Scientists have discovered a mutation in the SARS-CoV-2 virus that is responsible for causing COVID-19, which plays a crucial role in its ability to infect the central nervous system. This discovery could help researchers better understand the neurological symptoms associated with the virus, as well as the phenomenon of “long COVID.” Furthermore, this finding may ultimately lead to the development of specific treatments designed to protect and clear the virus from the brain. The study was a collaborative effort between scientists at Northwestern University and the University of Illinois-Chicago.
The study focused on mutations in the spike protein of the SARS-CoV-2 virus, which is the outer part of the virus responsible for helping it enter cells. The researchers found that these mutations enhanced the virus’s ability to infect the brains of mice. Specifically, viruses with a specific deletion in the spike protein were much more effective at infecting the brains of the animals compared to those found in the lungs. This unexpected discovery has the potential to significantly impact the development of treatments for neurological symptoms in COVID-19 patients.
In sequencing the genomes of viruses that replicated in the brains and lungs of mice infected with SARS-CoV-2, researchers observed significant differences in the spike protein. While the spike protein in the lung closely resembled the virus originally used to infect the mice, in the brain, most viruses had a deletion or mutation in a critical region of the spike protein that affects how the virus enters a cell. Interestingly, when viruses with this specific deletion were used to directly infect the brains of mice, the deletion was largely repaired once the virus traveled to the lungs. This suggests that the spike protein is a key regulator of the virus’s ability to enter the brain.
The study underscores the importance of understanding how SARS-CoV-2 interacts with the central nervous system, as the virus has been linked to various neurological symptoms such as loss of smell and taste, brain fog, and long COVID. The mystery of long COVID, which involves persistent symptoms beyond the acute phase of infection, remains unanswered. It is still unclear whether long COVID is caused by direct infection of brain cells or by some adverse immune response that lingers after the infection is cleared. If the former is true, the study suggests that there may be specific treatments that could be more effective in clearing the virus from the central nervous system.
The research was supported by funding from the National Institutes of Health, the Department of Defense, and institutional support for the Center for Pathogen Genomics and Microbial Evolution at Northwestern University. The findings of this study, which will be published in Nature Microbiology, have significant implications for understanding the neurological manifestations of COVID-19 and could pave the way for the development of targeted treatments to address these symptoms. This collaborative effort between researchers at Northwestern University and the University of Illinois-Chicago sheds new light on the underlying mechanisms of SARS-CoV-2 infection in the central nervous system and its potential impact on long-term health outcomes for COVID-19 patients.