mortality/aging
• most mice die a few hours after symptoms (ataxia and paralysis) appear at either 3 (4 of 5) or 4 (1 of 5) days post HSV1 infection; while only 3 of 5 wild-type mice die by 6 days after infection
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immune system
• marked reduction in IFN-alpha and IFN-beta in response to HSV1 infection
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• marked reduction in IFN-alpha and IFN-beta in response to HSV1 infection
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• lung fibroblasts transfected with interferon stimulatory DNA or herring testis DNA fail to produce any detectable level of IFN-beta
• induction of IFN-beta in lung fibroblasts infected with the DNA viruses; herpes simplex virus 1 (HSV1), vaccinia virus (VACV) and a mutant strain of HSV1called d109 is largely abolished
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• production of IFN-beta and TNF in bone marrow derived macrophages transfected with interferon stimulatory DNA or herring testis DNA are defective
• induction of IFN-beta in l bone marrow derived macrophages infected with VACV or HSV1 strains d109 or 7134 is largely abolished
• induction of IFN-beta in l bone marrow derived macrophages infected with HSV1 is severely but not completely blocked
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• cultured conventional dendritic cells fail to induce IFN-alpha or IFN-beta following transfection with interferon stimulatory DNA or herring testis DNA
• cultured conventional dendritic cells fail to induce IFN-beta following infections with HSV1 strain d109 or VACV and induction by wild-type HSV1 is partially inhibited
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• induction of IFN-alpha and IFN-beta by interferon stimulatory DNA, poly[dA:dT], and genomic DNA from E. coli and Vibrio cholerae in the presence of liposome is abolished
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• following intravenous infection with HSV1, levels of IFN-alpha and IFN-beta are reduced, 4 of 5 mice develop ataxia and paralysis by 3 days after infection
• high levels of HSV1 are found in the brain at day 3 after infection in mutants but not in wild-type controls
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• most mice die a few hours after symptoms (ataxia and paralysis) appear at either 3 (4 of 5) or 4 (1 of 5) days post HSV1 infection; while only 3 of 5 wild-type mice die by 6 days after infection
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homeostasis/metabolism
• marked reduction in IFN-alpha and IFN-beta in response to HSV1 infection
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• marked reduction in IFN-alpha and IFN-beta in response to HSV1 infection
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hematopoietic system
• production of IFN-beta and TNF in bone marrow derived macrophages transfected with interferon stimulatory DNA or herring testis DNA are defective
• induction of IFN-beta in l bone marrow derived macrophages infected with VACV or HSV1 strains d109 or 7134 is largely abolished
• induction of IFN-beta in l bone marrow derived macrophages infected with HSV1 is severely but not completely blocked
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