Use of Coxsackievirus B3 as a Model of Acute Pancreatitis

Hall, Jonathan H.

doi:10.3998/panc.2016.33

Cited by 1 publication

(1 citation statement)

References 29 publications

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“…Heart damage and the levels of VP1 in the myocardium of both mice groups were similar ( S7A and S7B Fig ). In addition, CVB3 cause extensive pancreatic tissue damage in experimental animal model [ 38 , 39 ]. Histological examinations of the pancreas using hematoxylin and eosin staining indicated pancreatic tissue damage with inflammation.…”

Section: Resultsmentioning

confidence: 99%

Interaction between coxsackievirus B3 infection and α-synuclein in models of Parkinson’s disease

2021

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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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Section: Resultsmentioning

confidence: 99%