MEDICAL TERMINOLOGY 6) Original Antigenic Sin
MEDICAL TERMINOLOGY 6) Original Antigenic Sin
If you read and understood yesterday's post, then you already understand Original Antigenic Sin
EXECUTIVE SUMMARY: These articles provide proof that vaccine-induced “protective antibodies” might not be protective at all and might actually indicate 1) a weakened immune response, and/or 2) antibody-mediated enhancement of viral infection, resulting in a more prolonged and severe course of the illness.
Good News & Bad News
Bad news: Few medical phrases are as retarded and meaningless as “Original Antigenic Sin”, but regardless of its awkwardness and ambivalence, it is a specific and recognized term, so we have to work with it, even if we don’t like it.
Good news: The good new is that if you read yesterday’s post on “MEDICAL TERMINOLOGY 5) linked epitope suppression” then you already understand “Original Antigenic Sin” because they are one and the same. If any distinction exists, it is that “Original Antigenic Sin” is a weak immune response following a natural infection while “linked epitope suppression” is a weak immune response following artificial vaccination.
These concepts should seem at least a little confusing because they are the exact opposite to the central conventional dogma of Immunology and Vaccine Sales.
Transition from yesterday’s article
Segue/transition: Let’s start today’s essay by using yesterday’s article to help us transition to a deeper understanding of this topic. On page 5 of yesterday’s article, the author wrote,
“The concept of original antigenic sin in influenza was suggested more than 60 years ago. The immunologic memory of children is such that with a second influenza A infection, the major antibody response is directed at the strain with which they were infected originally and not to the new infecting strain.”
Yesterday’s article focused on how a relatively poorly designed vaccine could cause LINKED EPITOPE SUPPRESSION which is the same as ORIGINAL ANTIGENIC SIN, as both of these cumbersome phrases indicate a defective or less robust second immune response following a first immune response that was either directed toward 1) a poorly designed vaccine—see yesterday’s example of the acellular pertussis vaccine, or 2) a sequence of two natural infections wherein the second immune response is misdirected toward the immunologic memory that was directed toward the first infection.
These concepts should seem at least somewhat confusing because they are the exact opposite to the central conventional dogma of Immunology and Vaccine Sales:
The central dogma of IMMUNOLOGY states that the first exposure to a microbe or vaccine prepares the immune system for a more rapid/robust/effective immune response on second/subsequent exposures. This is the underlying dogma of “protective immunity” and the absolute underpinning/foundation for the entirety of the vaccine paradigm.
The central dogma of VACCINE PARADIGM AND SALES states that the first exposure to a vaccine prepares the immune system for a more rapid/robust/effective immune response on second/subsequent exposures. This is the sales pitch of the vaccine industry.
LINKED EPITOPE SUPPRESSION and ORIGINAL ANTIGENIC SIN show us that the second exposure following either vaccination or natural infection can actually be **weaker** than the first response, because the immune system activates the original response program that was directed toward antigens of a different infection or an incompetent vaccine.
LINKED EPITOPE SUPPRESSION and ORIGINAL ANTIGENIC SIN show us that the second exposure following either vaccination or natural infection can actually be **weaker** than the first response, because the immune system activates the original response program that was directed toward antigens of a different infection or an incompetent vaccine.
Antibody Dependent Enhancement Due to Original Antigenic Sin and the Development of SARS
Now, let’s focus on a different article this time “Antibody Dependent Enhancement Due to Original Antigenic Sin and the Development of SARS” published in Frontiers in Immunology 2020Jun; you can open my annotated PDF below or see the open-access version at the publisher’s site: doi.org/10.3389/fimmu.2020.01120. This is an excellent article to use as a discussion piece because it segues from linked epitope suppression (LES) to original antigenic sin (OAS) and then to antibody-dependent enhancement (ADE).
Combining the information from both of these (and a few other) articles allows us to understand the following:
SECOND IMMUNE RESPONSE MIGHT BE WEAKER THAN THE FIRST via “Original Antigenic Sin” = “linked epitope suppression”
SECOND IMMUNE RESPONSE MIGHT BE WEAKER THAN THE FIRST: Instead of being stronger, the second immune response following either a natural infection or a vaccination can actually be weaker if the original exposure to similar antigens (in the infection or the vaccination) was “close but not close enough”, thereby essentially leaving the immune system misdirected and a bit confused, as it tries to use the original response against the subsequent exposure, but because of important differences between the original exposure and the second exposure the second response fails to provide protection.
