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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