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Journal of Virology, March 1999, p. 2563-2567, Vol. 73, No. 3
Departments of
Medicine1 and
Pathology,2 Columbia University College
of Physicians & Surgeons, New York, New York 10032
Received 16 September 1998/Accepted 18 November 1998
Interleukin-1
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Resistance of Interleukin-1
-Deficient Mice to
Fatal Sindbis Virus Encephalitis
(IL-1
) 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-1
in CNS viral pathogenesis, we compared the
natural histories of IL-1
-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-1
/
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-1
/
mice
could be detected. These results suggest that IL-1
deficiency is
protective against fatal Sindbis virus infection by a mechanism that
does not involve resistance to CNS virus-induced apoptosis or histopathology.
*
Corresponding author. Mailing address: Department of
Medicine, Columbia University College of Physicians & Surgeons, P & S 8-444, 630 W. 168th St., New York, NY 10032. Phone: (212) 305-7312. Fax: (212) 305-7290. E-mail:
Levine{at}cuccfa.ccc.columbia.edu.
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