Yesterday, I posted the article, Is Luc Montagnier Correct About the Variants Showing Up After Mass Vaccination?
This article is about a study that shows the mechanism of why resistant variants develop.
The SARS-CoV-2 constantly mutates.
RNA viruses like the SARS-CoV-2 continuously mutate. The antibody may neutralize some if they encounter an antibody, but some variants that arose from mutations can escape. Those escaped mutations will continue to survive and replicate and then transmit to another host.
Nature.com recently released a study about the A.30 variant of the SARS-CoV-2. The spike protein of SARS-CoV-2 variant A.30 is heavily mutated and evades vaccine-induced antibodies with high efficiency will be published on print at Cellular and Molecular Immunology.
The study showed that A3.0 or A.VOI.V2 could resist antibodies induced by the Pfizer BNT162b2 and the ChA-dOx1 nCoV AstraZeneca vaccines. The level of resistance is almost higher than the Beta variant. Among the early variants, the Beta variant has the highest level of resistance.
What makes the A.30 antibody resistant to the vaccines?
The spike protein of the A.30 has ten amino acid substitutions and five deletions. All deletions and four substitutions are in the N-terminal domain targeted by some neutralizing antibodies.
Three other mutations are in the receptor-binding domain (RBD). Those mutations make the RBD of the virus unrecognizable to the existing anti-RBD antibodies.
Plus, two other mutations in the spike protein make it easier for the virus to fuse and enter human cells. Not only that, additional testing with cell line series showed that it could spread faster from the lungs.
The image below compares the A.30, Eta (B.1.525), and the Beta (B1.351.1) variants. The amino acid mutations are in red. The horizontal bars are the domains or parts of the SARS-CoV-2. RBD means receptor-binding domain. RBDs attach to human cells. S1 and S2 subunits are parts of the spike proteins.
Notice that the A.30 has more mutations in the N-terminal and RBD that make it antibody resistant.
A.30 is resistant to vaccine-induced antibodies from Pfizer and AstraZeneca
This research showed that A.30 is resistant to the antibodies induced by the Pfizer BNT2162b2 and AstraZeneca ChAdOx1 vaccines. More than the Beta and Alpha variants.
In summary, the A.30 variant can quickly enter the cells and spread throughout the body and are resistant to the antibodies produced from the Pfizer and AstraZeneca vaccines.
Where is the A.30 now?
The A.30 was detected in several patients in Angola and Sweden in spring 2021 and likely originated in Tanzania.
The image below is from https://www.gisaid.org/hcov19-variants/. It shows all the variants as they branch and spread. The variant names and color codes are on the left. The right side represents the number of variants detected based on protein sequencing. If you go to the site, you can get more details about each colored dot.
I drew a turquoise line around the A.30 variants. The A.30 are in orange.
The A3.0 was detected in the following states: Maryland, Virginia, Mexico, Iowa, Arizona, Utah, Kansas, North Carolina, Georgia, Connecticut, Arkansas, Maine, Oregon, and Missouri.
The A.30 may be in other countries now since travel is easy, but if there is no sequencing done, it may not be detected.
The A.30 is resistant to antibodies produced by the Pfizer and AstraZeneca vaccines and spreads fast within the human body. It may become the dominant variant in the future.
What is the solution?
Early treatment is essential for COVID-19. Ivermectin works using the host cells and does not depend on viral mechanisms. That makes Ivermectin suitable for any variants.
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Reference:
Arora, P., Rocha, C., Kempf, A. et al. The spike protein of SARS-CoV-2 variant A.30 is heavily mutated and evades vaccine-induced antibodies with high efficiency. Cell Mol Immunol (2021). https://doi.org/10.1038/s41423-021-00779-5
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