cellular phenotype

• multifocal hepatic necrosis
  • with syncytial cell formation at necroscopy
  (MGI Ref ID J:31325)

mortality/aging

• lethality at weaning, complete penetrance
  • mice fail to thrive, with death occurring withing 48 hours of weaning
  (MGI Ref ID J:31325)

digestive/alimentary phenotype

• abnormal intestine morphology
  • intestinal lesions of necrotic foci with syncytial giant cells at necroscopy, incomplete penetrance
  (MGI Ref ID J:31325)

growth/size/body region phenotype

• decreased body size
  (MGI Ref ID J:31325)

hematopoietic system phenotype

• abnormal leukocyte physiology
  • splenocytes and macrophages failed to respond transcriptionally after exposure to IFN-gamma
  (MGI Ref ID J:31325)

immune system phenotype

• abnormal leukocyte physiology
  • splenocytes and macrophages failed to respond transcriptionally after exposure to IFN-gamma
  (MGI Ref ID J:31325)

• increased susceptibility to Coronaviridae infection
  • observed in conventional facility, where mouse hepatitis virus was common
  (MGI Ref ID J:31325)

• increased susceptibility to Riboviria infection
  • observed when exposed to vesicular stomatitis virus (VSV) under specific pathogen-free conditions
  (MGI Ref ID J:31325)

• increased susceptibility to viral infection
  • observed in conventional facility, where mouse hepatitis virus was common
  (MGI Ref ID J:31325)

liver/biliary system phenotype

• multifocal hepatic necrosis
  • with syncytial cell formation at necroscopy
  (MGI Ref ID J:31325)

hematopoietic system phenotype

• abnormal MHC II cell surface expression on macrophages
  • unstimulated bone marrow derived macrophages have much lower expression of class II on cell surface
  (MGI Ref ID J:130622)

mammalian phenotype

• immune system phenotype
  • Normal - mice are not susceptible to infection with an adapted human coronavirus 229E (HCoV-229E) that was produced by propagating the virus for 4 passages at 37 degrees Celsius on primary embryonic fibroblasts (HCoV-229E-37), showing no virus growth in lung, liver, spleen or small intestine
  (MGI Ref ID J:99728)

• vision/eye phenotype
  • Normal - lens development is normal
  (MGI Ref ID J:88422)

homeostasis/metabolism phenotype

• increased circulating interferon-gamma level
  • LPS administration leads to about 10-fold higher levels of IFN-gamma in the sera of mice compared to wild-type mice treated with LPS
  (MGI Ref ID J:130622)

immune system phenotype

• abnormal MHC II cell surface expression on macrophages
  • unstimulated bone marrow derived macrophages have much lower expression of class II on cell surface
  (MGI Ref ID J:130622)

• decreased level of surface class I molecules
  • unstimulated bone marrow derived macrophages have lower expression of class I on the cell surface
  (MGI Ref ID J:130622)

• decreased susceptibility to endotoxin shock
  • no mice die of LPS at a dose of 37 mg/kg body weight compared to 80% of Stat1^tm1Tdec homozygotes dying at this dose
  (MGI Ref ID J:130622)

• increased circulating interferon-gamma level
  • LPS administration leads to about 10-fold higher levels of IFN-gamma in the sera of mice compared to wild-type mice treated with LPS
  (MGI Ref ID J:130622)

• increased susceptibility to bacterial infection
  • mice all die when infected with 10⁴ or higher Listeria monocytogenes bacteria while all wild-type mice survive
  (MGI Ref ID J:130622)

• increased susceptibility to Riboviria infection
  • primary fibroblasts pre-treated with IFN-gamma and then exposed to vesicular stomatitis virus are all dead 24 hours later regardless of the amount of IFN-gamma used
  (MGI Ref ID J:130622)

• increased susceptibility to viral infection
  • primary fibroblasts pre-treated with IFN-gamma and then exposed to vesicular stomatitis virus are all dead 24 hours later regardless of the amount of IFN-gamma used
  (MGI Ref ID J:130622)

immune system phenotype

• increased susceptibility to Herpesvirales infection
  • slighty more susceptible to MCMV viral infection than wild-type
  (MGI Ref ID J:81243)

• increased susceptibility to Togaviridae infection
  • slighty more susceptible to Sindbis viral infection than wild-type
  (MGI Ref ID J:81243)

• increased susceptibility to viral infection
  • slighty more susceptible to MCMV and Sindbis viral infection than wild-type
  (MGI Ref ID J:81243)

endocrine/exocrine gland phenotype

• increased mammary adenocarcinoma incidence
  • mice develop spontaneous mammary adenocarcinoma with a median tumor onset of 14.5 months
  (MGI Ref ID J:216040)

integument phenotype

• increased mammary adenocarcinoma incidence
  • mice develop spontaneous mammary adenocarcinoma with a median tumor onset of 14.5 months
  (MGI Ref ID J:216040)

neoplasm

• increased mammary adenocarcinoma incidence
  • mice develop spontaneous mammary adenocarcinoma with a median tumor onset of 14.5 months
  (MGI Ref ID J:216040)

hematopoietic system phenotype

• abnormal NK cell physiology
  • NK cells have less proliferation in response to IFN-alpha treatment compared to controls and thus do not have the 2- to 6-fold gains in liver NK cell numbers that wild-type controls do
  (MGI Ref ID J:79552)
  • proportions of spleen NK cells expressing intracellular IFN-gamma from MCMV infected mice are increased
  (MGI Ref ID J:79552)
  • there is 75% less actively proliferating NK cells in the spleen after MCMV infection compared to controls
  (MGI Ref ID J:79552)

• impaired natural killer cell mediated cytotoxicity
  • NK cells fail to increase their cytolytic activity when treated with recombinant IFN-alpha
  (MGI Ref ID J:79552)
  • NK cells from MCMV-infected mice have about 3-fold less cytotoxicity than wild-type NK cells
  (MGI Ref ID J:79552)

homeostasis/metabolism phenotype

• increased circulating interferon-gamma level
  • serum IFN-gamma levels are 6-fold higher than controls in mice infected with MCMV
  (MGI Ref ID J:79552)

• increased circulating interleukin-12b level
  • mice infected with LCMV have 5-fold higher levels of IL-12 p40 than in controls
  (MGI Ref ID J:79552)

immune system phenotype

• abnormal NK cell physiology
  • NK cells have less proliferation in response to IFN-alpha treatment compared to controls and thus do not have the 2- to 6-fold gains in liver NK cell numbers that wild-type controls do
  (MGI Ref ID J:79552)
  • proportions of spleen NK cells expressing intracellular IFN-gamma from MCMV infected mice are increased
  (MGI Ref ID J:79552)
  • there is 75% less actively proliferating NK cells in the spleen after MCMV infection compared to controls
  (MGI Ref ID J:79552)

• impaired natural killer cell mediated cytotoxicity
  • NK cells fail to increase their cytolytic activity when treated with recombinant IFN-alpha
  (MGI Ref ID J:79552)
  • NK cells from MCMV-infected mice have about 3-fold less cytotoxicity than wild-type NK cells
  (MGI Ref ID J:79552)

• increased circulating interferon-gamma level
  • serum IFN-gamma levels are 6-fold higher than controls in mice infected with MCMV
  (MGI Ref ID J:79552)

• increased circulating interleukin-12b level
  • mice infected with LCMV have 5-fold higher levels of IL-12 p40 than in controls
  (MGI Ref ID J:79552)