We are a non-profit organisation that has been researching SARS-CoV-2 since early March 2020. We have no competing or conflicting interests. Our work takes a facts-based and evidence-based approach. Our work to date can be illustrated as a timeline:
2020
March
Identification that SARS-CoV-2 is no more dangerous than seasonal or winter flu (A(H1N1)/(H3N2)).
Identification that nucleic acid testing is not an appropriate measure of infection and therefore no basis for effective decision-making.
April
Assessment of the T1/2 of the virion in respect of various fomites.
Identification that SARS-CoV-2 is less dangerous than seasonal or winter flu (A(H1N1)/(H3N2)).
Initial identification of the key importance of viral dosage and relationship between viral dosage & viral load. Identification of importance of burst size and the upper respiratory tract.
Identification of associated deaths being included with actual deaths when reporting COVID-19 mortality figures.
Calculation that non-COVID-19 deaths were exceeding COVID-19 deaths.
Initial assessment of environmental factors causing increased mortality rates in European countries, including the use of NSAIDs; levels of vitamin D deficiency and relevance of latitude, humidity & ambient temperature.
May
Initial assessment of lockdown and identification that it causes negative outcomes, including causing more deaths than it might prevent.
Validation that the innate immune response is capable of overcoming infection with SARS-CoV-2
Initial evaluation of the R0 ratio and identification of its incorrect use by government and healthcare leaders.
Confirmation of deliberate misreporting of COVID-19 deaths as a result of F66 Guidance Notes.
Calculation of peak infection and peak death dates in the UK, and identification that SARS-CoV-2 is beginning to attenuate.
June
Calculation of the UK mortality rate as being 11.2x the worldwide average, despite continuing to attenuate in the UK.
July
Second assessment of environmental factors causing increased mortality rates in European countries. Confirmation that degrees of latitude, humidity & ambient temperature contribute to mortality rates.
Detailed evaluation of vitamin D’s role in SARS-CoV-2 infection, both through deficiency and the relevance of the vitamin D→eNOS→NO pathway, especially in the upper respiratory tract.
August
Initial confirmation that nucleic acid testing is neither effective nor suitable as a measure of infection due to error rates and inaccuracies in cycling/amplification.
Calculation that SARS-CoV-2 continues to attenuate.
September
Presentation of a timeline for SARS-CoV-2, including TMRCA and identification of likely recombination with embecovirus/lineage A betacoronavirus HCoV-OC43.
Evaluation that SARS-CoV-2 came into existence around 2013 and was incorrectly designated ‘new’ rather than ‘newly-discovered’.
Second confirmation that nucleic acid testing is neither effective nor suitable as a measure of infection.
Second assessment of lockdown and confirmation that it causes negative outcomes, including causing more deaths than it might prevent.
Calculation of number of actual deaths caused by lockdown and social distancing.
Identification of the negative outcomes caused by wearing non-surgical face coverings, including increased infectivity from greater viral load in those wearing them and extending periods of infection.
October
Identification of the relevance of the renin-angiotensin system and key importance of angiotensin II, including the relevance of SARS-CoV-2-induced imbalance in the ACE2→ Angiotensin1-7→ Mas / ACE→ angiotensin II→ AT1 receptor axes.
Validation of our work that lockdown causes negative outcomes.
Detailed assessment of the role of NSAIDs in increasing SARS-CoV-2 pathogenesis and mortality.
Assessment of pyrexia and ILIs causing pyrexia. Conclusion that temperature testing is neither an effective nor suitable means of identifying SARS-CoV-2 infection or COVID-19 symptoms.
Second assessment of the upper respiratory tract and importance of NO as a viral countermeasure and secretory IgA as immunity.
Initial identification of antigen shift in SARS-CoV-2-S through dynamic glycosylation and glycan shielding.
Initial assessment of the dangers of RNA/mRNA experimental vaccines.
Initial evaluation that an antiviral offering passive immunity is a more effective solution than a vaccine.
Evaluation of Remdesivir, confirming its high level of reactogenicity and low level of immunogenicity.
Confirmation of non-COVID-19 deaths continuing to exceed COVID-19 deaths.
November
Confirmation that TLR7 & TLR8 recognise SARS-CoV-2 through general coronavirus PAMPs.
Validation of our work on Remdesivir’s lack of efficacy and confirmation of its reactogenecity.
Initial identification of the relevance of memory CD8 TC cells in providing a SARS-CoV-2-specific adaptive immune response in those without previous exposure to the antigen.
Confirmation that memory CD4 TH and CD8 TC cells recognise SARS-CoV-2 and trigger an adaptive immune response, through recognition of two nonstructural proteins and SARS-CoV-2-N.
