ArticleFrontiers in cellular neuroscience2021
SARS-CoV-2 S1 Protein Induces Endolysosome Dysfunction and Neuritic Dystrophy.
Article in Frontiers in cellular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- HIV-1 gp120-induced lysosomal stress responses are controlled by TRPML1 redox sensors.Redox report : communications in free radical research · 2026Article
- High-throughput marker-free screening of cytoplasmic vacuoles in adherent cells via Fourier ptychographic microscopy.Biomedical optics express · 2025Article
- SARS-CoV-2 spike triggers TLR7-dependent endolysosome dysfunction and senescence in human astrocytes.Journal of neuroinflammation · 2025Article
- Role of NRP1/HDAC4/CREB/RIPK1 Axis in SARS-CoV2 S1 Spike Subunit-Induced Neuronal Toxicity.FASEB bioAdvances · 2025Article
- SLC38A9 is directly involved in Tat-induced endolysosome dysfunction and senescence in astrocytes.Life science alliance · 2025Article
- Investigating post-infection anxiety- and depression-like behaviors in a SARS-CoV-2 mouse model.Theranostics · 2025Article
- SLC38A9 regulates SARS-CoV-2 viral entry.iScience · 2024Article
- Unraveling the SARS-CoV-2 spike protein long-term effect on neuro-PASC.Frontiers in cellular neuroscience · 2024Article
- Viral Entry Inhibitors Protect against SARS-CoV-2-Induced Neurite Shortening in Differentiated SH-SY5Y Cells.Viruses · 2023Article
- The Endolysosomal System: The Acid Test for SARS-CoV-2.International journal of molecular sciences · 2022Review
- Dimethoxycurcumin Acidifies Endolysosomes and Inhibits SARS-CoV-2 Entry.Frontiers in virology (Lausanne, Switzerland) · 2022Article
- Molecular Mechanisms in the Genesis of Seizures and Epilepsy Associated With Viral Infection.Frontiers in molecular neuroscience · 2022Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
SARS-CoV-2 is the viral cause of the COVID-19 pandemic. Increasingly, significant neurological disorders have been associated with COVID-19. However, the pathogenesis of these neurological disorders remains unclear especially because only low or undetectable levels of SARS-CoV-2 have been reported in human brain specimens. Because SARS-CoV-2 S1 protein can be released from viral membranes, can cross the blood-brain barrier, and is present in brain cells including neurons, we tested the hypothesis that SARS-CoV-2 S1 protein can directly induce neuronal injury. Incubation of primary human cortical neurons with SARS-CoV-2 S1 protein resulted in accumulation of the S1 protein in endolysosomes as well as endolysosome de-acidification. Further, SARS-CoV-2 S1 protein induced aberrant endolysosome morphology and neuritic varicosities. Our findings suggest that SARS-CoV-2 S1 protein directly induces neuritic dystrophy, which could contribute to the high incidence of neurological disorders associated with COVID-19.
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