The researchers sequenced 750 genomes of the novel coronavirus from infected individuals and analysed the mutations
Some mutations in the novel coronavirus may not only enable it to evade antibodies, but also make the virus unrecognisable to the immune system’s T-killer cells, says a new study which could aid in the further development of vaccines.
While antibodies dock directly onto viruses to neutralise them, the scientists, including those from the Medical University of Vienna in Austria, said the T-killer cells recognise viral protein fragments on infected cells and subsequently kill them to stop virus production.
In the current study, published in the journal Cell Immunology, the researchers sequenced 750 genomes of the novel coronavirus from infected individuals and analysed mutations for their potential to alter T cell epitopes.
These are regions on the virus recognised by the body’s T cells.
“Our results show that many mutations in SARS-CoV-2 are indeed capable of doing this,” said study co-author Andreas Bergthaler. “With the help of bioinformatic and biochemical investigations as well as laboratory experiments with blood cells from COVID-19 patients, we were able to show that mutated viruses can no longer be recognized by T-killer cells in these regions.”
According to the researchers, there are several epitopes available for recognition by T-killer cells in most natural infections, and if the virus mutates in one place, other sites on its surface may still indicate its presence to T cells.
They said the spike protein of the virus, which it uses to enter cells and against which most vaccines are targeted, has, on average, one to six of these T cell epitopes.
“If the virus mutates in one of these regions, the risk that the infected cells will not be recognized by the T-killer cells increases,” explained Johannes Huppa, another co-author of the study.
“Especially for the further development of vaccines, we therefore have to keep a close eye on how the virus mutates and which mutations prevail globally. Currently, we see few indications that mutations in T killer cell epitopes are increasingly spreading,” added Judith Aberle, another of the study’s co-authors from the Medical University of Vienna.
The scientists believe the findings provide important insights on how the novel coronavirus interacts with the immune system.
“Furthermore, this knowledge helps to develop more effective vaccines with the potential to activate as many T-killer cells as possible via a variety of epitopes,” the scientists said. “The goal is vaccines that trigger neutralizing antibody and T killer cell responses for the broadest possible protection.”