Viruses such as SARS-CoV-2, which caused Covid-19, can cause brain cells to fuse, initiating malfunctions that lead to chronic neurological symptoms, according to an international team of researchers.
This could explain brain fog, headaches, loss of taste and smell and other long-term neurological symptoms some patients experience as ‘long Covid’ months after their initial infection.
To understand, the teams from the universities of Queensland, Macquarie in Australia, and Helsinki in Finland explored how viruses alter the function of the nervous system.
Their research, published in the journal Sciences Advances, showed that Covid-19 causes neurons to undergo a cell fusion process, which has not been seen before.
“After neuronal infection with SARS-CoV-2, the spike S protein becomes present in neurons, and once neurons fuse, they don’t die,” said Professor Massimo Hilliard from the Queensland Brain Institute.
“They either start firing synchronously, or they stop functioning altogether.”
As an analogy, Professor Hilliard likened the role of neurons to that of wires connecting switches to the lights in a kitchen and a bathroom.
“Once fusion takes place, 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 the two independent circuits.”
The discovery offers a potential explanation for persistent neurological effects after a viral infection.
“In the current understanding of what happens when a virus enters the brain, there are two outcomes – either cell death or inflammation,” said Ramon Martinez-Marmol from the institute.
“But we’ve shown a third possible outcome, which is neuronal fusion.”
Martinez-Marmol said numerous viruses cause cell fusion in other tissues, but also infect the nervous system and could be causing the same problem there.
“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 happen during a viral infection. This is potentially a major cause of neurological diseases and clinical symptoms that is still unexplored.”
For their study, the team relied heavily on ‘mini-brains’, which allowed researchers to experiment on complex human neuronal networks resembling a live human brain.
Some of these mini-brains were infected with viruses, or viral surface fusogens — including the SARS-Cov-2 virus — and then compared with non-infected control mini-brains, using a remarkable breakthrough in brain experiment techniques.
This study is just one example of the huge research potential now possible thanks to the development of the mini-brains, which bridge the gap between non-living tissue and human subjects.
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