Abstract
Interleukin-1β (IL-1β) concentrations are frequently elevated in central nervous system (CNS) viral infections, but the pathophysiologic significance of such elevations is not known. To examine the role of IL-1β in CNS viral pathogenesis, we compared the natural histories of IL-1β- deficient and wild-type 129 SV(ev) mice infected with a neurovirulent viral strain, neuroadapted Sindbis virus (NSV). We found that the incidence of severe paralysis and death was markedly decreased in NSV-infected IL-1β(-/- ) mice compared to NSV-infected wild-type mice (4 versus 88%, P < 0.001). Despite this marked difference in clinical outcome, no differences in numbers of apoptotic cells or presence of histopathologic lesions in the brains of moribund wild-type mice and those of clinically healthy IL-1β(-/-) mice could be detected. These results suggest that IL-1̄ deficiency is protective against fatal Sindbis virus infection by a mechanism that does not involve resistance to CNS virus-induced apoptosis or histopathology.
Original language | English (US) |
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Pages (from-to) | 2563-2567 |
Number of pages | 5 |
Journal | Journal of virology |
Volume | 73 |
Issue number | 3 |
DOIs | |
State | Published - 1999 |
ASJC Scopus subject areas
- Microbiology
- Immunology
- Insect Science
- Virology