had had a mild case of Covid-19:

SARS-COV binding with ACE2 at the lung – how do you know you had a “mild” bout of that?

Now, as the piece goes on to tell, Yeadon did not respond – but then, if he wanted to defend his claim, he would have had to defy data such as that being discovered by a team at Boston University, that was reported on in a piece, published January 21, 2021, titled How Coronavirus Damages Lung Cells within Mere Hours (emphasis added):

Viruses can’t replicate themselves because they lack the molecular machinery for manufacturing proteins—that’s why they rely on infecting cells to hijack the cells’ internal machinery and use it to spread their own genetic material. When SARS-CoV-2 takes over, it completely changes the cells’ metabolic processes, [Andrew] Emili [a senior study investigator] says, and even damages the cells’ nuclear membranes within three to six hours after infection, which the team found surprising. In contrast, “cells infected with the deadly Ebola virus don’t show any obvious structural changes at these early time points of infection, and even at late stages of infection, the nuclear membrane is still intact,” [Elke] Mühlberger [a senior study investigator] says.

The nuclear membrane surrounds the nucleus, which holds the majority of a cell’s genetic information and controls and regulates normal cellular functions. With the cell nucleus compromised by SARS-CoV-2, things rapidly take a bad turn for the entire cell. Under siege, the cells—which normally play a role in maintaining the essential gas exchange of oxygen and carbon dioxide that occurs when we breathe—die. As the cells die, they also emit distress signals that boost inflammation, triggering a cascade of biological activity that speeds up cell death and can eventually lead to pneumonia, acute respiratory distress, and lung failure.

Notably, Mühlberger is reported as stating:

What makes this research unusual is that we looked at very early time points [of infection], at just one hour after the virus infects lung cells. It was scary to see that the virus already starts to damage the cells so early during infection.

Lots of this information the FBEL reader will have already known. What is confirmed, however, and what we inferred to have always been the case, is that Covid-19 requires medical attention very soon after taking hold. Interestingly, the NHS guidance for SARS states that “a person suspected of having SARS should be admitted to hospital immediately and kept in isolation under close observation.”

Now, it is true that there is a story that Covid-19 starts in the upper respiratory tract, and this would explain why people might have cold-like symptoms, and would be said to have a mild case which T-cells can clear up – and do it before the virus can get into the blood to be transported to the lungs. This scenario, however, has been rejected at FBEL because, although ACE2 will be presenting at other organs, it is only at the lungs where infection occurs, indicating that this organ has been reached through the entirety of the respiratory tract. In other words, the pathogen goes straight to the lungs (for more on this see, Covid-19 is not flu). Of course, that there has been misinformation in corporate and alternative media so as to conflate Covid-19 with flu is perhaps why the myth of the mild case could be established and persists. What people were actually having, when they thought they had Covid-19, was common cold or flu.

If it is possible to naturally survive a case of SARS-COV to ACE2 binding, and the rapid onset of the deterioration of the lungs, the thing that the author would put it down to would be non-facilitating levels of the enabling protein (ACE2) – which, again, is at the core of the issue. Arguably, even this kind of a case would still need hospitalisation. Above all else, it should be all too clear to the reader that anyone who dies of Covid-19 should have been a recipient of treatment in critical care.

Coming at last to the central point of this article, and to make an account of the research referred to in the title, the very fact that Covid-19 requires therapy is why there has been the development that we are about to discuss; a development which is about the controlling of ACE2: yet again, the key to Covid-19.

A treatment using something called interferons has been mentioned before hereabouts at FBEL, and for a fuller discussion, please see the article, No surprises as Covid-19’s exceptionality remains ignored and unreported; ACE2 crops up again. What was suspected in that article, that interferons created ACE2 prevalence and thus were problematic, is confirmed in research by people at the University of Southampton, let’s call it Lucas et al. The study, published in Nature Genetics, but also recounted at the website, where the author encountered the telling of it, claims to have found a way to get around a problem:

Naturally occurring antiviral proteins called interferons have shown promise in treating COVID-19. However, previous studies have shown that interferons increase levels of ACE2 – casting doubts over the potential for such treatments, with the possibility that increased ACE2 could see these drugs actually worsen COVID-19 impacts.

The researchers are saying that they have discovered a “short form” of ACE2 which basically lacks the equipment for binding to it. And what these researchers are saying is that the interferon treatment actually “predominantly” promoted “short” ACE2, thus, we should infer, paving the way to interferon based treatments. However, the crucial point is that, here again, just as was found in the Nebraska University study by Radhakrishnan et al  [that featured in the FBEL article, Forget Dangerous Infertility Causing Vaccines, Covid-19 Is Prevented By The Humble Pineapple (Say Researchers)], there is academic support for the notion that diminished expression of ACE2 is inextricably linked to prevention of Covid-19.

This is the key to Covid-19, thus – because it would fatally damage the construct that UK Government uses to implement its economic blockade – is it never, ever discussed in the sphere of public discourse (and that’s why all of your alternative media is controlled, reader). And again, it is left to this humble little site, in all the world, it seems, to state that the crucial question to answer is: what causes the initial ACE2 expression which makes the host susceptible to an infection (binding)? The theory proposed at FBEL is that it is due to prescription drugs: ACEIs and ARBs. See, Is “Covid-19” An NHS Prescribed Drug-Induced Pneumonia (Amongst Other Things)?

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  1. BeBop says:

    Excellent again

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