Coxsackie B virus infection of mice: inoculation by the oral route protects the pancreas from damage, but not from infection.

S. Bopegamage; J. Kovacova; A. Vargova; J. Motusova; A. Petrovicova; M. Benkovicova; P. Gomolcak; J. Bakkers; F. van Kuppeveld; W.J. Melchers; J.M. Galama

doi:10.1099/vir.0.81249-0

Coxsackie B virus infection of mice: inoculation by the oral route protects the pancreas from damage, but not from infection.

S. Bopegamage, J. Kovacova, A. Vargova, J. Motusova, A. Petrovicova, M. Benkovicova, P. Gomolcak, J. Bakkers, F. van Kuppeveld, W.J. Melchers, J.M. Galama

Hubrecht Institute

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Abstract

The pathogenesis of coxsackie B virus (CVB) infections is generally studied in mice by intraperitoneal (i.p.) injection, whereas the gastrointestinal tract is the natural porte d'entree in humans. The present study was undertaken to compare systematically the influence of infection route on morbidity and pathology. Swiss Albino mice were infected with CVB3 (Nancy) at different doses (5 x 10(3), 5 x 10(5), 5 x 10(7), 5 x 10(9) TCID50), given either i.p. or orally. Virus could be isolated from several organs (heart, spleen and pancreas), indicating systemic infection, irrespective of the infection route. Virus titres were 1-2 logs higher after i.p. infection, but kinetics were largely independent of infection route. Organs became negative for virus isolation after 21 days, with the exception of spleen tissue, which remained positive for up to 49 days. Thereafter, virus was detected only by immunohistochemistry and PCR up to 98 days post-infection (oral route). Histopathology showed mild inflammation and necrosis in heart tissue of all mice during the acute phase, with repair at later stages. Strikingly, pancreatic lesions were confined to the exocrine pancreas and observed only after i.p. infection. Under all experimental conditions, the pancreatic islets were spared. In contrast, immunohistochemistry showed the presence of viral VP1, protein 3A and alpha interferon (IFN-alpha) in exocrine as well as endocrine pancreas of all mice, irrespective of route and dose of infection. It is concluded that infection via the oral route protects the pancreas from damage, but not from infection, a process in which IFN-alpha is not the only factor involved.

Original language	English
Pages (from-to)	3271-3280
Journal	Journal of General Virology
Volume	86
Issue number	Pt 12
DOIs	https://doi.org/10.1099/vir.0.81249-0
Publication status	Published - 2005

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Bopegamage, S., Kovacova, J., Vargova, A., Motusova, J., Petrovicova, A., Benkovicova, M., Gomolcak, P., Bakkers, J., van Kuppeveld, F., Melchers, W. J., & Galama, J. M. (2005). Coxsackie B virus infection of mice: inoculation by the oral route protects the pancreas from damage, but not from infection. Journal of General Virology, 86(Pt 12), 3271-3280. https://doi.org/10.1099/vir.0.81249-0

@article{150d802429484d11bb1ef2e7e79127da,

title = "Coxsackie B virus infection of mice: inoculation by the oral route protects the pancreas from damage, but not from infection.",

abstract = "The pathogenesis of coxsackie B virus (CVB) infections is generally studied in mice by intraperitoneal (i.p.) injection, whereas the gastrointestinal tract is the natural porte d'entree in humans. The present study was undertaken to compare systematically the influence of infection route on morbidity and pathology. Swiss Albino mice were infected with CVB3 (Nancy) at different doses (5 x 10(3), 5 x 10(5), 5 x 10(7), 5 x 10(9) TCID50), given either i.p. or orally. Virus could be isolated from several organs (heart, spleen and pancreas), indicating systemic infection, irrespective of the infection route. Virus titres were 1-2 logs higher after i.p. infection, but kinetics were largely independent of infection route. Organs became negative for virus isolation after 21 days, with the exception of spleen tissue, which remained positive for up to 49 days. Thereafter, virus was detected only by immunohistochemistry and PCR up to 98 days post-infection (oral route). Histopathology showed mild inflammation and necrosis in heart tissue of all mice during the acute phase, with repair at later stages. Strikingly, pancreatic lesions were confined to the exocrine pancreas and observed only after i.p. infection. Under all experimental conditions, the pancreatic islets were spared. In contrast, immunohistochemistry showed the presence of viral VP1, protein 3A and alpha interferon (IFN-alpha) in exocrine as well as endocrine pancreas of all mice, irrespective of route and dose of infection. It is concluded that infection via the oral route protects the pancreas from damage, but not from infection, a process in which IFN-alpha is not the only factor involved.",

author = "S. Bopegamage and J. Kovacova and A. Vargova and J. Motusova and A. Petrovicova and M. Benkovicova and P. Gomolcak and J. Bakkers and {van Kuppeveld}, F. and W.J. Melchers and J.M. Galama",

