Phenotypes for Tg(CD46)2Gsv MGI:3689178 MGI Mouse

premature death ( J:109895 )

• 94% of transgenic mice (mortality of all transgenics is similar, regardless of background) die within 3 weeks of infection (regardless of background), but no non-transgenic littermates become ill

abnormal chemokine level ( J:109895 )

• CC chemokines (RANTES, MIP-alpha and -beta, and MCP-1) and CXC chemokines (IP-10 and TCA-3, or MIG) are detected in brains of infected mice but EOTXN, LTN and MIP-2 are not

abnormal cell-mediated immunity ( J:109895 )

• infected transgenic mice that were primed with LCMV virus 60-90 days earlier can not mount an MHC-restricted cytotoxic T lymphocyte response to LCMV-infected targets

decreased cytotoxic T cell cytolysis ( J:109895 )

• cytotoxic T cells can only lyse LCMV-infected MHC class I but not class II targets

abnormal humoral immune response ( J:109895 )

• humoral immune response is suppressed in infected transgenic mice; no antibody response to sheep red blood cells is generated while transgenic mice inoculated with vehicle instead of MV generated a significant antibody response

abnormal cytokine secretion ( J:109895 )

• at 6 days postinfection, a 6-fold increase in Il-12 expression (RNA), an 11-fold increase in lymphotoxin-beta and a 17-fold increase in TNFalpha expression are detected in brains of transgenic mice

increased susceptibility to Paramyxoviridae infection ( J:109895 )

• multiple cell types from transgene-expressing mice, including transgenic mice on various other mixed or congenic backgrounds can be infected with measles virus (MV); cells become infected, express virus antigens, and release infectious viral progeny when cocultivated with permissive Vero cells (African green monkey kidney epithelial) compared to wild-type mouse cells

• neurons and lymphoid cells in the blood, spleen and lymph nodes express viral proteins and RNA upon injection of 10³ pfu; in spleen and lymph nodes, MV is expressed primarily in T cell-enriched areas whereas cells from non-transgenic mice don't express viral proteins

abnormal response to transplant ( J:113644 )

• transplanted hearts expressing the transgene slow down initially upon human serum perfusion, but recover while non-transgenic hearts (8/8) cease beating entirely

abnormal heart morphology ( J:113644 )

• transgenic and normal hearts develop white discoloration upon slowing or cessation of heart beat after normal human serum perfusion, but transgenic hearts resume beating and normal coloration within 15 minutes

• 7/10 transgenic hearts resume functioning after ~3-5 minutes and begin beating normally within 15 minutes

decreased heart rate ( J:113644 )

• heart rate of transgenic hearts perfused with normal human serum after transplantion slows down similar to normal hearts perfused with decomplemented human serum; all non transgenic hearts perfused with normal human serum slow down immediately, resulting in white discoloration and complete cessation of heart beat within 3-5 minutes

increased neuron apoptosis ( J:109895 )

• MV-infected transgenic mice have 50 to 100-fold more apoptotic primary neurons than innoculated non-transgenic mice or transgenic mice that received a needle wound in the brain

astrocytosis ( J:109895 )

• generalized astrocytosis accompanies MV replication and spread, with infiltration of CD4+ and some CD8+ T cells into the brain parenchyma

abnormal neuron morphology ( J:109895 )

• viral proteins and RNA are expressed in the CNS after inoculation; numerous MV nucleocapsids are present in neurons in optic tegmentum, cerebral cortex, hippocampus and cerebellum, moving into axons with normal and disorganized microtubules