immune system
• following infection with herpes simplex virus type 1 (HSV-1), vaccinia virus (VACV) or murine cytomegalovirus (MCMV) DNA viruses, serum C-X-C motif chemokine 10 (CXCL10) levels are significantly lower than those in wild-type controls
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• following infection with HSV-1, VACV or MCMV DNA viruses, serum IFN-beta levels are significantly lower than those in wild-type controls
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• following infection with HSV-1, VACV or MCMV DNA viruses, serum IL-6 levels are significantly lower than those in wild-type controls
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• mice exhibit impaired innate immune response to DNA viruses
• cytosolic dsDNA- and DNA virus-triggered induction of downstream effector genes is inhibited in primary mouse immune cells and embryonic fibroblasts
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• mice are more susceptible to VACV-induced death than wild-type controls
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• at 6 days after intranasal infection with herpes simplex virus type 1 (HSV-1), mice exhibit significantly higher HSV-1 genomic copy numbers and viral titers in the brain and greater infiltration of immune cells and tissue damage in the lungs than similarly-infected wild-type controls
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• mice are more susceptible to HSV-1-induced death than wild-type controls
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homeostasis/metabolism
• following infection with herpes simplex virus type 1 (HSV-1), vaccinia virus (VACV) or murine cytomegalovirus (MCMV) DNA viruses, serum C-X-C motif chemokine 10 (CXCL10) levels are significantly lower than those in wild-type controls
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• following infection with HSV-1, VACV or MCMV DNA viruses, serum IFN-beta levels are significantly lower than those in wild-type controls
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• following infection with HSV-1, VACV or MCMV DNA viruses, serum IL-6 levels are significantly lower than those in wild-type controls
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mortality/aging
• mice are more susceptible to HSV-1-induced death than wild-type controls
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• mice are more susceptible to VACV-induced death than wild-type controls
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