HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Vella, C. Articles by McCarthy, D. A. Search for Related Content PubMed PubMed Citation Articles by Vella, C. Articles by McCarthy, D. A. Agricola Articles by Vella, C. Articles by McCarthy, D. A.

Coxsackievirus B4 infection of the mouse pancreas: acute and persistent infection

C. Vella^1,

¹ Department of Immunology, The London Hospital Medical College, Turner Street, London E1
² Institute of Pathology, London Hospital, London E1
and³ School of Biological Sciences, Queen Mary and Westfield College, Mile End Road, London E1, U.K.

The course of infection of a pancreas-adapted isolate of coxsackievirus B4 was followed over a 10 month period in a murine model. Following intraperitoneal inoculation a typical acute infection was seen in nine of 10 inbred mouse strains. Virus rapidly infected the exocrine pancreas, titres peaking 3 to 4 days post-infection (p.i.). Lesions were almost exclusively confined to pancreatic acinar cells and varied in severity among the inbred strains. Virus shed into the blood-stream was not cell-associated. Evidence of persistent infection was found in nine mouse strains and infective virus was recovered from the pancreas of seven strains for up to 10 months p.i. Approximately 28% of pancreases examined beyond the acute phase showed focal inflammation and 22% showed focal necrosis (cell death). Virus was occasionally recovered from other organs (heart, liver and spleen), but lesions were rarely seen. Virus-specific antigen was localized to small groups of pancreatic acinar cells using an indirect immunogold silver staining technique. These observations suggested that the virus persists in pancreatic tissues because it seems unlikely that virus disseminated from distant sites would cause such localized infection. In three of these strains, the course of infection may have been influenced by superinfection with mouse hepatitis virus.

Present address: National Institute for Biological Standards and Control, Blanche Lane, South Mimms, Potters Bar, Hertfordshire EN6 3QG, U.K.

Received 11 November 1991; accepted 5 February 1992.

This article has been cited by other articles:

				T. R. Jerrells, D. Vidlak, and J. M. Strachota Alcoholic pancreatitis: mechanisms of viral infections as cofactors in the development of acute and chronic pancreatitis and fibrosis J. Leukoc. Biol., February 1, 2007; 81(2): 430 - 439. [Abstract] [Full Text] [PDF]

				D. M. Potvin, D. W. Metzger, W. T. Lee, D. N. Collins, and A. I. Ramsingh Exogenous Interleukin-12 Protects against Lethal Infection with Coxsackievirus B4 J. Virol., August 1, 2003; 77(15): 8272 - 8279. [Abstract] [Full Text] [PDF]

				M. Roivainen, S. Rasilainen, P. Ylipaasto, R. Nissinen, J. Ustinov, L. Bouwens, D. L. Eizirik, T. Hovi, and T. Otonkoski Mechanisms of Coxsackievirus-Induced Damage to Human Pancreatic {beta}-Cells J. Clin. Endocrinol. Metab., January 1, 2000; 85(1): 432 - 440. [Abstract] [Full Text]

				P. E. Tam and R. P. Messner Molecular Mechanisms of Coxsackievirus Persistence in Chronic Inflammatory Myopathy: Viral RNA Persists through Formation of a Double-Stranded Complex without Associated Genomic Mutations or Evolution J. Virol., December 1, 1999; 73(12): 10113 - 10121. [Abstract] [Full Text]