Published On: Tue, Oct 6th, 2020

Covid-19 is not flu

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It’s probably true to say that right from the start of the UK Government’s operation to use “Covid-19” as a pretext for imposing economically debilitating restrictions (that are for the vast majority of the time facilitated by people volunteering to obey them), influenza has commonly been conflated with an illness that develops from a virus that has been called SARS-COV2.

To cut through the confusion, let us be clear that there are two positions regarding an illness that develops from SARS-COV2. The first is that of the official narrative, where SARS-COV2 leads to Covid-19. The second is advocated by the author and it is one where SARS-COV2 has never been isolated, can’t be shown to exist, and where it is in fact the original SARS-COV that is causing a relatively obscure ailment that sometimes can develop to the death of the patient. And let us be totally clear again, none of this discussion involves “Covid-19” – Covid-19 in quotation marks – which is actually the death of hospital population, by various causes but attributed to a new disease, to create the appearance of a scary viral pandemic.

In fact, the conflation of Covid-19 with flu is everything to do with the public relations exercise surrounding the demise of around 50,000 people who had their death pathway management withdrawn so that they would die more or less immediately thereafter for the effect. Indeed, if one separates flu and Covid-19 out from each other, one can see how the conflation would have been entirely necessary (pointing to it being thought up as part of a plan) to present an impression of a new illness that was also as terrible a killer as was flu, but more importantly, could kill in a similar way as flu was supposed to.

As far as those looking to capitalise on a pandemic-scare crisis would have been concerned, SARS-COV – the virus that is suspected by the author to be at the root of Covid-19 – was a big disappointment in its first outing in 2003 as virulent microbiological catastrophe bringer. 811 deaths worldwide, according to the Wikipedia entry. It is entirely understandable that it would need a lot of public relations help to generate great fear of it in any new project to exploit it – and in the UK≠, that exterminated hospital population would have been the bedrock of the exercise. The disease would need a different name too.

A crucial element for creating belief that there had been great death from the all new Covid-19 was that very conflation with flu, and this activity is something that happened across the board of broadcast media, with the alternative sort, unsurprisingly, also failing to insist on a distinction. And this is why UK Government has been able to get away with having its NHS operatives dole out “mention of Covid-19”, often expressed as “death with coronavirus”, as an official cause of death. The impression it is meant to give is that, while Covid-19 has not directly killed the patient, it was a contributory factor – just like flu is popularly imagined to be.

Reality is completely different. Covid-19 is a pneumonia, manifested in a specific way directly related to the causative agent, that brings on death of its own accord – and this is what FBEL readers, at all times, have been asked to understand. Indeed, at this site, there was eventual rejection of the other phrase used by alternative media and assigned-to-be-dissident corporate-media, “death from coronavirus”, which was used for creating a dislocated sceptical perception. “Death from coronavirus” was used to give the impression that a good deal, if not all, of the hospital population death that had been attributed to the disease “Covid-19” had actually died of it. As was discussed at FBEL in May, saying that there was death from or with coronavirus amounted to the same thing: it allowed that “Covid-19” was real – something that would have been harder to do if there had not been conflation with flu.

Now, of course, it is possible to say of flu that it causes pneumonia, and indeed it can do that. But again, this would be about erroneously and maliciously, even, conflating flu with Covid-19, which is pneumonia, not the possibility of it occurring from a viral infection. When it was thought to have first emerged in China, Covid-19 was called NCIP: novel coronavirus-infected pneumonia.

Despite the (deliberately created) confusion, it is quite possible to discern two key characteristics of flu and Covid-19 by which they can be separated, and be seen as different beasts. The first is the way in which the virus, whichever one it may be, is distributed to the lung, and the second is what happens at that point of arrival. In fact, the characteristics of flu being a potential large scale killer, and Covid-19 being a pharmaceutical company’s big disappointment are all tied up in these differences. And that’s why, we can in our suspicion realise, that there is nobody else in any media who tries to not conflate the two.

The influenza virus, and the variety of it doesn’t matter, gets started in the upper respiratory tract. And this is also what is said of SARS-COV2, and so in this respect it would differ from is evolutionary ancestor, SARS-COV, which, as had been thought, had to be inhaled₸, potentially all the way into the lung, where it would nevertheless behave in exactly the same way as SARS-COV2 does at that organ.

However, logic dictates that it cannot be guaranteed that SARS-COV2 will exploit the upper respiratory tract to reach the lower respiratory tract in the same way that a flu virus does, and this ultimately is an argument for why SARS-COV2 is indeed the same old, useless SARS-COV.

As we all know by now, SARS-COV (and SARS-COV2, if it must be mentioned), performs its cell-invading via a protein on the surface of the cell: ACE2. A flu virus doesn’t need this gateway agent to attack a cell. At the commencement of an infection, the flu virus attaches to epithelial cells in the upper respiratory tract – epithelial cells being those that line the surfaces of the body. The medium in which a spread of infection from the upper to the lower respiratory tract appears to be mucus.

ACE2, when one investigates this, is a substance that can have varying levels of expression. This is understood to be true because medication to inhibit ACE appears to “upregulate”, which is the Orwellian medical word for “increasing levels of”, ACE2 (please see previous FBEL articles to understand the relation between ACE and ACE2).

