Cellular prion protein prevents brain damage after encephalomyocarditis virus infection in mice

Cellular prion protein prevents brain damage after encephalomyocarditis virus infection in mice Cellular prion protein (PrP C ), a cell-surface glycoprotein normally associated with neurons, is also expressed in other cell types such as glia and lymphocytes. To further elucidate these roles of PrP C , wild-type prion protein gene ( Prnp +/+ ) mice and Prnp -deficient ( Prnp −/− ) mice were infected with encephalomyocarditis virus B variant (EMCV-B) via an intracranial route. EMCV-B causes encephalitis and apoptotic cell death in vivo. Histopathological studies revealed that Prnp +/+ mice infected with 600 pfu of EMCV-B showed more severe infiltration of inflammatory cells, accompanied by higher activation of microglia cells around the hippocampus, than Prnp −/− mice; viz., no differences in the brain virus titer between these two lines of mice. Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP, nick end-labeling (TUNEL) staining of the brain specimens revealed that the CA1 hippocampal pyramidal cells showed a larger number of apoptotic neurons in Prnp −/− than Prnp +/+ mice. Based on all these findings, PrP C may play certain roles in the induction of inflammation and inhibition of apoptosis in vivo. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Cellular prion protein prevents brain damage after encephalomyocarditis virus infection in mice

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Publisher
Springer Vienna
Copyright
Copyright © 2008 by Springer-Verlag
Subject
Biomedicine; Infectious Diseases; Medical Microbiology ; Virology
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-008-0086-x
Publisher site
See Article on Publisher Site

Abstract

Cellular prion protein (PrP C ), a cell-surface glycoprotein normally associated with neurons, is also expressed in other cell types such as glia and lymphocytes. To further elucidate these roles of PrP C , wild-type prion protein gene ( Prnp +/+ ) mice and Prnp -deficient ( Prnp −/− ) mice were infected with encephalomyocarditis virus B variant (EMCV-B) via an intracranial route. EMCV-B causes encephalitis and apoptotic cell death in vivo. Histopathological studies revealed that Prnp +/+ mice infected with 600 pfu of EMCV-B showed more severe infiltration of inflammatory cells, accompanied by higher activation of microglia cells around the hippocampus, than Prnp −/− mice; viz., no differences in the brain virus titer between these two lines of mice. Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP, nick end-labeling (TUNEL) staining of the brain specimens revealed that the CA1 hippocampal pyramidal cells showed a larger number of apoptotic neurons in Prnp −/− than Prnp +/+ mice. Based on all these findings, PrP C may play certain roles in the induction of inflammation and inhibition of apoptosis in vivo.

Journal

Archives of VirologySpringer Journals

Published: Jun 1, 2008

References

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