Viruses like SARS-CoV-2, which caused Covid-19, can fuse brain cells, triggering a malfunction that leads to chronic neurological symptoms, according to an international team of researchers. This may explain the brain fog, headache, loss of taste and smell, and other long-term neurological symptoms some patients experience as ‘long COVID’ months after their initial infection.
To understand, teams from the Universities of Macquarie in Queensland, Australia and Helsinki in Finland explored how the virus alters nervous system function. Their research, published in the journal Science Advances, showed that COVID-19 causes neurons to undergo a cell fusion process, which has not been observed before.
“After neuronal infection with SARS-CoV-2, the spike S protein becomes present in neurons, and once neurons fuse, they do not die,” said Professor Massimo Hilliard from the Queensland Brain Institute. “They either start firing synchronously, or they stop working altogether.”
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As an analogy, Professor Hilliard compared the role of neurons to the wires connecting the switches to the lights in the kitchen and bathroom. “Once the fusion is done, each switch either turns on both the kitchen and bathroom lights at the same time, or neither of them,” he said.
“It’s bad news for two independent circuits.” The finding offers a possible explanation for persistent neurological effects following viral infection. “Current understanding of what happens when a virus enters the brain suggests two outcomes – either cell death or inflammation,” said the institute’s Ramon Martinez-Marmol.
“But we have shown a third possible outcome, which is neuronal fusion.” Martinez-Marmol said that many viruses cause cell fusion in other tissues, but also infect the nervous system and can cause the same problems. “These viruses include HIV, rabies, Japanese encephalitis, measles, herpes simplex virus and Zika virus,” he said.
“Our research reveals a new mechanism for the neurological events that occur during a viral infection. This is potentially a major cause of neurological diseases and clinical symptoms that is still unclear.”
For their study, the team relied heavily on ‘mini-brains’, which allowed researchers to conduct experiments on complex human neuronal networks similar to those of a living human brain.
Some of these mini-brains were infected with viruses, or viral surface fusogens – including the SARS-Cov-2 virus – and then compared to non-infected control mini-brains, a remarkable breakthrough in brain experimentation techniques used Went.
This study is just one example of the enormous research potential now possible for the development of mini-brains that bridge the gap between non-living tissue and human subjects.