According to the Wikipedia entry for ACE2, it is expressed on endothelial cells, which are also surface-lining cells, but they form barriers between blood and lymph vessels (tubes) and tissue, and control the flow of substances and fluid into and out of the tissue – and this would make sense of why there is the phenomenon of low blood oxygen that is associated with Covid-19. Indeed, this might make us think that SARS-COV must spread by way of the blood. In fact, it is this transfer mechanism that is claimed by the medical professional who was encountered on Twitter by the author, and with whom an exchange was had, after which an account was written up in the article, A twitter encounter with a zealot from the cult at the forefront of tyrannising the country (an equivalent of the Nazi SS). There was no effort by this medical professional to explain how SARS-COV travels from the upper to the lower respiratory tract, but instead, in fact, it was claimed that the disease was more of a cardiovascular one – due to the whole infection of blood cell angle of attack – and not like SARS (from SARS-COV): in other words, not a respiratory one. This, of course, is wrong. Covid-19 is a respiratory disease – but then this medical professional didn’t seem to know the difference between ACE and ACE2. In short, the scenario proposed by the medical professional (and we can suppose that it has been parroted from an official medical industrial complex in-house explanation) bypasses the problem of the means of spread by the respiratory tract by opting to think of the disease as something that it is not.

ACE2 – which, if the reader didn’t see this told hereabouts before, quite conveniently came along at about the same time as SARS (“discovered” in 2000, according to one particular paper‡) – is found at most organs in the body, but there does not seem to be binding with SARS-COV at any other place than the lung in the mechanics of Covid-19. This would suggest that the virus doesn’t get into the blood, and the fact that associated low blood oxygen level is, by some, reckoned to be caused by the pulmonary fibrosis by SARS-COV binding, further suggests that communication between blood and lung is being sealed off rather than opened up. Of course, opening up the blood system by cell damage at the lung to a broader viral infection of the body is said to be a feature of flu. This is why the author says that Covid-19 is as different to flu as flu is to warts.

How, then, does SARS-COV move from the upper to the lower respiratory tract? Putting aside what medium it would have to travel in, there needs to be a presence of ACE2 because without this there can be no exploitation of the environment – and so we revisit the point that there must be uncertainty of any fact of this in the upper respiratory tract, for a number of reasons (i.e. ACE2 levels – which, if they are variable can presumably be as low as to be ineffective – and the fact that ACE2 primarily appears to be an organ-blood barrier phenomenon). The author gravitates to the idea that SARS-COV2 must be inhaled into the lung† – so the distributing medium is air – which suits his idea that the virus is in fact SARS-COV. In turn, this suits the idea that people have for a long time, and are still getting sick with SARS, and SARS variant, an obscure illness where perhaps a long term and usually dormant resident mircoorganism (because, unless one lives in an effective air pollutant chamber like Wuhan, what are the daily chances of breathing in SARS-COV?) kicks in on changes in the microbiome (“upregulated” ACE2 levels). It is an illness, then, that , up until this point when it was picked on to form the basis of a great deception, would probably usually have been misidentified as the much more common flu-induced pneumonia.

 

≠ The author can only comment on what happened in the UK, but if the matter of who died of what in foreign hospitals was looked into, we might anticipate discovering that the same scenario played out time again all over that part of the world where the Anglo-globalists needed economic readjustment.

₸ See the Amoy Gardens, Hong Kong, outbreak, where

SARS was capable of going airborne, spreading through… faulty plumbing and ventilation systems to the people who lived on the estate. “The infections [were] officially attributed to faulty toilet traps which were thought to have aerosolized patients’ virus when the toilet was flushed, allowing dispersal of the virus to other residents,” [Stephen] Morse [professor of epidemiology at Columbia University Mailman School of Public Health] explained.

‡ See: A Novel Angiotensin-Converting Enzyme–Related Carboxypeptidase (ACE2) Converts Angiotensin I to Angiotensin 1–9, Donoghue et al, Circulation Research 2000;87:E1–E9.

† True that researchers/scientists/lab technicians have supposedly discovered SARS-COV2 in the upper respiratory tract, but as always we must ask, how do they know they have discovered SARS-COV2? The reader is referred to the article, SARS-COV-2 doesn’t exist, but don’t take anyone else’s word for it:

Imagine there is this RNA that everyone has a matter of course in their microbiome, and perhaps people create slightly different variations in their own bodies. This material gets detected at the same time that people are suffering from a pneumonia caused by a toxic environment (see Wuhan), and so it becomes to be believed to be a virus and the causation agent for an illness. After it is analysed, as best it can be without the biological matter it comes from ever having been properly isolated, and a genetic record is placed in international databases, it becomes a model for other material to be recognised, but not precisely – only in a cluster of very alike genetic patterns

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Displaying 7 Comments
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  1. theguvnor says:

    I’m getting lost! What are they testing for or more precisely what are they suggesting is throwing up positiv?
    https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30453-7/fulltext

    • P W Laurie says:

      This: “In March and early April, 2020, most people tested in the UK were severely ill patients admitted to hospitals with a high probability of infection”, and this:

      “At present [Sep 29th], only about a third of swab tests are done in those with clinical needs or in health-care workers (defined as the pillar 1 community in the UK), while the majority are done in wider community settings (pillar 2). At the end of July, 2020, the positivity rate of swab tests within both pillar 1 (1·7%) and pillar 2 (0·5%) remained significantly lower than those in early April, when positivity rates reached 50%.”

      In fact, as FBEL spotted, the very first thing the NHS did was it went hunting for “Covid-19” with PCR tests on its own wards – patients who had already been admitted. Anything sets off the PCR test, again as covered here. So, what is suggested here is that the hospital population that were about to be killed off were so lousy with various pathogen that a PCR test performed on them had a field day.

  2. theguvnor says:

    PW What happened to your latest article which was up Sat afternoon but seems to have disappeared?

  3. theguvnor says:

    I must apologise. In a slightly inebriated state following my team in virtual rugby I googled rather than use bookmark and it sent me into an article on Government racketeering which was dated March. I have never seen the article before and consider it an real eye opener and very prescient for the state we are now in. Needless to say I have linked it on various other blogs but in our world of 24hr news it doesn’t seem to be getting much attention. Sorry for inconvenience

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