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SARS-CoV-2 S1 Protein Induces Endolysosome Dysfunction and Neuritic Dystrophy
Gaurav Datta1, Nicole M Miller1, Peter W Halcrow1
1Department of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND, United States.
Frontiers in Cellular Neuroscience
|November 15, 2021
Summary
The SARS-CoV-2 S1 protein directly injures neurons by disrupting endolysosome function, potentially explaining COVID-19 neurological complications. This study reveals a direct mechanism for viral-induced brain damage.
Area of Science:
- Neuroscience
- Virology
- Cell Biology
Background:
- COVID-19, caused by SARS-CoV-2, is increasingly linked to neurological disorders.
- The exact mechanisms driving these neurological issues are unclear, as the virus is rarely detected in brain tissue.
Purpose of the Study:
- To investigate if the SARS-CoV-2 S1 protein can directly cause neuronal injury.
- To explore the potential role of S1 protein in COVID-19-associated neurological dysfunction.
Main Methods:
- Primary human cortical neurons were incubated with purified SARS-CoV-2 S1 protein.
- Changes in endolysosome function, morphology, and neuronal structures were analyzed.
Main Results:
- SARS-CoV-2 S1 protein accumulated in neuronal endolysosomes, leading to de-acidification.
- Abnormal endolysosome morphology and neuritic varicosities were observed in neurons exposed to S1 protein.
- These changes indicate S1 protein induces neuritic dystrophy.
Conclusions:
- The SARS-CoV-2 S1 protein can directly induce neuronal injury, specifically neuritic dystrophy.
- This direct neurotoxic effect of the S1 protein may contribute to the neurological symptoms observed in COVID-19 patients.
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