Share this with your doctor…
Doctors For Covid Ethics has sent the following letter to tens of thousands of doctors in Europe, summarising four scientific findings critical to the covid-19 vaccination programme.
Four recent scientific discoveries alter the entire landscape of the covid-19 pandemic, and they force us to reassess the merits of vaccination against SARS-CoV-2.
Rapid and efficient memory-type immune responses occur reliably in virtually all unvaccinated individuals who are exposed to SARS-CoV-2. The effectiveness of further boosting the immune response through vaccination is therefore highly doubtful. Vaccination may instead aggravate disease through antibody- dependent enhancement (ADE).
SARS-CoV-2 spike protein circulates shortly after vaccination
SARS-CoV-2 proteins were measured in longitudinal plasma samples collected from 13 participants who received two doses of Moderna mRNA-1273 vaccine . With 11 of the 13, the SARS-CoV-2 spike protein was detected in the blood within only one day after the first vaccine injection.
Spike protein molecules were produced within cells that are in contact with the bloodstream — mostly endothelial cells — and released into the circulation.
This means that:
a) the immune system will attack those endothelial cells, and
b) the circulating spike protein molecules will activate thrombocytes
Both effects will promote blood clotting. This explains the many clotting-related adverse events — stroke, heart attack, venous thrombosis — that are being reported after vaccination.
Rapid, memory-type antibody response after vaccination
Several studies have demonstrated that circulating SARS-CoV-2-specific IgG and IgA antibodies became detectable within 1-2 weeks after application of mRNA vaccines [1–3].
Attempts to develop vaccines to the original SARS virus, which is closely related to SARS-CoV-2, repeatedly failed…
Rapid production of IgG and IgA always indicates a secondary, memory-type response that is elicited through re-stimulation of pre-existing immune cells. Primary immune responses to novel antigens take longer to evolve and initially produce IgM antibodies, which is then followed by the isotype switch to IgG and IgA.
A certain amount of IgM was indeed detected alongside IgG and IgA in some studies [1,4]. Importantly, however, IgG rose faster than IgM , which confirms that the early IgG response was indeed of the memory type.
This memory response indicates pre-existing, cross-reactive immunity due to previous infection with ordinary respiratory human coronavirus strains. The delayed IgM response most likely represents a primary response to novel epitopes which are specific to SARS-CoV-2.
Memory-type responses have also been documented with respect to T-cell-mediated immunity [5–7].
…our immune system efficiently recognizes SARS-CoV-2 as “known” even on first contact.
Overall, these findings indicate that our immune system efficiently recognizes SARS-CoV-2 as “known” even on first contact. Severe cases of the disease thus cannot be ascribed to lacking immunity.
Instead, severe cases might very well be caused or aggravated by pre-existing immunity through antibody-dependent enhancement (ADE, see below).
SARS-CoV-2 elicits robust adaptive immune responses regardless of disease severity
Serum antibody profiles were reported for 203 individuals following SARS-CoV-2 infection . 202 (>99%) of the participants exhibited SARS-CoV-2 specific antibodies.
With 193 individuals (95%), these antibodies prevented SARS-CoV-2 infection in cell culture and also inhibited binding of the spike protein to the ACE2 receptor. Furthermore, CD8+ T-cell responses specific for SARS-CoV-2 were clear and quantifiable in 95 of 106 (90%) HLA-A2-positive individuals.
This study confirms the above assertion that the immune response to initial contact with SARS-CoV-2
is of the memory type. In addition, it shows that this reaction occurs with almost all individuals, and particularly also with those who experience no manifest clinical symptoms.
The goal of the vaccination is to stimulate production of antibodies to SARS-CoV-2, but we now know that such antibodies can and will be rapidly generated by everyone upon the slightest viral challenge, even without vaccination.
Even though the antibody response to the first injection is of the memory type, the small time lag after the injection may mitigate adverse reactions, because the abundance of spike protein on the cells in the blood vessel walls and in other tissues may have already passed its peak when the antibodies arrive.
The situation changes dramatically with the second injection. Then the spikes are produced and protrude
into the bloodstream that is already swarming with both reactive lymphocytes and antibodies.
The antibodies will cause the complement system [9,10] and also neutrophil granulocytes to attack the spike protein-bearing cells. The possible consequences of all-out self-attack by the immune system are frightening.
Antibody-dependent enhancement of disease
As described, memory-type immune responses ensure the rapid rise of antibody titres after initial exposure to SARS-CoV-2, rendering the benefit of vaccine-induced antibody response response (a “cytokine storm”) that will amplify the damage to the lungs, liver and other organs of the body.
Attempts to develop vaccines to the original SARS virus, which is closely related to SARS-CoV-2, repeatedly failed due to ADE.
The vaccines did induce antibodies, but when the vaccinated animals were subsequently infected with the virus, they became more ill than the unvaccinated controls (see e.g. ).
The possibility of ADE was not adequately addressed in the clinical trials on any of the covid-19 vaccines. It is therefore prudent to avoid the danger of inducing ADE through vaccination and instead rely on proven forms of treatment  for dealing with clinically severe covid-19 disease.
The collective findings discussed above clearly show that the benefits of vaccination are highly doubtful.
In contrast, the harm the vaccines do is very well substantiated, with more than 15,000 vaccination-associated deaths now documented in the EU drug adverse events database (EudraVigilance), and over 7,000 more deaths within the UK and the US 
Source: The Light Paper (issue 12)
- Ogata, A.F. et al. (2021) Circulating SARS-CoV-2 Vaccine Antigen Detected in the Plasma of mRNA-1273 Vaccine Recipients. Clin. Infect.
- Amanat, F. et al. (2021) SARS- CoV-2 mRNA vaccination induces functionallydiverse antibodies to NTD, RBD and S2. Cell
- Wisnewski, A.V. et al. (2021) Human IgG and IgA responses to COVID-19 mRNA vaccines. PLoS One 16:e0249499
- Qu, J. et al. (2020) Profile of Immunoglobulin G and IgM Antibodies Against Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Clin. Infect. Dis. 71:2255-2258
- Le Bert, N. et al. (2020) SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls. Nature 584:457-462
- Grifoni, A. et al. (2020) Targets of T Cell Responses to SARS- CoV-2 Coronavirus in Humans with COVID-19 Disease and Unexposed Individuals. Cell 181:1489-1501.e15
- Gallais, F. et al. (2021) Intrafamilial Exposure to SARS-CoV-2 Associated with Cellular Immune Response without Seroconversion. Emerg. Infect. Dis. 27
- Nielsen, S.S. et al. (2021) SARS-CoV-2 elicits robust adaptive immune responses regardless of disease severity. EBioMedicine 68:103410
- Magro, C.M. et al. (2020) Docked severe acute respiratory syndrome coronavirus2 proteins within thecutaneous and subcutaneous microvasculature and their role in the pathogenesis of severe coronavirus disease 2019.Hum. Pathol. 106:106-116
- Magro, C.M. et al. (2021) Severe COVID-19: A multifacetedviral vasculopathy syndrome. Annals of diagnostic pathology 50:151645
- Tseng, C. et al. (2012) Immunization with SARS coronavirus vaccines leads to pulmonary immunopathology on challenge with the SARS virus. PLoS One 7:e35421
- McCullough, P.A. et al. (2021) Pathophysiological Basis and Rationale for Early Outpatient Treatment of SARS-CoV-2 (COVID-19) Infection. Am. J. Med. 134:16-22
- Johnson, L. (2021) Official Vaccine Injury and Fatality Data: EU, UK and US.