ArticlePLoS pathogens2021
Interaction between coxsackievirus B3 infection and α-synuclein in models of Parkinson's disease.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- Alpha-synuclein at the crossroads of host-virus interactions: immunological roles beyond the nervous system.Journal of virology · 2026Review
- Viral Infections and Neurodegenerative Diseases: Reinterpreting the Crosstalk Through a Dual-Role Lens.Current microbiology · 2026Review
- NeuroViOme: a viral orfeome collection for studies of neurodegenerative disease.Journal of neurovirology · 2026Review
- Potential new drug sources for the treatment of Parkinson's disease: flavonoid O-glycosides.Molecular biology reports · 2025Review
- Underestimated virus impaired cognition-more evidence and more work to do.Frontiers in immunology · 2025Review
- Positive-strand RNA virus replication organelles at a glance.Journal of cell science · 2024Review
- Global landscape of coxsackieviruses in human health.Virus research · 2024Review
- Neurotropic virus infection and neurodegenerative diseases: Potential roles of autophagy pathway.CNS neuroscience & therapeutics · 2024Review
- Environmental risk factors provoke new thinking for prevention and treatment of dementia with Lewy bodies.Heliyon · 2024Review
- Integration of National Health Insurance claims data and animal models reveals fexofenadine as a promising repurposed drug for Parkinson's disease.Journal of neuroinflammation · 2024Article
- Infections in the Etiology of Parkinson's Disease and Synucleinopathies: A Renewed Perspective, Mechanistic Insights, and Therapeutic Implications.Journal of Parkinson's disease · 2024Review
- Monitoring α-synuclein Aggregation Induced by Preformed α-synuclein Fibrils in anExperimental neurobiology · 2023Article
- Enterovirus infection and its relationship with neurodegenerative diseases.Memorias do Instituto Oswaldo Cruz · 2023Article
- Identification of key genes and signaling pathways associated with dementia with Lewy bodies and Parkinson's disease dementia using bioinformatics.Frontiers in neurology · 2023Article
- Viruses in neurodegenerative diseases: More than just suspects in crimes.PLoS pathogens · 2022Review
- Mitochondrial Sirtuins in Parkinson's Disease.Neurochemical research · 2022Review
- Picornavirus May Be Linked to Parkinson's Disease through Viral Antigen in Dopamine-Containing Neurons of Substantia Nigra.Microorganisms · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is one of the most common neurodegenerative diseases. PD is pathologically characterized by the death of midbrain dopaminergic neurons and the accumulation of intracellular protein inclusions called Lewy bodies or Lewy neurites. The major component of Lewy bodies is α-synuclein (α-syn). Prion-like propagation of α-syn has emerged as a novel mechanism in the progression of PD. This mechanism has been investigated to reveal factors that initiate Lewy pathology with the aim of preventing further progression of PD. Here, we demonstrate that coxsackievirus B3 (CVB3) infection can induce α-syn-associated inclusion body formation in neurons which might act as a trigger for PD. The inclusion bodies contained clustered organelles, including damaged mitochondria with α-syn fibrils. α-Syn overexpression accelerated inclusion body formation and induced more concentric inclusion bodies. In CVB3-infected mice brains, α-syn aggregates were observed in the cell body of midbrain neurons. Additionally, α-syn overexpression favored CVB3 replication and related cytotoxicity. α-Syn transgenic mice had a low survival rate, enhanced CVB3 replication, and exhibited neuronal cell death, including that of dopaminergic neurons in the substantia nigra. These results may be attributed to distinct autophagy-related pathways engaged by CVB3 and α-syn. This study elucidated the mechanism of Lewy body formation and the pathogenesis of PD associated with CVB3 infection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.