mortality/aging
• all mice die within 4 days after VSV
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immune system
N |
• at 18 h after i.v. injection with the DNA HSV-1 virus (1 107 pfu per g body weight), mice show normal induction of Ifna, Ifnb1, Ifit1 and Il6 mRNA levels in liver, spleen and lung, and no differences in serum IFN-alpha, IFN-beta and IL-6 levels or in lung pathology relative to HSV-1-infected wild-type controls
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• isolated peritoneal macrophages show a marked reduction in VSV-dependent induction of phosphorylated IRF3 (p-IRF3), consistent with a reduced antiviral innate response to RNA viruses
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• at 18 h after i.v. VSV infection (2 106 pfu per g body weight), mice show significantly lower serum IFN-alpha levels than wild-type controls
• at 24 h after intranasal injection with influenza virus strain A/Puerto Rico/1981 H1N1 (PR8), mice show significantly lower serum IFN-alpha levels than wild-type controls
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• at 18 h after i.v. VSV infection (2 106 pfu per g body weight), mice show significantly lower serum IFN-beta levels than wild-type controls
• at 24 h after intranasal injection with influenza virus strain A/Puerto Rico/1981 H1N1 (PR8), mice show significantly lower serum IFN-beta levels than wild-type controls
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• at 18 h after i.v. VSV infection (2 106 pfu per g body weight), mice show significantly lower serum IL-6 levels than wild-type controls
• at 24 h after intranasal injection with influenza virus strain A/Puerto Rico/1981 H1N1 (PR8), mice show significantly lower serum IL-6 levels than wild-type controls
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• at 18 h after i.v. VSV injection, mice exhibit a significantly lower induction of Ifit1 mRNA levels (an IFN-stimulated gene) in liver, spleen and lung relative to wild-type controls
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• at 12h after VSV infection, isolated peritoneal macrophages produce significantly less IFN-alpha than wild-type cells
• at 18 h after i.v. VSV infection, mice show a significantly lower induction of Ifna mRNA levels in liver, spleen and lung relative to wild-type controls
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• at 12h after VSV infection, isolated peritoneal macrophages produce significantly less IFN-beta than wild-type cells
• at 18 h after i.v. VSV infection, mice exhibit a significantly lower induction of Ifnb1 mRNA levels in liver, spleen and lung relative to wild-type controls
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• at 12h after VSV infection, isolated peritoneal macrophages produce significantly less IL-6 than wild-type cells
• at 18 h after i.v. VSV infection, mice exhibit a significantly lower induction of Il6 mRNA levels in liver, spleen and lung relative to wild-type controls
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• at 18 h after i.v. VSV
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• all mice die within 4 days after VSV
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homeostasis/metabolism
• at 18 h after i.v. VSV infection (2 106 pfu per g body weight), mice show significantly lower serum IFN-alpha levels than wild-type controls
• at 24 h after intranasal injection with influenza virus strain A/Puerto Rico/1981 H1N1 (PR8), mice show significantly lower serum IFN-alpha levels than wild-type controls
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• at 18 h after i.v. VSV infection (2 106 pfu per g body weight), mice show significantly lower serum IFN-beta levels than wild-type controls
• at 24 h after intranasal injection with influenza virus strain A/Puerto Rico/1981 H1N1 (PR8), mice show significantly lower serum IFN-beta levels than wild-type controls
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• at 18 h after i.v. VSV infection (2 106 pfu per g body weight), mice show significantly lower serum IL-6 levels than wild-type controls
• at 24 h after intranasal injection with influenza virus strain A/Puerto Rico/1981 H1N1 (PR8), mice show significantly lower serum IL-6 levels than wild-type controls
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hematopoietic system
• isolated peritoneal macrophages show a marked reduction in VSV-dependent induction of phosphorylated IRF3 (p-IRF3), consistent with a reduced antiviral innate response to RNA viruses
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