note = "Reporting year: 2005",

year = "2005",

doi = "10.1099/vir.0.81249-0",

language = "English",

volume = "86",

pages = "3271--3280",

journal = "Journal of General Virology",

issn = "0022-1317",

publisher = "Society for General Microbiology",

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Bopegamage, S, Kovacova, J, Vargova, A, Motusova, J, Petrovicova, A, Benkovicova, M, Gomolcak, P, Bakkers, J, van Kuppeveld, F, Melchers, WJ & Galama, JM 2005, 'Coxsackie B virus infection of mice: inoculation by the oral route protects the pancreas from damage, but not from infection.', Journal of General Virology, vol. 86, no. Pt 12, pp. 3271-3280. https://doi.org/10.1099/vir.0.81249-0

TY - JOUR

T1 - Coxsackie B virus infection of mice: inoculation by the oral route protects the pancreas from damage, but not from infection.

AU - Bopegamage, S.

AU - Kovacova, J.

AU - Vargova, A.

AU - Motusova, J.

AU - Petrovicova, A.

AU - Benkovicova, M.

AU - Gomolcak, P.

AU - Bakkers, J.

AU - van Kuppeveld, F.

AU - Melchers, W.J.

AU - Galama, J.M.

N1 - Reporting year: 2005

PY - 2005

Y1 - 2005

N2 - The pathogenesis of coxsackie B virus (CVB) infections is generally studied in mice by intraperitoneal (i.p.) injection, whereas the gastrointestinal tract is the natural porte d'entree in humans. The present study was undertaken to compare systematically the influence of infection route on morbidity and pathology. Swiss Albino mice were infected with CVB3 (Nancy) at different doses (5 x 10(3), 5 x 10(5), 5 x 10(7), 5 x 10(9) TCID50), given either i.p. or orally. Virus could be isolated from several organs (heart, spleen and pancreas), indicating systemic infection, irrespective of the infection route. Virus titres were 1-2 logs higher after i.p. infection, but kinetics were largely independent of infection route. Organs became negative for virus isolation after 21 days, with the exception of spleen tissue, which remained positive for up to 49 days. Thereafter, virus was detected only by immunohistochemistry and PCR up to 98 days post-infection (oral route). Histopathology showed mild inflammation and necrosis in heart tissue of all mice during the acute phase, with repair at later stages. Strikingly, pancreatic lesions were confined to the exocrine pancreas and observed only after i.p. infection. Under all experimental conditions, the pancreatic islets were spared. In contrast, immunohistochemistry showed the presence of viral VP1, protein 3A and alpha interferon (IFN-alpha) in exocrine as well as endocrine pancreas of all mice, irrespective of route and dose of infection. It is concluded that infection via the oral route protects the pancreas from damage, but not from infection, a process in which IFN-alpha is not the only factor involved.

AB - The pathogenesis of coxsackie B virus (CVB) infections is generally studied in mice by intraperitoneal (i.p.) injection, whereas the gastrointestinal tract is the natural porte d'entree in humans. The present study was undertaken to compare systematically the influence of infection route on morbidity and pathology. Swiss Albino mice were infected with CVB3 (Nancy) at different doses (5 x 10(3), 5 x 10(5), 5 x 10(7), 5 x 10(9) TCID50), given either i.p. or orally. Virus could be isolated from several organs (heart, spleen and pancreas), indicating systemic infection, irrespective of the infection route. Virus titres were 1-2 logs higher after i.p. infection, but kinetics were largely independent of infection route. Organs became negative for virus isolation after 21 days, with the exception of spleen tissue, which remained positive for up to 49 days. Thereafter, virus was detected only by immunohistochemistry and PCR up to 98 days post-infection (oral route). Histopathology showed mild inflammation and necrosis in heart tissue of all mice during the acute phase, with repair at later stages. Strikingly, pancreatic lesions were confined to the exocrine pancreas and observed only after i.p. infection. Under all experimental conditions, the pancreatic islets were spared. In contrast, immunohistochemistry showed the presence of viral VP1, protein 3A and alpha interferon (IFN-alpha) in exocrine as well as endocrine pancreas of all mice, irrespective of route and dose of infection. It is concluded that infection via the oral route protects the pancreas from damage, but not from infection, a process in which IFN-alpha is not the only factor involved.

U2 - 10.1099/vir.0.81249-0

DO - 10.1099/vir.0.81249-0

M3 - Article

SN - 0022-1317

VL - 86

SP - 3271

EP - 3280

JO - Journal of General Virology

JF - Journal of General Virology

IS - Pt 12

ER -

Coxsackie B virus infection of mice: inoculation by the oral route protects the pancreas from damage, but not from infection.

Abstract

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