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Revealing How SARS-CoV-2 Infiltrates the Brain at SfN 2021
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Revealing How SARS-CoV-2 Infiltrates the Brain

Revealing How SARS-CoV-2 Infiltrates the Brain at SfN 2021
News

Revealing How SARS-CoV-2 Infiltrates the Brain

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A press conference held one week prior to the opening of the Society for Neuroscience (SfN)’s Neuroscience 2021 conference highlighted a series of studies that will be presented online between November 8–11. These studies reveal the impact of SARS-CoV-2 on the brain – looking at the ways in which the virus might enter and disrupt the brain and the extent and duration of these effects. This important research provides new light on an unclear aspect of SARS-CoV-2 infection, as the ability of the virus to infect neurons and other cells of the nervous system has been hard to pin down.

Opening the press briefing was the All India Institute of Medical Science, Patna’s Professor Ashutosh Kumar, who looked at the mechanisms that may permit the virus to access our brain. His team identified a pair of molecules – the receptor protein neuropilin 1 and the protease furin – as potential mediators of SARS-CoV-2 entry. Neuropilin-1 is capable of, in combination with furin, cleaving the SAR-CoV-2 spike protein, an essential step in viral cell entry.

A complementary study, looking at how the virus might enter the peripheral nervous system, was presented by Virginia Tech’s Jonathan D. Joyce. Joyce’s presentation contained a stark reminder of why this research is such a focus of the SfN program in 2021 – 80% of people with COVID-19 develop neurological symptoms, ranging from loss of taste and smell to nerve pain. Joyce’s work looked at ganglia – groups of neuronal cell bodies that are found in the peripheral nervous system. By using mouse models of COVID-19, Joyce’s team revealed that SARS-CoV-2 was capable of infecting peripheral nerves beyond those responsible for smell. Every single peripheral sensory and autonomic nerve tested had the viral genome present, and infectious virus was also detected in a subset of these nerves. This finding, said Joyce, may explain some of the constellation of neurological symptoms reported by COVID-19 patients.

SARS-CoV-2’s profound effect on our sense of smell, while far from being the most severe or debilitating symptom of COVID-19, is an unusual and potent clinical sign that sets the disease apart from other respiratory viruses. Investigating this phenomenon in detail was John H Morrison, a professor of neurology at UC Davis. Are such neurological effects a direct result of the virus invading the brain, or of some other biological response to the virus?

Morrison and colleagues, using a primate model, showed that seven days after exposure, SARS-CoV-2 proteins could be found in multiple brain areas, with transport through the brain apparently facilitated via brain circuits. Notably, Morrison’s team showed that entry to the brain appeared to be through the olfactory system and that aged, diabetic animals had more aggressive brain infection.

A final study presented was by Dr. Allison Sekuler, a chair in cognitive neuroscience at Baycrest’s Rotman Research Institute and a professor at McMaster University and the University of Toronto. Her multi-institutional team used a neuroimaging-based approach to examine the long-term effects of COVID-19 on cognition. Using an innovative portable electroencephalography (EEG) device, they showed that brain power was reduced in people who had tested positive for COVID-19 up to seven months after infection.

Together, these studies show the neuroscience field’s commitment to revealing the remaining ambiguous effects of COVID-19 on the brain, which will help bring clarity to both those battling the disease and those still feeling its side effects months later. 

Meet The Author
Ruairi J Mackenzie
Ruairi J Mackenzie
Senior Science Writer
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