Scientific Research Relating To What’s Wrong With A Covid-19 Vaccine

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When we are FIRST exposed to a virus, we respond the most to it. Subsequent exposures can actually slow or stop an immune response against that virus. This is called Original Antigenic Sin, after a researcher who first observed it in 1960.

The problem is, if a vaccine “exposure” is all we have, we ruin our first chance of exposure to that virus or whatever it is, and often we don’t mount much of a defense afterwards when we should.

This is one of the critical things wrong with vaccine strategy in general.

Original Antigenic Sin is designed to prevent the immune system in overdrive.

But, without constant exposure, vaccines stop working. We need to swim in a sea of viruses for the immunity to last, unless the immunity is at a cellular level, which doesn’t happen with vaccines. At a cellular level vaccines can confer true lifetime immunity but especially when we are exposed from time to time to that virus.

Without the recurrent exposure, we lose immunity.

Immune history and influenza virus susceptibility

Antibody responses to influenza viruses are critical for protection, but the ways in which repeated viral exposures shape antibody evolution and effectiveness over time remain controversial. Early observations demonstrated that the history of viral exposures has a profound effect on the specificity and magnitude of antibody responses to a new viral strain, a phenomenon called “original antigenic sin.” Although “sin” might suppress some aspects of the immune response, so far there is little indication that hosts with pre-existing immunity are more susceptible to viral infections compared to naïve hosts. However, the tendency of the immune response to focus on previously recognized conserved epitopes when encountering new viral strains can create an opportunity cost when mutations arise in these conserved epitopes. Hosts with different exposure histories may continue to experience distinct patterns of infection over time, which may influence influenza viruses’ continued antigenic evolution. Understanding the dynamics of B cell competition that underlie the development of antibody responses might help explain the low effectiveness of current influenza vaccines and lead to better vaccination strategies.

 

[ecstatichamster]

While it is clear that antibody responses against childhood viral strains are efficiently boosted by antigenically novel strains, early reports conflicted about whether boosting comes at the expense of generating strong antibody responses against the new strain. The original study by Francis in 1947 found no difference in post-infection antibody titers to the new viral strain between recent recipients of the mismatched vaccine strain, whose titers were boosted, and non-recipients [3]. Similar results were found in animals sequentially infected with different influenza viruses [11]. The magnitude of the responses elicited by an antigenically distinct influenza virus in these studies was the same in animals with and without prior influenza exposure.

Other studies have suggested that prior exposures actively suppress the magnitude or quality of antibody responses to new viral strains. For example, Davenport & Hennessy [6] noted a “suppressive effect” on the antibody response to some viral strains in children, depending on the order in which they received monovalent vaccinations, and cited similar patterns of apparent suppression in other immunization studies [4,13]. Antibody responses tend to decline during repeated vaccinations [14]. de St. Groth & Webster [11] described the secondary response in immunized rabbits as “inadequate” because antibodies in the secondary response reacted better with the first antigen than the second. However, most studies that report inhibitory effects of prior exposures rely on the hemagglutination-inhibition assay, which only measures antibodies that block viral attachment to sialic acid. It is possible that sequential vaccinations in these studies elicit cross-reactive antibodies against other epitopes (such as the HA stalk) that are not detected in classical hemagglutination-inhibition assays. Thus, these studies might indicate that prior exposures affect the specificity of antibody responses, but this change in specificity might not affect overall protection.