Histopathological follow-up of the pancreas and small intestines of mice, experimentally infected by the oral and intraperitoneal routes
Abstract number: 902_p911
Coxsackieviruses belong to genus Human Enterovirus of the family Picornaviridae. The natural infection is acquired by the faecaloral route, whereas in mouse studies the intraperitoneal route is used. We have established a new mouse model with infection by the oral route.
To compare the histological changes, viral persistence and localisation of the virus in the pancreas and the small intestines of mice, experimentally infected by oral or intraperitoneal route.
Mice were infected with CVB 3 (Nancy) by the oral or intraperitoneal route. Doses ranged from 5 × 103 to 5 × 109 TCID50. Selected organs from each mouse were embedded into paraffin and sections were attached on silanised slides. For histological observation the sections were stained by Mayer's haematoxylin eosin method. For localisation of the antigen by immunohistochemical staining, the VP1 protein served as an indicator for the presence of the virus. The method was standardised. The tissue sections were processed and stained by the avidinbiotin method, using the monoclonal mouse anti-enterovirus antibody against VP1 protein.
The histological observations reveal that the tissue of exocrine pancreas showed inflammatory changes on the 3rd, 7th, 10th, 14th and 21st day post-infection in exocrine pancreas of the intraperitoneally infected mice. After oral infection no destruction of the exocrine pancreas was observed, but on day 35th post-peroral infection liposis was seen. VP1 was detected mainly on the third and seventh days after infection in the small intestine. We found differences in VP1 localisation between oral and intraperitoneal infection. In small intestine of orally infected mice positive staining was localised in smooth intestinal muscles whereas after intraperitoneal infection. VP1 was detected within the villi. There was no correlation between the virus concentration and tissue damage.
The pathogenesis of CVB3 infection is influenced by the route of virus administration, which has direct implications for the use of mouse models to study the pathogenesis of Coxsackieviruses."
|Session name:||XXIst ISTH Congress|
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