by Patrick ➕follow (55) 💰tip ignore
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the UK’s most recent vaccine surveillance report (you can find it HERE) had a funny little tidbit in the notes to the week 42 update. it goes like this:
the reason to track it is simple: if you get vaccinated with any of the currently existing covid-19 vaccines, they teach you to respond to and attack S-1 proteins. this is what you learn, express, and carry antibodies for. so, if you test a vaccinated person for S antibodies, you’ll find them.
but you will NOT find antibodies to N proteins. those will ONLY be found in those who got covid, recovered, and acquired resistance. ...
but if having been vaccinated later prevents you from mounting as strong an N antibody response, then it may actually be significantly reducing the effectiveness of the immunity acquired from exposure to covid, which is, BY FAR the strongest immunity currently known.
this would imply that the vaccines:
not only do not stop you from getting covid and may well make it more likely,
but also that they prevent you from getting the full benefit of the immunity you require when you GET covid.
if this suppression is substantial enough, it might even render your recovery acquired immunity non-sterilizing and leave you active as a carrier and spreader by preventing the immune response that seems to be generating effective sterilization and replacing it with one known not to.
this might make the vaccinated into durable or even perpetual carriers even if they have had disease and recovered.
obviously, that would be BAD.
this is not an unheard of idea. there is, in fact, a name for it: original antigenic sin (OAS). this sounds biblical, but it’s not. it’s a well studied immune phenomenon.
it works like this: (read through this carefully)
Original antigenic sin, also known as antigenic imprinting or the Hoskins effect,[1] refers to the propensity of the body's immune system to preferentially utilize immunological memory based on a previous infection when a second slightly different version of that foreign pathogen (e.g. a virus or bacterium) is encountered. This leaves the immune system "trapped" by the first response it has made to each antigen, and unable to mount potentially more effective responses during subsequent infections. Antibodies or T-cells induced during infections with the first variant of the pathogen are subject to a form of original antigenic sin, termed repertoire freeze.
The phenomenon of original antigenic sin has been described in relation to influenza virus, dengue fever, human immunodeficiency virus (HIV) [2] and to several other viruses.[3]
This phenomenon was first described in 1960 by Thomas Francis Jr. in the article "On the Doctrine of Original Antigenic Sin".[4][5] It is named by analogy to the theological concept of original sin. According to Francis as cited by Richard Krause:[5]
The original antigenic sin: When the body first encounters an infection it produces effective antibodies against its dominant antigens and thus eliminates the infection. But when it encounters the same infection, at a later evolved stage, with a new dominant antigen, with the original antigen now being recessive, the immune system will still produce the former antibodies against this old "now recessive antigen" and not develop new antibodies against the new dominant one, this results in the production of ineffective antibodies and thus a weak immunity
the bottom line is this:
the UKHSA is in possession of what looks like it might be some very interesting information. it seems to have been referenced in passing, but getting the rest of that story seems like a useful and important undertaking.
What's so unbelievable is that anyone with even a single year of undergrad biology, could figure this out.
I don’t think journalists take any of that. Undergrad biology can be tough, after all!
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