Researchers at the Vanderbilt University Medical Center found that people recovering from COVID-19 and those vaccinated with the causative virus, SARS-CoV-2, produce the same clone or group of antibody-producing white blood cells. I found that I would do it.
Their findings were reported in the journal this week Cell reportSheds light on the selective pressure that drives the emergence of SARS-CoV-2 mutants that may escape spontaneous development antibody And those induced by vaccination.
Current vaccines, including those that use Genetic material, MRNA, Viral protein It is primarily protective against delta mutants, which currently dominate unvaccinated populations worldwide, to elicit an immune response. Still, scientists are worried that other more toxic and contagious variants of what has already been vaccinated may emerge.
Findings reported this week could help scientists design more effective vaccines, Antibody therapy Researchers have concluded for a wider range of varieties.
“I was surprised to discover that there are so many shared antibodies among individuals after SARS-CoV-2 infection, which is a good sign,” said the corresponding author of the paper, the director of the Vanderbild Vaccine Center. One James Crow Junior Doctor of Medicine said. ..
“It was encouraging to discover that the mRNA vaccine also induces these clones, which explains in part why these antibodies work so well for so many people.” Crow, who holds the Anscott Karel Chair and is a professor of pediatrics and pathology, microbiology, said. & Immunology at VUMC.
Antibodies are proteins produced by special things White blood cells They are called B lymphocytes or B cells. When the virus binds to the surface of a B cell, it stimulates the cell to divide and mature into a clone of the same cell.
Mature B cells, called plasma cells, secrete millions of antibodies into the bloodstream and lymphatic system, some of which attach to the virus and prevent it from becoming infected. Target cell..
Researchers have identified 27 public chronotypes that are clones of genetically similar antibodies shared by survivors of COVID-19 and non-infected individuals vaccinated with SARS-CoV-2. did.
Most of the published chronotypes were formed against “spike” on the surface of the virus or some of the S proteins that attach to specific receptors on the surface. cell In the lungs and other tissues.
This part of the S protein is variable, meaning that it can change or mutate in a way that effectively obscures the virus from circulating antibodies.
If many independently make the same antibody against the variable portion of the S protein, this can put selective pressure on it to mutate.
Scientists believe this led to a delta variant of SARS-CoV-2. It is more infectious than the original strain of the virus and is much more susceptible to human-to-human transmission.
In this study, researchers first discovered two public chronotypes that recognize another more conserved portion of the S protein that fuses with the cell membrane. When fusion occurs, SARS-CoV-2 enters its target cell, where it hijacks the cell’s genetic machinery and copies itself.
Neutralizing antibodies that bind to the conserved portion of the S protein have this portion protein It is less likely to mutate.
SARS-CoV-2 variants may be less likely to evade vaccines and antibody therapies when targeting the less mutated “Achilles tendon.”
The study was conducted in collaboration with colleagues at Washington University in St. Louis, University of Arizona School of Medicine in Tucson, and Integral Molecular in Philadelphia.
Elaine Chen, a graduate student at Crowe Lab, was the first author of this treatise. Other VUMC co-authors are Pavlo Gilchuk, Ph.D., Seth Zost, Ph.D., Naveen Suryadevara, Ph.D., Elad Binshtein, Ph.D., Rachel Sutton, Jessica Rodriguez, Sam Day, Luke. Myers, Andrew Trivette, MS, and Robert Carnahan, Ph.D.
Elaine C. Chen et al, Convergent antibody response to SARS-CoV-2 peplomer in convalescent and vaccinated individuals, Cell report (2021). DOI: 10.1016 / j.celrep.2021.109604
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Shared Antibodies May Push COVID Variants: Study
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