Key quote: “The phenomenon of “original antigenic sin” was initially described for influenza. It particularly plays a role in vaccination. Depending on the antigen against which antibodies are made in a first infection or immunization, in a second immunization with a different antigen of influenza, the immune system is only boosting the antibodies against the old antigen and does not recognize the new antigen. Therefore, a new specific protection is not built up and, consequently, the patient is not protected against the new virus.”
SECOND IMMUNE RESPONSE MIGHT MAKE THE INFECTION WORSE via Antibody-dependent enhancement (ADE)
SECOND IMMUNE RESPONSE MIGHT MAKE THE INFECTION WORSE: The authors repeatedly note that an early IgG response might signal that LES-OAS is occurring to result in a relatively weak immune response to infection and that this same LES-OAS could actually make the infection worse because of ADE. Note again that this is contrary to the advertising hype from vaccine salesmen who repeatedly say that a rise in IgG indicates the production of “protective antibodies” and that this alone indicates that “the vaccine is working”; these are absurd assumptions that are not supported by anything but the most superficial and optimistic interpretations of basic Immunology. Note again that injected vaccine-induced IgG antibodies do not protect the mucosa (because they do not result in sIgA production) and thus do not defend against infection acquisition nor infection transmission.
ANTIBODY-DEPENDENT ENHANCEMENT (ADE): Antibodies can make viral infections worse by 1) binding to the virus, and then 2) serving to transport the virus into the cell where it is replicated to then continue/exacerbate the infection. Viruses usually enter a cell by use of a receptor on the cell surface; in the case of ADE, the antibody which is commonly assumed to be protective actually binds to and transports the virus into the cell, thus acting as a specific receptor for the virus.
Key quote: “The worst scenario would be when such cross-reactive memory antibodies to related coronaviruses would not only be non-protective but even enhance infection and the clinical course. Such a phenomenon of antibody dependent enhancement (ADE) has already been described in several viral infections. Thus, the development of IgG against SARS-CoV-2 in the course of COVID-19 might not be a simple sign of viral clearance and developing protection against the virus. On the contrary, due to cross-reaction to related coronavirus strains from earlier infections, in certain patients IgG might enhance clinical progression due to ADE.”
VACCINE-INDUCED ANTIBODY-DEPENDENT ENHANCEMENT (viADE): Vaccines can induce production of IgG antibodies which provide little or no protection from most viral infections but which can serve to facilitate virus infection of cells by aiding the transport of viruses into cells for replication.
“Such a phenomenon of antibody dependent enhancement (ADE) has already been described in several viral infections. In the course of development of a vaccine against Respiratory Syncytial Virus (RSV) it was shown that 80% of the vaccinated children required hospitalization during a subsequent infection with RSV, where two children died, whereas only 5% of the [nonvaccinated] controls had a severe course.”
MORE IgG ANTIBODIES = MORE DISEASE: The authors of this pre-Cv19-vaccination era article (2020 June) were already very clear that higher and earlier IgG response correlated with more severe and prolonged infection. These early findings directly refute the sales pitch that people need Cv19 vaccines with repeated “boosters” to keep antibody levels high. The idea that IgG antibodies need to be kept “high” is absurd and is inconsistent with the majority of what is known in Immunology; it is a simplistic notion that appears medically reckless and commercially motivated. The idea that humans need to have consistently high antibody levels to any or all infectious agents is not supported by any idea in Immunology or Pathology or Microbiology; consistently high antibody levels lead to diseases such as vasculitis and kidney damage.
[in patients with COVID-19] “stronger [IgG] antibody response was associated with delayed viral clearance and increased disease severity.
[Earlier/stronger IgG response = delayed virus clearance] Patients with a strong IgG response (> 2-fold of cutoff value) showed only in 9% a virus clearance at day 7 after IgG developed, whereas weak IgG responders cleared the virus in 57%.
[Earlier/stronger IgG response = increased severity of Cv19] Further, it was found that earlier IgG response, concurrently with IgM, and higher IgG antibody titers were associated with enhanced disease severity.”
There you have it: Proof that vaccine-induced “protective antibodies” might not be protective at all and might actually indicate 1) a weakened immune response, and/or 2) antibody-mediated enhancement of viral infection, resulting in a more prolonged and severe course of the illness.
This might (partly) explain why the FDA uses antibodies to sell vaccine uptake but then paradoxically states that antibodies have no value in determining immunity.
