Epitopes And Paratopes.
Apparently the killer virus of death (the one that continues to not kill people, especially those it infects) has now mutated into an even more killer strain. If that’s true – which it isn’t, read on to find out why – then wonderdrug vaccine BNT126b2 is nothing of the sort: it was never going to be effective and now won’t work on the killer mutation of death. This is because the vaccine is designed to artificially create SARS-CoV-2’s antigen – its structural spike glycoprotein – in vivo in order to generate an antigen-specific adaptive immune response. Well, if the virus really has ‘mutated’, resulting in mutations to its epitopes, then the paratopes of vaccine-stimulated antibodies won’t recognise it.
In order to understand the differences between a vaccine and antiviral you can read our earlier article here as well as why an experimental vaccine is truly dangerous here and why an antiviral offering passive immunity to high risk groups is a far better focus here.
BNT126b2 has been touted as the solution to the pandemic and therefore is supposed to be a pandemic vaccine, except a pandemic vaccine only works where the pathogen has a high stability genetic sequence with low or zero antigen shift or drift. As we’ve highlighted on many previous occasions, SARS-CoV-2 contains an exoribonuclease within nonstructural protein 14 (nsp14-ExoN) which functions as a ‘proof reader’, ensuring high stability RNA transcription within its replication. So in theory, it is prevented from ‘mutating’ but don’t let that get in the way of the latest lie to be excreted from the diseased orifice of the invertebrate, mass-murdering, cowardly Death Secretary.
Spike Glycoprotein Shift And Drift.
What is happening is the spike glycoprotein is undergoing antigen shift and antigen drift, a dynamic and continuous process undertaken by viruses to ensure their survival. In this context, the nature of the shift & drift relates to the antigen itself and not phylogenetic evolution. SARS-CoV-2 knows that its spike glycoprotein is the target of viral countermeasures because that houses its antigen. Without antigen, it is inert and not pathogenic. Therefore, it deploys a range of tactics to try and ensure virulence through immunoevasion. This includes two of the nonstructural proteins working to alter the 5′-end of mRNA from Cap-0 to Cap-1 to mimic host RNA. However, the principal means of immunoevasion is varying the degree & location of the glycan shielding on the trimeric spike glycoprotein as this shifts the postioning & accessibility of the main epitopes.
Spike glycoprotein epitopes S6P2, S14P5, S20P2 & S21P2 that are detected by paratopes on IgG antibodies [Amrun et al, 2020].
It Contiues To Weaken.
A virus’ sole objective is survival and altering its appearance is a key part of this process. ‘Mutation’ sounds scary and conjures up images of Hollywood science fiction blockbusters. In reality it is a natural process that in no way justifies the ever-more hysterical response. Mathematical fact – not the sciency-fiction projections that the government peddles – shows that SARS-CoV-2 continues to attenuate. As we set out here at the end of August, the Active Cases were 99% mild/1% serious or critical and Closed Cases were 95% recovered or discharged and 5% deaths. We revisited the data three months later, at the end of November, when the figures had changed to Active 99.4%/0.6% and Closed 97%/3%.
The current figures are Active 99.5%/0.5% and Closed 97%/3% (source Johns Hopkins Coronavirus Resource Center and Worldmeters, @ 0500UTC 20/12/20). So despite the third wave and killer mutant of death, it is less virulent than a month ago and still less dangerous than four months ago…while having always been less dangerous than seasonal or winter flu (A(H1N1)/(H3N2)).
Over time, SARS-CoV-2 is now becoming more like its lineage A betacoronavirus relatives, common-cold causing HCoV-HKU1 and HCoV-OC43. We’ve written previously about how the pattern recognition receptors of the innate immune system recognise the pathogen-associated molecular patterns of coronaviruses as they have been doing for the 7,163 years since alphacoronaviruses and betacoronaviruses phylogenetically diverged [Woo et al., 2020].
More And More Like The Common Cold.
In reality, the virus is not mutating but rather undergoing its constant quest for survival through recombination around its spike glycoprotein, a quest made more difficult now that memory T cells conserved from previous exposure to common colds are recognising the homology of its peptide chains with other alpha and beta genera coronaviruses.
Maizel-Lenk dot plot showing the homology of HCoV-OC43’s genetic sequence with that of HCoV-229E and SARS-CoV. Identical matches are indicated by dots, [Vijgen et al, 2005].
Both elements of the body’s immune response – the innate and adaptive — recognise SARS-CoV-2 as non-self pathogen in general and in particular its similarity to the other four common-cold causing coronaviruses:
Cross-reactive epitopes of SARS-CoV-2 and the other four common-cold causing coronaviruses, [Shrock et al, 2020].
Peak infections were 19th March and peak deaths 8th April. Since then, the government’s response has simply prolonged its existence with increasingly pointless and harmful measures that have killed tens of thousands and caused distress, hardship & misery to tens of millions.
Do not panic. Do not worry. Do not follow government advice.