Prof. Dolores Cahill of Ireland (Immunologist) believes that in a

Comment on Are mRNA Vaccines for COVID-19 helpful or harmful? by Sean Pitman.

Prof. Dolores Cahill of Ireland (Immunologist) believes that in a few months people will start dying of cytokine storms from the mRNA vaccines. This video is just over 10 minutes long–please debunk this info…if you can. Following also is a paper abstract from PubMed–you’re also welcome to try and debunk this one too. I may be a retired carpenter, but I do know when I’m being lied to.

First of, you’re mixing apples and oranges here. Aside from being a well-known anti-vaxx conspiracy theorist (with a retracted anti-vaxx paper), Dr. Cahill is talking about the SARS vaccine against the SARS virus that emerged in China in 2002. This is different from the mRNA vaccines against the COVID-19 virus that hit the world in 2020. Now, it is true that some of the earlier attempts at a SARS vaccine showed ADE (Antibody-dependent enhancement) effects in mouse models. Further work showed that this seemed to be linked, not so much to the antibody response, as to the T-cell response. Specifically, a “Th2” heavy response (as opposed to more Th1 or a balance between the two), was linked to lung pathology. Those are subdivisions of the CD4+ T cells, based on which cytokines they produce, and these results alerted everyone to keep an eye out for that. Mouse immunogenicity studies with the current mRNA vaccine candidates against COVID-19, in particular, did not show these effects… This has been why we’ve seen that the makers of the mRNA vaccines against COVID-19 take so much care to put the Spike protein into its “perfusion” conformation (so that it doesn’t attach itself to human cell membranes). The worry has been that if antibodies are generated to it after it’s had a chance to bind to human cells, that gives you a better chance for non-neutralizing antibodies (and thus a higher risk for ADE). A high proportion of outright neutralizing antibodies is a safeguard against antibody-driven enhancement of ADE disease – which is what the mRNA vaccines against COVID-19 have shown. (Dr. Derek Lowe, December 18, 2020)

As far as the paper you cite published by Timothy Cardozo and Ronald Veazey (October, 2020) cited concerns over what is known as “antibody-dependent enhancement” of vaccines – with the potential to increase a negative response to the actual viral infection as compared to those who never had the vaccine. This concern is based on the very real observation of more severe diseases occurring in individuals who received vaccines to other viruses in the past – such as the one for dengue fever. In a 2018 study, scientists at La Jolla Institute for Immunology showed that newborn mouse pups harboring anti-Zika antibodies were more vulnerable to death from dengue exposure than mice that lacked anti-Zika antibodies. Certainly, this is an example of antibody-dependent enhancement (ADE). However, ADE has not been shown to occur in individuals that received COVID-19 vaccines during the double-blinded trials over many months or since the mRNA vaccines have started to be given to medical providers (like me).

Now, the reasons why ADE isn’t a significant concern for the mRNA vaccines against the COVID-19 virus is partly due to the fact that the COVID-19 virus does not infect macrophages in a way that is pro-inflammatory:

SARS-CoV infection of macrophages is abortive and does not alter the pro-inflammatory cytokine gene expression profile after antibody-dependent uptake4. Findings to date argue against macrophages as productive hosts of SARS-CoV-2 infection (Link).

For more specific details regarding the underlying science of immunology, see:

Vaccines that elicit neutralizing antibodies against the S protein reliably protect animals from SARS-CoV challenge without evidence of enhancement of infection or disease. These data suggest that human immunization strategies for SARS-CoV-2 that elicit high neutralizing antibody titres have a high chance of success with minimal risk of ADE. For example, subunit vaccines that can elicit S-specific neutralizing antibodies should present lower ADE risks (especially against S stabilized in the prefusion conformation, to reduce the presentation of non-neutralizing epitopes8). These modern immunogen design approaches should reduce potential immunopathology associated with non-neutralizing antibodies… It is encouraging that a recent assessment of an inactivated SARS-CoV-2 vaccine elicited strong neutralizing antibodies in mice, rats and rhesus macaques, and provided dose-dependent protection without evidence of enhanced pathology in rhesus macaques (Lee, et. al., 2020).

