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SARS-CoV-2-Mimicking Pseudoviral Particles Accelerate α-Synuclein Aggregation In Vitro
Gianluca Zilio1, Anna Masato1, Michele Sandre1,2
1Department of Biology, University of Padova, Padova 35131, Italy.
ACS Chemical Neuroscience
|December 22, 2023
Summary
The SARS-CoV-2 virus
Area of Science:
- Neuroscience
- Virology
- Pathology
Background:
- COVID-19 (SARS-CoV-2) infection is linked to neurological issues and long-term brain symptoms.
- Evidence suggests SARS-CoV-2 can invade the nervous system.
- Viral infections can cause parkinsonism; COVID-19 may impact dopaminergic neurons and Parkinson's disease (PD) pathogenesis.
Purpose of the Study:
- To investigate the potential of SARS-CoV-2 proteins to induce α-synuclein aggregation.
- To explore the role of viral structure in promoting amyloid formation relevant to Parkinson's disease.
Main Methods:
- In vitro experiments assessing the effects of SARS-CoV-2 spike and nucleocapsid proteins on α-synuclein.
- Microscopic analysis to observe protein aggregation and fibril formation.
Main Results:
- Both SARS-CoV-2 spike and nucleocapsid proteins independently promote α-synuclein aggregation.
- The corona-like structure of the spike protein on the viral envelope accelerates amyloid fibril formation.
Conclusions:
- SARS-CoV-2 proteins can directly induce α-synuclein aggregation, a key process in Parkinson's disease.
- The viral spike protein's structure may be critical in initiating rapid amyloid formation, potentially contributing to PD pathogenesis.
