The vast majority of people infected with SARS-CoV-2 clear the virus, but those with compromised immunity—such as individuals receiving immune-suppressive drugs for autoimmune diseases—can become chronically infected. As a result, their weakened immune defenses continue to attack the virus without being able to eradicate it fully. Now, a new study led by Harvard Medical School scientists offers a look into this interplay, shedding light on the ways in which compromised immunity may render SARS-CoV-2 fitter and capable of evading the immune system.

The research, published March 16 in Cell, shows that a mutated SARS-CoV-2 from a chronically infected immune compromised patient is capable of evading both naturally occurring antibodies from COVID-19 survivors as well as lab-made antibodies now in clinical use for treatment of COVID-19.

The patient case was originally described Dec. 3, 2020, as a New England Journal of Medicine report by scientists at Brigham and Women's Hospital a few weeks before the U.K. and South African variants were first reported to the World Health Organization. Interestingly, the patient-derived virus contained a cluster of changes on its spike protein—the current target for vaccines and antibody-based treatments—and some of these changes were later detected in viral samples in the U.K. and South Africa, where they appear to have arisen independently, the researchers said.

The newly published study, which builds on the initial case report, shows something more alarming still. Some of the changes found in the patient-derived virus have not been identified yet in dominant viral variants circulating in the population at large. However, these changes have been already detected in databases of publicly available viral sequences. These mutations remain isolated, the authors of the report said, but they could be harbingers of viral mutants that may spread across the population.

The researchers emphasize that variants initially detected in the U.K. and South Africa remain vulnerable to currently approved mRNA vaccines, which target the entire spike protein rather than just portions of it. Nonetheless, the study results could also offer a preview into a future, in which current vaccines and treatments may gradually lose their effectiveness against next-wave mutations that render the virus impervious to immune pressures.

Regards

John
Editorial Assistant
Immunogenetics Open Access