Herd immunity with new COVID variants?

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SUMMARY

The discussion centers on the immunity provided by natural COVID-19 infection versus vaccination against new variants. Antibodies from natural infection generate a diverse response, while vaccines like Pfizer produce a targeted subset of antibodies that effectively block viral entry. Despite reduced effectiveness against new variants, T cell responses from both natural infection and vaccination remain robust, ensuring continued protection against severe disease. Key studies referenced include findings on SARS-CoV-2 RBD antibodies and their implications for therapeutic development.

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  • Understanding of SARS-CoV-2 and its variants
  • Knowledge of antibody responses from natural infection versus vaccination
  • Familiarity with T cell immunity and its role in viral protection
  • Awareness of receptor-binding domain (RBD) antibodies and their significance
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  • Research the role of T cells in COVID-19 immunity
  • Explore the differences between natural infection and vaccine-induced immunity
  • Investigate the implications of SARS-CoV-2 RBD antibodies for future vaccine development
  • Learn about the latest studies on COVID-19 variants and their impact on public health
USEFUL FOR

This discussion is beneficial for immunologists, healthcare professionals, vaccine developers, and anyone interested in understanding COVID-19 immunity and the effectiveness of current vaccines against emerging variants.

ElliotSmith
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TL;DR
Do natural COVID antibodies protect against the new variants?
If someone has had the original COVID-19 strain and survived, does this mean that they have any immunity to the new variants? Or do the new variants completely ignore any antibodies that someone who survived the original virus has?
 
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The difference between the antibodies you get from an invection vs. antibodies you might get from the new immunizations they are now producing, is that the immunizations produce antibodies to only a single part of the virus, a part deeply involed involved in infecting cells. If the antibody binding this site (epitope) doesn't directly lead to the virus's destruction, it will physically block the virus's ability to a gain entry to a cells to infect.
Antibodies acquired by being infected can be from any exposed molecular surface of the viruses (several proteins, with many different places an antibody could bind).
Antibodies, to parts of the virus's surface not targeted in the immunizations, can act as signals to immune cells to remove the virus, but until that happens, the virus is still infective.

Summary:
The antibodies from a natural infection, will raise a lot of different antibodies.
The antibodies raised by the immunization will be a sub-set of those raised by an infection, but they will be very effective.
Not all of the antibodies from a natural infection will be equally effective in fighting new challenges.
 
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An important thing to keep in mind is that even if antibodies protect less against new variants, the T cells protection developed by natural infection or by Pfizer vaccines has been negligibly affected by variants. The T cell responses may help explain why the vaccines continue to provide good protection against severe disease, even though their ability to protect from infection has decreased.
https://doi.org/10.1016/j.xcrm.2021.100355
https://immunology.sciencemag.org/content/6/59/eabj1750
https://www.nature.com/articles/s41586-021-03681-2
 
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SARS-CoV-2 RBD antibodies that maximize breadth and resistance to escape​

Here we comprehensively characterize escape, breadth and potency across a panel of SARS-CoV-2 antibodies targeting the receptor-binding domain (RBD). Despite a trade-off between in vitro neutralization potency and breadth of sarbecovirus binding, we identify neutralizing antibodies with exceptional sarbecovirus breadth and a corresponding resistance to SARS-CoV-2 escape. One of these antibodies, S2H97, binds with high affinity across all sarbecovirus clades to a cryptic epitope and prophylactically protects hamsters from viral challenge. Antibodies that target the angiotensin-converting enzyme 2 (ACE2) receptor-binding motif (RBM) typically have poor breadth and are readily escaped by mutations despite high neutralization potency. Nevertheless, we also characterize a potent RBM antibody (S2E128) with breadth across sarbecoviruses related to SARS-CoV-2 and a high barrier to viral escape. These data highlight principles underlying variation in escape, breadth and potency among antibodies that target the RBD, and identify epitopes and features to prioritize for therapeutic development against the current and potential future pandemics.
https://www.nature.com/articles/s41586-021-03807-6
 

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