Health
Spike mutation helps SARS-CoV-2 infect the brain
Scientists have discovered a mutation in SARS-CoV-2, the virus that causes COVID-19, that plays a key role in its ability to infect the central nervous system. The discovery could help scientists unravel the mysteries of neurological symptoms and “long COVID” and may even lead to the development of specific treatments in the future to protect and clear the virus from the brain.
A new collaborative study by scientists from Northwestern University and the University of Illinois at Chicago has uncovered a series of mutations in SARS-CoV-2's spike protein — the outer part of the virus that helps it enter cells — that enhance its ability to infect the brains of mice.
“When we looked at the genomes of the viruses we found in the brain compared to the lungs, we found that viruses with specific deletions in the spike were much better at infecting the brains of these animals,” said co-corresponding author Judd Hultquist, assistant professor of medicine (infectious diseases) and of microbiology and immunology at Northwestern University Feinberg School of Medicine. “This was totally unexpected and very exciting.”
The study will be published on August 23rd. Nature Microbiology.
Variations in the spike help the virus infect different cells in the body
In the study, the researchers infected mice with SARS-CoV-2 and sequenced the genome of the virus that replicated in the brain and lungs. In the lungs, the spike protein was highly similar to the virus used to infect the mice. However, in the brain, most of the viruses had a deletion or mutation in a critical region of the spike that determines how it enters cells. When they used a virus with this deletion to directly infect the brains of mice, it was largely restored when it traveled to the lungs.
“The virus needed a change in the spike protein to move from the lungs to the brain, a change that is already known to dictate how the virus enters different types of cells,” Hultquist said. “We believe that this spike region is a key regulator of whether the virus enters the brain, which could have major implications for the treatment and management of neurological symptoms reported by COVID-19 patients.”
SARS-CoV-2 has long been associated with a variety of neurological symptoms, including loss of smell and taste, “brain fog,” and “long COVID.”
“We don't yet know whether Long COVID is caused by a direct infection of brain cells or some kind of adverse immune response that continues after infection,” Hultquist said. “If it is caused by an infection of cells in the central nervous system, our study suggests that there may be certain treatments that are more effective than others at clearing the virus from this part of the body.”
Other Northwestern authors on the study include Lacey M. Simmons, Tanushree Dangi, Egon A. Ozer, Pablo Penaloza McMaster and Ramon Lorenzo Redondo.
The study, “SARS-CoV-2 Evolution in the Mouse Central Nervous System Drives Viral Diversification,” was funded by the National Institutes of Health (grants R01AI150672, R56DE033249, R21AI163912, U19AI135964), the Department of Defense (grant MS200290), and institutional support from the Center for Pathogen Genomics and Microbial Evolution and the Northwestern University Institute for Clinical and Translational Sciences (NUCATS).
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Sources 2/ https://www.sciencedaily.com/releases/2024/08/240823120055.htm The mention sources can contact us to remove/changing this article |
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