First Author | Manchester M | Year | 1999 |
Journal | J Neuroimmunol | Volume | 96 |
Issue | 2 | Pages | 207-17 |
PubMed ID | 10337919 | Mgi Jnum | J:343089 |
Mgi Id | MGI:7562602 | Doi | 10.1016/s0165-5728(99)00036-3 |
Citation | Manchester M, et al. (1999) Characterization of the inflammatory response during acute measles encephalitis in NSE-CD46 transgenic mice. J Neuroimmunol 96(2):207-17 |
abstractText | Expression of the human measles virus receptor, CD46, in the murine central nervous system allows infection and replication by wild-type human measles virus (MV) strains (Rall, G.F., Manchester, M., Daniels L.R., Callahan, E., Belman, A., Oldstone, M.B.A., 1997. A transgenic mouse model for measles virus infection of the brain. Proc. Natl. Acad. Sci. U.S.A. 94, 2243-2248). MV replicates in neurons in focal lesions of the cortex, hippocampus and thalamus, leading to death of the animals. In MV-infected CD46 transgenic mice, infiltration of CD4+ and CD8+ T-lymphocytes, B-lymphocytes and macrophages was seen. Upregulation of MHC class I and class II molecules was observed, along with reactive astrocytosis and microgliosis. Increased chemokine mRNAs, especially RANTES and IP-10, and cytokine RNAs IL-6, TNF-alpha, and IL1-beta were observed. Apoptosis of neurons also was increased. No MV replication or inflammation was seen in similarly inoculated nontransgenic littermates. These results further characterize the MV-induced encephalitis in CD46 transgenic mice and highlight similarities to MV infection of the human CNS. |