by Dr. Lynn Fynn
Vaccines serve a purpose. The first vaccine was created in 1796 for the eradication of smallpox. Since then, the purpose has remained the same; vaccines mitigate death and stop the spread of a virulent infectious disease among the populous. This goal is achieved by introducing a non-infectious, antigenic portion of said infectious disease agent to the subject’s immune system to aid in the body’s recognition of the agent. This means that the body is primed to respond differently to the disease in the future. The body can signal its defenses and neutralize the agent before it can replicate and cause disease. Those people who have previously recovered from such an infection (convalescence) have thereby acquired the ability to recognize that disease and can effectively neutralize the infection before it takes hold. This is basic immunology.
There are many concerns with immunizing the immune. Besides it being unduly taxing on the body, the chief concern is the potential to induce Antibody Dependent Enhancement. (ADE). This mechanism occurs as antibodies to a specific portion of a pathogenic complex can be enhanced and activated when exposed in high concentration in the future. This phenomenon is common with such infections as Dengue, HIV, SARS, and Ebola.
In the case of human Coronaviruses, can there be too much of a good thing? Yes, there can be. The worst-case scenario, immunologically, would be when cross-reactive memory antibodies to related coronaviruses can not only become non-protective but can actually enhance infection in the clinical course. Such a phenomenon of antibody dependent enhancement (ADE) has already been described in several viral infections.
The development of IgG against SARS-CoV-2 in the course of COVID-19 might not be a simple sign of viral clearance and augmentation of protection against the virus. On the contrary, due to cross-reaction to related coronavirus strains from earlier infections, a patient’s viral history of coronavirus infection might be crucial to the severity of the course of the current infection with SARS-CoV-2. This is a phenomenon that has been called in the context of influence infections “original antigenic sin.” This is particularly concerning when injecting mRNA because it signals the patient’s cells to produce trillions of pathogenic spike proteins to elicit another immune response which could potentially enhance disease in the subject.
The current mRNA vaccines in mass distribution contain concerning epitopes that could facilitate ADE. Peptide S597-603 induced antibodies have enhanced infection both in vitro and in non-human primates by using an epitope sequence-dependent (ESD) mechanism. This peptide exhibited a high level of serological reactivity (64%), which resulted from the additive responses of two tandem epitopes (S597-603 and S604-625) combined with a long-term human B-cell memory response with antisera from convalescent SARS patients.
Do convalescents fail to exhibit long-term immunity? That seems to be the excuse for why vaccinating the recovered is necessary but, there is NO evidence to support this argument. In fact there is more evidence that shows long-term immunity in many forms, protects the convalescent patient in the long term. Historical science, and numerous studies, like the well-powered SIREN study support lifetime immunity.
So why diminish immunity in the convalescent? Why would you enforce an experimental immune-modulation injection in someone that exhibits prior immunity? Fully screening a patient for prior immunity is of utmost importance before determining whether to vaccinate. With many adverse events reported daily to VAERS, the vaccine adverse event reporting system, why add unnecessary risk? Such jeopardy has markedly increased this year in persons who basically have mitigated risk through immunity?
Determining immunity to SARS CoV2 in the population involves much more than a typical nucleocapsid IgM and IgG assay. The immune system is complex and effective. Though that is a great place to start, there are so many other forms of defense against this virus. One that was initially overlooked was T-cell activity and their contribution to protective immunity. Measuring SARS2-specific CD-4 and CD-8 T-cells is just as important in determining immunity as B cells. This is because there is clear cross-reactivity against this pathogen and it is prevalent in much of the population previously exposed to a Coronavirus from the common cold. CD-4 T-cell responses were detected in 40%–60% of unexposed individuals. This may be reflective of some degree of cross-reactive, pre-existing immunity to SARS-CoV-2.
In addition to T-cells, another relevant form of measurement of prior exposure is that of Immunoglobulins. IgG titers specifically indicate “the big guns” for lasting immunity. IgG titers to the nucleocapsid proteins of SARS2 show immunity gained from prior infection, and those that are spike-specific show there was either exposure to the virus, or the subject was vaccinated. Both are necessary to discern which exposure elicited which Ig population.
This is the most common assay ordered for Serology; however, as you can see, it is not the only way to measure one’s immunity to SARS CoV-2.
Prior to COVID-19, the CDC contra-indicated vaccines in the previously exposed/recovered. Historically, we would run titers for previous infection, and if convalescent antibodies were present, we would refrain from additional immunization. We see no reason to revise the definition of immune or change what has clearly worked.