There are concerns about the potential for more serious adverse events—enhanced respiratory disease (ERD) following infection and a subtype of ERD, antibody-dependent enhancement (ADE) following infection after vaccine administration. There are two mechanisms of ADE, both of which “occur when non-neutralizing antibodies or antibodies at sub-neutralizing levels bind to viral antigens without blocking or clearing infection.” In ADE via enhanced infection, non-neutralizing antibodies bound to the virus enhance infection rates in target cells, such as macrophages, leading to more severe disease. In the second type described by Lee et al., ADE via enhanced immune activation, binding of non-neutralizing antibody to the virus leads to the formation of immune complexes in lung tissues, which, in turn, lead to “secretion of pro-inflammatory cytokines” and “activation of the complement cascade”. “The ensuing inflammation can lead to airway obstruction and can cause acute respiratory distress syndrome in severe cases.” A recognized example of this type of enhanced respiratory disease results from some infections with measles after measles vaccination and has been seen with vaccines for RSV, dengue, and SARS. “Existing evidence suggests that immune complex formation, complement deposition and local immune activation present the most likely ADE mechanisms in COVID-19 immunopathology.” (Lee, et. al., 2020)

Vaccine developers are well aware of ADE and have pursued approaches that make ADE less likely. This includes selecting specific epitopes within the receptor binding domain of the spike protein as targets for a neutralizing antibody response. It is encouraging that some early clinical trials reports have indicated both a strong neutralizing antibody response and and a strong type 1 helper T cell (TH1) response, rather than the TH2 response associated with immunopathology. (Anderson, et. al., 2020)

Table of Contents

1 Sean Pitman Also Commented
- 1.1 Recent Comments by Sean Pitman
2 Related

Sean Pitman Also Commented

Are mRNA Vaccines for COVID-19 helpful or harmful?
I don’t know about Dr. Botha, in particular, but others have made similar claims. Of course, I see no credible evidence to support such sensational claims…

Are mRNA Vaccines for COVID-19 helpful or harmful?
Just because the effectiveness of vaccines may wane over time doesn’t mean that they aren’t working. They are working, very well. The vast majority of those who are being hospitalized right now with severe COVID-19 infections are the unvaccinated – by a ratio of more than 10:1 over the vaccinated.

Here’s an explanation from Shane Crotty, Ph.D. (Immune system and vaccine scientist. Professor, La Jolla Institute for Immunology (LJI), a non-profit research institute): Link

Are mRNA Vaccines for COVID-19 helpful or harmful?

As of June 11, 2021, approximately 296 million doses of mRNA COVID-19 vaccines had been administered in the United States, with 52 million administered to persons aged 12–29 years; of these, 30 million were first and 22 million were second doses. Within the Vaccine Adverse Event Reporting System (VAERS) (4), the national vaccine safety passive monitoring system, 1,226 reports of myocarditis after mRNA vaccination were received during December 29, 2020–June 11, 2021. Among persons with reported myocarditis after mRNA vaccination, the median age was 26 years (range = 12–94 years), with median symptom onset interval of 3 days after vaccination (range = 0–179). Among 1,194 reports for which patient age was known, 687 were among persons aged <30 years and 507 were among persons aged ≥30 years; of 1,212 with sex reported, 923 were male, and 289 were female.§§ Among 1,094 patients with number of vaccine doses received reported, 76% occurred after receipt of dose 2 of mRNA vaccine; cases were reported after both Pfizer-BioNTech and Moderna vaccines. Informed by early reports, CDC prioritized rapid review of myocarditis in persons aged <30 years reported during May 1–June 11, 2021; the 484 patient records in this subset were evaluated by physicians at CDC, and several reports were also reviewed with Clinical Immunization Safety Assessment Project investigators,¶¶ including cardiologists. At the time of this report, 323 of these 484 cases were determined to meet criteria in CDC’s case definitions for myocarditis, pericarditis, or myopericarditis by provider interview or medical record review (Table 1). The median age of the 323 patients meeting CDC’s case definitions was 19 years (range = 12−29 years); 291 were male, and 32 were female. The median interval from vaccination to symptom onset was 2 days (range = 0−40 days); 92% of patients experienced onset of symptoms within 7 days of vaccination. Of the 323 persons meeting CDC’s case definitions, 309 (96%) were hospitalized. Acute clinical courses were generally mild; among 304 hospitalized patients with known clinical outcomes, 95% had been discharged at time of review, and none had died. Treatment data in VAERS are preliminary and incomplete; however, many patients have experienced resolution of symptoms with conservative treatment, such as receipt of nonsteroidal antiinflammatory drugs. Follow-up is ongoing to identify and understand longer-term outcomes after myocarditis occurring after COVID-19 vaccination. (Link)

In comparison, those who are infected with COVID-19 have a much higher rate of myocarditis as well as a much MUCH higher rate of long-term injuries and death. Up to a third of otherwise young healthy people, including athletes and even children, end up with myocarditis following even mild infections with COVID-19.