A new study has found that changes in the spike protein of the coronavirus enhance its ability to infect the brain, potentially explaining the brain-related symptoms of long COVID, such as brain fog. The spike protein guides the SARS-CoV-2 virus into human cells, leading to COVID-19 infection.

While the precise causes of long COVID and its neurological effects remain unclear and are the subject of extensive research, this study could provide crucial insights. Researchers from Northwestern University, the University of Illinois-Chicago, and the UK suggest that these findings might lead to targeted treatments to protect the brain and eliminate the virus.

Published in Nature Microbiology, the study involved infecting mice with the coronavirus. Researchers compared the spike proteins of the virus in the brain to those in the lungs. They observed that while the spike protein in the lungs closely resembled that of the infecting virus, the spike proteins in the brain often had deletions or mutations in a key region responsible for cell entry.

“We discovered that viruses with specific deletions in the spike protein were significantly more effective at infecting the brain,” said Judd Hultquist, an assistant professor of medicine (infectious diseases) at Northwestern University and the study’s corresponding author. The mutated spike proteins also weakened the virus’s ability to infect the lungs.

The researchers concluded that these viruses are better suited to infect the brain and central nervous system, suggesting that the spike protein plays a crucial role in determining whether the virus can access the brain.

These findings may have significant implications for treating and managing neurological symptoms associated with COVID-19. If long COVID is linked to brain infection, specific treatments could be developed to more effectively clear the virus from the central nervous system, Hultquist noted.