alexa Implication of Uncoupling Protein 2 in Immunity to Herpes Simplex Virus Type I in Resistant and Susceptible Mouse Strains | OMICS International | Abstract
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Journal of Neuroinfectious Diseases
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Research Article

Implication of Uncoupling Protein 2 in Immunity to Herpes Simplex Virus Type I in Resistant and Susceptible Mouse Strains

Laurie Rouger1, Yan Sergerie2, Denis Arsenijevic3, Eric Paradis1, Guy Boivin2, and Denis Richard1*

1Research Center of the Quebec City University Institute for Cardiology and Pneumology, 2725 Chemin Sainte-Foy, Sainte Foy, QC G1V 4G5, Canada

2Research Center in Infectious Diseases, CHUQ-CHUL and Laval University, Quebec City, QC G1V 4G2, Canada

3Division of Physiology, Department of Medicine, Faculty of Science, University of Fribourg, CH-1700 Fribourg, Switzerland

*Corresponding Author:
Denis Richard
Research Center of the Quebec City University Institute for Cardiology and Pneumology
2725 Chemin Sainte-Foy, Sainte Foy, QC G1V 4G5, Canada
E-mail: [email protected]

Received Date: 6 January 2011; Revised Date: 26 February 2011; Accepted Date: 7 March 2011

Abstract

The present results demonstrate resistance to HSV-1 in C57Bl6 mice is associated with differential temporal body weight and GSH changes, compared to susceptible 129Sv mouse strain. Strong brain viral load TK and TLR-2 induction in the brain precedes TNF-α, iNOS, IκBα and UCP2 expression in 129Sv mice. Interestingly, we observe that UCP2 brain expression differs: UCP2 is found in higher quantities in the mid and hind brain in susceptible mice and in the forebrain in resistant mice. In contrast with previous data, UCP2 KO mice did not show differences in terms of survival, inflammatory gene expression and neurodegeneration compared to their WT controls. UCP2 brain expression is therefore a marker of resistance/susceptibility to infection but does not play a role in viral load or survival. In conclusion, UCP2s role in host survival to infection may be pathogen specific and largely subordinate to the direct effect of the toxicity of changes in antioxidants on the infectious agent itself.

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