As usual, Geert Vanden Bossche (GVB) skirts the entire issue of T-cells and their breadth of antigenic virus recognition and appears to want to base his fear mongering solely on the role of antibodies. As for the mechanism of host protection I describe - which is absolutely classical & not considered theoretical at all - how else does GVB propose host immunity works?
If you’ve acquired immunity from surviving infection or having been vaccinated, but then don’t see the virus again for months, most likely you won’t have appreciable quantities of circulating antibodies. But you will have circulating T-cells capable of recognising up to several dozen virus short peptides, which he’s right to point out are presented in conjunction with appropriate MHC. It’s therefore also true that some of your cells do need to become infected before your immune system recognises that the virus is present. And this is fine, because
immunity doesn’t necessarily prevent SUBCLINICAL infection but it does protect you against CLINICAL illness.
No variant so far differs sufficiently from the original virus to have ANY chance of escaping immunity conferred in the way which has been demonstrated in several peer reviewed journal articles over the last year. If this wasn’t true, by now we’d be seeing reinfection accompanied by CLINICAL illness all over the world. And we’re not seeing that, anywhere.
Do please remember, PCR tests don’t distinguish reliably clinical illness from sub-clinical infection (or downright errors in the test). So when I see news articles claiming reinfection,
notice they always & only speak of the distorted language of ‘cases’, entirely the wrong term for a symptomless person with a positive PCR at high cycle threshold.
SARS-CoV-2 creates a great many variants but it’s easiest to distinguish the effect of these on resilience of host protection by reference to how DIFFERENT these variants are from the original virus. If you were to create an image of the original virus & then superimpose all the variants, one after another, it would seem as if the virus remains where it is, vibrating, as it were.
Much activity, but little change in its overall structure.
In every case to date, the changes are irrelevantly tiny, a handful of amino acids out of almost 10,000. This means the majority of those MHC-restricted peptides are unchanged from variant to variant.
Our immune systems have absolutely no difficulty whatsoever in recognising these as a virus we’ve encountered before & this means we rapidly recruit T-cell clones, selected-for during the acquisition of immune memory, and it is these rapidly available T-cells which protect us from clinical illness by killing those small numbers of virus-infected cells. This all happens without us even becoming aware of our wonderful protective immune system.
We will not remain sub-clinically infected for long enough to grow a sufficiently large virus load to become infectious. So this notional selection pressure won’t get much of a chance to operate. In fact, think about it: when was the longest time during which the virus was able to replicate unhindered? That’s right: during the initial infection.
That allowed several days to a couple of weeks before an immunocompetent host mounts a sufficient response to overwhelm the virus. And it’s during that process that a selection pressure could operate, yet it’s out of this activity that the variants arose.
Yet still, almost everyone clears the infection. So much for “variants formed under selection pressure are likely to be more dangerous & escape immunity”.
Clearly, this is precisely NOT occurring.
The only variants forming are those so close-in to the original virus that they’re not escaping immunity at all. To state again: the number of variants of SARS-CoV-2 formed is theoretically very large but,
so long as they are all nearly identical to the original - which ALL of them are - they’re irrelevant from an immunological standpoint. (I recognise that some might have different behaviours as infectious agents, but that’s a separate topic entirely).
I'd be interested in GVB’s response to my characterisation so far, because I genuinely don’t understand his narrative at all & I have tried, having listened to two of his long-form interviews. Is he saying that the variants of SARS-CoV-2 are much more different from the original sequence than I’m relating? If yes, please provide a link to this. I’m not seeing any such larger changes in the literature.
Or, is he saying that a change as tiny as I’m talking about (0.3% or so in the primary sequence) is enough to no longer be recognised as a pathogen we’ve seen before? If so, perhaps he’d like to comment on how that could be, and in particular I’d be very interested in his thoughts on these two papers:
The above paper by Le Bert et al (2020) shows that
those who recovered from infection with SARS in 2003 still retain good T-cell immune recognition 17y later AND also recognise SARS-CoV-2, which they’d NOT encountered before. Now, that’s cross protection, and these two viruses differ by more than 20%. Rather destroys any argument that the tiny extent of drift of SARS-CoV-2 requires the planetary obsession of which GVB is part, does it not?
The above paper by Tarke et al (2021) shows that a large number of T-cell epitopes are selected & form part of the repertoire in immunity (there’s another set of smaller, overlapping but non-identical set of epitopes against which antibodies are raised). The authors themselves conclude that their findings remove concern that small changes in the virus, such as we’ve seen so far, will enable immune escape.
The same group also showed that subjects who’d survived infection by SARS-COV-2, or had been vaccinated,
ALL recognised ALL the variantswhich the investigators had available.
By the way, I’d be be interested in his reactions to this in-depth review on the clinical efficacy of ivermectin. It's been subject to ruthless censorship for at least SIX MONTHS, resulting in countless avoidable deaths.
I argue that if it, along with the other useful treatments, (which have been beautifully summarised in a protocol for targeted, sequential, multi drug treatment of covid19, which Dr Peter McCullough & others have drafted & posted on the website of the American Association of Physicians & Surgeons), were more widely appreciated & APPLIED in clinical practise, we could control Covid19 much better than we do now, and CANCEL the Emergency Use Authorisations for all the experimental, gene-based, spike protein inducing ‘vaccines’.
Does GVB agree, or is he interested only in peddling further, also experimental vaccines?
Ivermectin review:
Review of the Emerging Evidence Demonstrating the Efficacy of Ivermectin in the Prophylaxis and Treatment of COVID-19
McCullough et al multi-drug treatment of Covid19:
And also:
Bottom line for me is that
the extent of variation in SARS-COV-2 simply isn’t concerning. There’s no hint of immune escape nor would it be expected, based on both theoretically & empirically.
If the picture changes, so too will my view.
This means THERE'S NO JUSTIFICATION WHATSOEVER FOR VACCINES AGAINST VARIANTS!!
Anyone know what’s in those “3rd jab vials”?
I’m often asked “So why do we require new vaccines against influenza each year?”
This is because the way flu changes its structure is COMPLETELY DIFFERENT from the slow, antigenic drift we observe in SARS-COV-2. Instead, flu can undergo reassortment or antigenic SHIFT, exchanging whole sections of genetic information. In terms of the movement analogy, for flu, it’s as if it has its ‘seven league boots on’. It can combine these methods and,
in a year, evolve so much that, when it cones round again in the next season, it can actually present to our immune systems as if it was a new pathogen entirely.
www.bitchute.com
