New York: US researchers have found that people recovering from Covid-19 and those vaccinated against SARS-CoV-2 produce identical clones, or groups, of antibody-producing white blood cells.
Antibodies are proteins produced by specialised white blood cells called B lymphocytes, or B cells. When a virus binds to the surface of a B cell, it stimulates the cell to divide and mature into a clone of identical cells.
The 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 infecting its target cell.
The study, published in the journal Cell Reports, identified 27 public clonotypes, genetically similar clones of antibodies, which were shared by Covid-19 survivors and by uninfected people who had been vaccinated against SARS-CoV-2.
“We were surprised to discover that there are so many shared antibodies between individuals after SARS-CoV-2 infection, but that is a good sign,” said James Crowe, Jr., Professor of Pediatrics and Pathology, Microbiology and Immunology from Vanderbilt University Medical Center in Tennessee, US.
“It was encouraging to find that an mRNA vaccine also induces those clones, which in part explains why these antibodies work so well in so many people,” said Crowe.
Most of the public clonotypes were formed against part of the viral surface “spike” or S protein that attaches to a specific receptor on the surface of cells in the lungs and other tissues.
This part of the S protein is variable, meaning that it can change, or mutate, in ways that can make the virus virtually invisible to circulating antibodies.
If many people independently make the same antibody against the variable part of the S protein, this may exert selective pressure on it to mutate.
Scientists believe this is what led to the delta variant of SARS-CoV-2, which is more infectious than the original strain of the virus, and much more transmissible from person to person.
In this study, researchers for the first time found two public clonotypes recognising another, more conserved part of the S protein that fuses with the cell membrane. Once fusion occurs, SARS-CoV-2 enters its target cell, where it hijacks the cell’s genetic machinery to copy itself.
Neutralising antibodies that bind the conserved part of the S protein are of interest because this part of the protein is less likely to mutate. Variants of SARS-CoV-2 may be less likely to evade vaccines and antibody therapies when its less mutable “Achilles heel” is targeted.
The findings could help scientists design more effective vaccines and antibody therapies against a broader range of variants, the researchers said.