| First Author | Sauder C | Year | 2000 |
| Journal | J Virol | Volume | 74 |
| Issue | 19 | Pages | 9267-80 |
| PubMed ID | 10982374 | Mgi Jnum | J:64497 |
| Mgi Id | MGI:1889418 | Doi | 10.1128/jvi.74.19.9267-9280.2000 |
| Citation | Sauder C, et al. (2000) Chemokine gene expression in astrocytes of Borna disease virus-infected rats and mice in the absence of inflammation. J Virol 74(19):9267-80 |
| abstractText | Borna disease virus (BDV) causes CD8(+) T-cell-mediated meningoencephalitis in immunocompetent mice and rats, thus providing a valuable animal model for studying the mechanisms of virus-induced central nervous system (CNS) immunopathology. Chemokine-mediated leukocyte recruitment to the CNS is a crucial step in the development of neurological disease. We found increased mRNA levels of IP-10 and other chemokines in brains of adult rats following infection with BDV. The marked increase in chemokine gene expression at about day 8 postinfection seemed to immediately precede the inflammatory process. In brains of rats infected as newborns, in which inflammation was only mild and transient, sustained expression of IP-10 and RANTES genes was observed. In situ hybridization studies revealed that astrocytes were the major source of IP-10 mRNAs in brains of rats infected as newborns and as adults. In brains of infected mice lacking CD8(+) T cells (beta2m(0/0)), transcripts encoding IP-10 and RANTES were also observed. IP-10 transcripts were also present in a small number of scattered astrocytes of infected knockout mice lacking mature B and T cells as well as functional alpha/beta and gamma interferon receptors, indicating that BDV can induce chemokine synthesis in the absence of interferons and other B- or T-cell-derived cytokines. These data provide strong evidence that CNS-resident cells are involved in the early localized host immune response to infection with BDV and support the concept that chemokines are pivotal for the initiation of virus-induced CNS inflammation. |
