Prior research suggests that antibodies encoded by IGHV3-53 are generally present, at least in small numbers, in healthy people's blood. The results therefore offer hope that using a vaccine to boost levels of these ever-present antibodies will protect adequately against the virus. Snip The team started by analyzing 294 different SARS-CoV-2-neutralizing antibodies isolated from COVID-19 patients' blood over the past few months. Antibodies are Y-shaped proteins made in immune cells called B-cells. Each B-cell makes a specific antibody type, or clone, which is encoded by a unique combination of antibody genes in the cell. The scientists found that an antibody gene called IGHV3-53 was the most common of the genes for the 294 antibodies, encoding about 10 percent of them. Snip The IGHV3-53 antibodies had yet another property suggesting that boosting their numbers would be a good and achievable aim for a SARS-CoV-2 vaccine: They appeared to have mutated only minimally from the original versions that would be circulating, initially in small numbers, in the blood of healthy people.
Normally, when activated by an encounter with a virus to which they fit, B-cells will start proliferating and also mutating parts of their antibody genes, in order to generate new B-cells whose antibodies fit the viral target even better. The more mutations needed for this "affinity maturation" process to generate virus-neutralizing antibodies, the harder it can be to induce this same process with a vaccine.
Fortunately, the IGHV3-53 antibodies found in the study seemed to have undergone little or no affinity maturation and yet were already very potent at neutralizing the virus—which hints that a vaccine may be able to induce a protective response from these potent neutralizers relatively easily.
"Coronaviruses have been around for hundreds to thousands of years, and one can imagine that our immune system has evolved in such a way that we carry antibodies like these that can make a powerful response right off the bat, so to speak" Wilson says.
