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

Vella, Cherelyn; Brown, C. L.; McCarthy, D.

doi:10.1099/0022-1317-73-6-1387

Cited by 28 publications

(17 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This finding is in direct contrast with experimental infections in mice where enteroviruses had a propensity to the exocrine compartment. Thus localisation studies on mouse pancreases have identified virus in acinar cells but not in islets [41,42,43,44,45,46,47,57]. In spite of almost complete destruction of the infected exocrine pancreas, the islets, ducts and connective tissue were selectively spared in mice infected with coxsackievirus B [42,44,46,47,58].…”

Section: Discussionmentioning

confidence: 99%

Enterovirus infection in human pancreatic islet cells, islet tropism in vivo and receptor involvement in cultured islet beta cells

Ylipaasto

Klingel

Lindberg³

et al. 2004

Diabetologia

261

248

View full text Add to dashboard Cite

Aims/hypothesis. It is thought that enterovirus infections cause beta-cell damage and contribute to the development of Type 1 diabetes by replicating in the pancreatic islets. We sought evidence for this through autopsy studies and by investigating known enterovirus receptors in cultured human islets. Methods. Autopsy pancreases from 12 newborn infants who died of fulminant coxsackievirus infections and from 65 Type 1 diabetic patients were studied for presence of enteroviral ribonucleic acid by in situ hybridisation. Forty non-diabetic control pancreases were included in the study. The expression and role of receptor candidates in cultured human islets were investigated with receptor-specific antibodies using immunocytochemistry and functional assays. Results. Enterovirus-positive islet cells were found in some of both autopsy specimen collections, but not in control pancreases. No infected cells were seen in exocrine tissue. The cell surface molecules, poliovirus receptor and integrin αvβ 3 , which act as enterovirus receptors in established cell lines, were expressed in beta cells. Antibodies to poliovirus receptor, human coxsackievirus and adenovirus receptor and integrin αvβ 3 protected islets and beta cells from adverse effects of poliovirus, coxsackie B viruses, and several of the arginine-glycine-aspartic acid motifs containing enteroviruses and human parechovirus 1 respectively. No evidence was found for expression of the decay-accelerating factor which acts as a receptor for several isletcell-replicating echoviruses in established cell lines. Conclusions/interpretation. The results show a definite islet-cell tropism of enteroviruses in the human pancreas. Some enteroviruses seem to use previously identified cell surface molecules as receptors in beta cells, whereas the identity of receptors used by other enteroviruses remains unknown. [Diabetologia (2004) 47:225-239]

show abstract

Section: Discussionmentioning

confidence: 99%

Enterovirus infection in human pancreatic islet cells, islet tropism in vivo and receptor involvement in cultured islet beta cells

Ylipaasto

Klingel

Lindberg³

et al. 2004

Diabetologia

261

248

View full text Add to dashboard Cite

show abstract

“…The lyric infection is controlled by the immune system which will become active within 5 to 7 days. For reasons which are not fully understood, the lytic infection can be limited to a chronic productive one with focal necrosis and expression of viral antigens in both surviving and necrotic cells (Vella et al, 1992). Therefore, it may be that the virus can be trapped in a few cells which do not immediately lyse, probably due to defective virus replication.…”

Section: Discussionmentioning

confidence: 99%

“…Several animal models have been developed, in which pancreatitis (Vella et al, 1992), cardiomyopathy (Gauntt et al, 1979) and myositis (Ray et al, 1979) are induced by infection with specific strains of coxsackie B viruses. Ray et al (1979) described a murine model for myositis induced by a coxsackievirus B1 infection of suckling mice.…”

Section: Introductionmentioning

confidence: 99%

Coxsackievirus B1-induced murine myositis: no evidence for viral persistence

Zoll¹,

Jongen

Galama³

et al. 1993

Journal of General Virology

View full text Add to dashboard Cite

The persistence of coxsackievirus B1 in the muscles of mice with coxsackievirus Bl-induced chronic myositis was investigated. Neonatal CD1 Swiss mice were inoculated with a myositis-causing variant of coxsackievirus B1 (Tucson strain). Hamstring muscle samples of diseased mice obtained at various times after inoculation were examined for the presence of infectious virus, viral RNA and histological abnormalities. Viral RNA was detected up to 4 weeks after initiation of infection, whereas virus could be isolated from hamstring muscles for up to 2 weeks. Thereafter no sign of infection was demonstrated although histological abnormalities remained present for the entire observation period of 16 weeks. That viral RNA was detectable for only 2 weeks after tissues became negative for infectious virus suggests that the infection slowly waned rather than the viral RNA persisting. Hence, it is concluded that coxsackievirus B1 plays an essential role in the initiation of myositis but not in the maintenance of the chronic phase.

show abstract

“…have demonstrated its persistence in this tissue (see Vella et al, 1991Vella et al, , 1992. During acute infection, NK cells appear to play a role in the control of virus replication because lesions are least severe in the three strains with the highest endogenous levels of NK cell activity.…”

Section: Discussionmentioning

confidence: 99%

“…(Table 1). The histological changes seen in the 10 strains examined are presented fully elsewhere (Vella et al, 1992). Briefly, lesions of the exocrine pancreas were seen in all strains by 4 days p.i.…”

Section: Virus Isolation and Histological Findingsmentioning

confidence: 99%

Coxsackievirus B4 infection of the mouse pancreas: the role of natural killer cells in the control of virus replication and resistance to infection

Vella

Festenstein²

1992

Journal of General Virology

Self Cite

View full text Add to dashboard Cite

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

Cited by 28 publications

References 11 publications

Enterovirus infection in human pancreatic islet cells, islet tropism in vivo and receptor involvement in cultured islet beta cells

Enterovirus infection in human pancreatic islet cells, islet tropism in vivo and receptor involvement in cultured islet beta cells

Coxsackievirus B1-induced murine myositis: no evidence for viral persistence

Coxsackievirus B4 infection of the mouse pancreas: the role of natural killer cells in the control of virus replication and resistance to infection

Contact Info

Product

Resources

About