Validation of our work that SARS-CoV-2 has been in existence for a period of years and was not ‘new’ in early 2020.
Confirmation that exposure to any coronavirus can create SARS-CoV-2 immunity through persistent antigen exposure.
Confirmation that SARS-CoV-2 continues to attenuate and assessment it is becoming more like embecovirus/lineage A betacoronavirus HCoV-OC43.
December
Evaluation of the dangers of autoimmunity, immunopathology and ADE caused by potential SARS-CoV-2 vaccines, in particular RNA/mRNA experimental vaccines.
Detailed assessment of SARS-CoV-2 immunity gained through persistent antigen exposure caused by regular exposure to the common cold.
Assessment of putative new mutant strain, including infectiousness and infectivity, and conclusion it is antigen shift and natural phylogenetic evolution.
Detailed evaluation of the homology of embeco/lineage A and sarbeco/lineage B betacoronavirus genomes. Identification of antibody cross-reactivity across epitopes of alpha and beta genera coronaviruses.
Confirmation nucleic acid testing is picking up the common cold.
Confirmation that all current and pending vaccines use IM/ID delivery and will not provide sterilising / protective immunity, as they avoid the upper respiratory tract and prevent secretory IgA expression.
2021
January
Confirmation that SARS-CoV-2 continues to attenuate and validation of our work on SARS-CoV-2 becoming more like embecovirus/lineage A betacoronavirus HCoV-OC43.
Second calculation of actual deaths caused by lockdown.
Evaluation of S-VoC / N501Y variant, including confirmation it is no more dangerous.
Assessment of antibody-dependent enhancement in SARS-CoV-2.
Initial assessment of ChAdOx1.
Validation by the WHO of our assessment of the flaws in nucleic acid testing.
Review of NORSTM nasal spray. Validation of the significance of the upper respiratory tract and our previous assessment of nitric oxide as an effective viral countermeasure.
Validation of our identification of the significance of viral load and relevance of burst size.
Evaluation of the change in spike protein trimers leading to increased vulnerability to neutralising antibodies.
February
Third calculation of actual deaths caused by lockdown.
Identification of significant rise in UK mortality rate since the start of lockdown 3 and use of ChAdOx1 antiviral.
Second validation of our evaluation that nitric oxide synthesised from vitamin D provides a significant reduction in disease severity and significant improvement in clinical outcomes.
Third validation of our identification of fundamental flaws in nucleic acid testing and failure of testing as an effective response to SARS-CoV-2.
Identification of cell-to-cell fusion by standalone spike proteins migrating direct from endoplasmic reticulum rather than transported to ERGIC for virion assembly. Assessment of this function in immunoevasion of IgG antibodies and subsequent weakness of ChAdOx1 treatment.
Assessment of valosin-containing protein VCP/p97 as a viral countermeasure to trigger chain termination in SARS-CoV-2’s replication process.
March
Identification of the homology of SARS-CoV-2 variants, including haplotype composition and function. Confirmation that amino acid substitutions N501Y and E484K are not geographically exclusive, having been in existence across the world for months before being labelled as originating in a single country.
Evaluation of the role of immunoglobulin A as the most effective isotype as a viral countermeasure and to achieve viral clearance. Identification that it has the fastest isotype seroconversion and is produced in greater numbers than IgM & IgG by plasmablasts in response to SARS-CoV-2.
Identification of the role of glycosylation and hinge structure in IgA2 subclass antibodies in increasing their binding affinity to S protein trimers.
Calculation of the reduction in effectiveness of BNT126b2 in response to SARS-CoV-2 variants, focusing upon B1.1.7(N501Y.v1); B1.1.28(E484K)(P1) and B1.351(N501Y.v2). Validation that the S protein is not an effective target for viral countermeasures.
Validation of our work that persistent antigen exposure to other common cold-causing viruses increases immunity to SARS-CoV-2.
April
Calculation of the reduction in effectiveness of mRNA-1273 in response to SARS-CoV-2 variants, focusing upon B1.1.7(N501Y.v1); B1.1.28(E484K)(P1) and B1.351(N501Y.v2). Further validation that the S protein is not an effective target for viral countermeasures.
Initial assessment of adverse side effects caused by BNT126b2; Janssen; mRNA-1273 and Vaxzeria treatments. Identification of thrombosis and anaphylaxis as serious adverse side effects.
Identification of the risk arising from the use of polyethylene glycol (PEG) in lipid nanoparticle coatings of antiivral treatments. Identification of the related increased risk of antiphospholipid syndrome through use of phospholipids in antiviral treatments.
Evaluation of ivermectin as a potential antiviral treatment.
