Viral pancreatitis: Ultrastructural pathological effects of coxsackievirus B3 infection in newborn mouse pancreas

Alyne K. Harrison; Sally P. Bauer; Frederick A. Murphy

doi:10.1016/0014-4800(72)90070-6

Viral pancreatitis: Ultrastructural pathological effects of coxsackievirus B3 infection in newborn mouse pancreas

Alyne K. Harrison, Sally P. Bauer, Frederick A. Murphy

Pathology

Research output: Contribution to journal › Article

21 Scopus citations

Abstract

An electron microscopic study of Coxsackievirus B3-infected newborn mice revealed pathological changes in both the endocrine and exocrine portions of the pancreas. Damage ranged from a focal degeneration in which small areas of individual cells were affected to a widespread necrosis and inflammation in which entire acini and islets were so changed that identification of individual cell types was difficult. Compound membrane-vesicle complexes typical of picornavirus infection and virus particles in various arrays were observed in the acinar cells and macrophages. Fibrosis of the islets and a thickening of the basal laminae of associated capillaries were noted also. Comparisons were made to the pancreatitis caused by this and other group B Coxsackieviruses in both human and experimental animals.

Original language	English (US)
Pages (from-to)	206-219
Number of pages	14
Journal	Experimental and Molecular Pathology
Volume	17
Issue number	2
DOIs	https://doi.org/10.1016/0014-4800(72)90070-6
State	Published - Oct 1972

ASJC Scopus subject areas

Pathology and Forensic Medicine
Molecular Biology
Clinical Biochemistry

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Harrison, A. K., Bauer, S. P., & Murphy, F. A. (1972). Viral pancreatitis: Ultrastructural pathological effects of coxsackievirus B3 infection in newborn mouse pancreas. Experimental and Molecular Pathology, 17(2), 206-219. https://doi.org/10.1016/0014-4800(72)90070-6

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abstract = "An electron microscopic study of Coxsackievirus B3-infected newborn mice revealed pathological changes in both the endocrine and exocrine portions of the pancreas. Damage ranged from a focal degeneration in which small areas of individual cells were affected to a widespread necrosis and inflammation in which entire acini and islets were so changed that identification of individual cell types was difficult. Compound membrane-vesicle complexes typical of picornavirus infection and virus particles in various arrays were observed in the acinar cells and macrophages. Fibrosis of the islets and a thickening of the basal laminae of associated capillaries were noted also. Comparisons were made to the pancreatitis caused by this and other group B Coxsackieviruses in both human and experimental animals.",

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