Q1. How can a virus containing an exoribonuclease mutate in the way you are saying?
Coronaviruses possess an exoribonuclease within nonstructural protein 14 (nsp14-ExoN). This functions as a proofreader during viral transcription and encoding, ensuring high fidelity replication. This minimises the potential for mutation, as shown by the fact that sarbecovirus/lineage B betacoronaviruses with their exoribonuclease removed mutate at 16x the rate of those with the exoribonuclease [Smith et al, 2010].
The killer mutation is nothing more than the antigen shift around the spike glycoprotein, something that is a constant and key part of a coronavirus’ attempt at immunoevasion.
Q2. If This Mutation Is True, Won’t It Render Your Vaccine Ineffective?
More than likely. The principal ‘vaccines’ (to understand the difference between a vaccine and an antiviral, read our explanation here) are BNT126b2 and now ChAdOx1. Both focus upon the structural spike glycoprotein which is usually described as SARS-CoV-2 Achilles’ Heel. It is the low-hanging fruit of an obvious target. To protect against this, the structural S protein recombines through glycosylation and dynamic glycan shielding. This means it evolves on a regular basis (that’s your ‘mutation’) but any vaccine that targets the spike protein is predicated upon it being static and not subject to change.
These new vaccines aim to stimulate antigen-specific antibodies but SARS-CoV-2-specific antibodies are gone by 56 days following viral clearance for IgM and by 80 days for IgG [Anding et al, 2020]. So your vaccine can create as many antibodies as it wants…the immune system will discard them once they are no longer required.
Professionally, we suggest that there are far more vulnerable elements to SARS-CoV-2, notably:
Integration of nsp10 (grey) and nsp-14 ExoN (yellow) of sarbecovirus/lineage B betacoronavirus [Ma et al, 2015].
- nonstructural proteins 7 & 13 as well as the structural nucleocapsid protein. Memory T cells conserved from previous infections with the common cold are recognising SARS-CoV-2’s nsp7, nsp13 & N protein with high affinity. That’s on top of the pathogen-associated molecular patterns of coronaviruses that are recognised by pattern recognition receptors TLR7 & TLR8.
Q3. Can You State That ANY Vaccine Given Rushed Approval Will Not Cause Trigger ANY Autoimmunity Or Cause ANY Immunopathology?
They can’t because prior to BNT126b2 having been given fast-track approval by conflicted healthcare agencies, no RNA/mRNA experimental vaccine had ever been approved for the treatment of any condition anywhere in the world.
Vaccines usually take up to 15 years to develop. How many corners are cut, especially in the crucial Phase III large-scale clinical trials under ‘real world’ conditions, when you compress 15 years into less than one year?
Timeline for standard and rushed COVID-19 vaccine development [Krammer et al, 2020].
Tseng et al [2012} proved that SARS-CoV vaccine candidates can trigger pulmonary immunopathology through Th2 proliferation. While Bolles et al [2011] used a double-inactivated type vaccine, they also showed pulmonary immunopathology.
If that weren’t enough, the risk of antibody-dependent enhancement (ADE) is greater, where a vaccine or antiviral increases the virulence of the pathogen it is supposed to treat. Previously, in respect of SARS-CoV Ho et al [2005] showed evidence of ADE and Zhao et al [2020] show evidence of ADE in respect of SARS-COV-2. These should all be red flags.
Q4. Does IM/ID Vaccine Delivery Prevent IgA-Induced Protective Or Sterilising Immunity?
Almost certainly.
BNT126b2’s intramuscular (IM) delivery and then intracellular bioactivation bypasses the upper respiratory tract and therefore prevents the creation of secretory immunoglobulin A (IgA). IgA is the immunoglobulin isotype expressed in mucus and dominant in the upper respiratory tract, whereas IgG is dominant in the lower respiratory tract. In other words, IgA is right where you want an antibody to be: the point of first contact. The respiratory tract is where virions activate through furin cleavage, are attenuated before reaching the ACE2 receptor and are expelled by mucal excretion. An intramuscular or intradermal (ID) delivery misses the upper respiratory tract.
All the vaccines now approved and in Phase III trials – mRNA1273; BNT126b2; AdV-5; CoronaVac; ChAdOx1 and NVX-CoV2373 – use IM delivery so none are likely to provide protective or sterilising immunity.
While BNT126b2 may trigger the creation of antigen-specific IgM and IgG antibodies, these may not be able to class switch to IgA or may not be effective as such, where the genetically-modified spike glycoprotein created by the vaccine differs from any subsequent exposure to the virion. In other words, the vaccine is unlikely to provide any protection through secretory IgA expression and therefore no sterilising immunity [Krammer et al; Doremalen et al; Yu et al].
Q5. Why Do You Confuse Infection With Severity?
The R0 ratio for varicella-zoster virus (chickenpox) is in the range 10 – 12. The R0 ratio for ebolavirus is 1.5 – 1.9. Which would you rather have?
The more infectious or contagious an illness becomes does not mean it also becomes more severe or dangerous.
The most infectious illness on the planet is the common cold.
SARS-CoV-2 has been weakening since August. It may be more infectious now but it is also less dangerous by a significant percentage.
Q6. What Proportion of ‘Coronavirus Tests’ Are Picking Up ANY Coronavirus Rather Than Sarbecovirus/Lineage B Betacoronavirus SARS-CoV-2?
Nucleic acid testing, also known as RT-PCR testing, looks for tiny fragments of viral RNA. Except coronaviruses have a high level of genetic homology. Embecovirus/lineage A betacoronaviruses share amino acids, peptide chains and proteins with sarbecovirus/lineage B betacoroaviruses. RT-PCR testing can’t tell them apart, so a large proportion of positive tests are positive tests for the common cold.
We first highlighted the fallacy of nucleic acid testing on 19th March 2020.
To understand the different types of testing, read our explanation here. The next time you hear or read about ‘rising COVID cases’ ask yourself is that rising SARS-CoV-2 positive nucleic acid tests or rising COVID-19-specific antibody tests: the two are completely different but deliberately conflating one with the other makes the situation seem far worse than it is. That’s before you take into consideration the false positives, as explained above.
Q7. How High Is The Positive Correlation Between Wearing Masks And Numbers Of Infections?
If proper surgical masks – defined as conforming to FFP2/N95 standards – only filter down to 0.3 micron and the SARS-CoV-2 virion is 0.1 micron, then just how effective is a piece of cloth you bought for 10p going to be? It will not stop the inhalation of virions.
It will however stop mucal excreta that may contain newly-replicated virions from being exhaled normally. It will prevent the normal action of viral clearance that the respiratory system is designed to facilitate, i.e. breathing out contaminants, whether dust or pathogen. Instead, you simply re-breathe your own infection for hours on end. With SARS-CoV-2 having a burst size of 103 you in effect self-dose, accumulating ever greater viral load in the upper respiratory tract until you merrily turn yourself into an improvised infectious device. “I wear a mask…to make myself sick” as the propaganda adverts would say if they told the truth.
The more people are told to wear non-surgical face coverings, the higher the number of moderate to severe infections. Non-surgical face coverings prolong the presence of the virion and make the situation worse not better.
Do not panic. Do not worry. Do not follow government advice.