Abstract |
We have evaluated the effect of rabies virus infection on interleukin-1 alpha (IL-1 alpha) production and its receptors in mouse brain. Study of virus dissemination in the central nervous system (CNS) showed a massive infection of main brain structures from day 4 post infection (p.i.) up to the agony stage on day 6 p.i. At the same time, IL-1 alpha concentrations increased in cortical and hippocampal homogenates, whereas no change was detected in serum. In non-infected mice, IL-1 alpha binding sites were observed in the dentate gyrus, the cortex, the choroid plexus, the meninges and the anterior pituitary. During rabies virus infection, a striking decrease in IL-1 alpha binding sites was observed on day 4 p.i. with a complete disappearance on day 6 p.i., except in the pituitary gland where they remained at control level. In conclusion, concomitantly with the early rabid pathological signs, brain IL-1 alpha production and IL-1 alpha binding sites are specifically and significantly altered by brain viral proliferation. These results indicate that IL-1 alpha could be involved in the brain response to viral infection as a mediator and could participate in the genesis of the rabies pathogeny.
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Authors | C Marquette, P E Ceccaldi, E Ban, P Weber, H Tsiang, F Haour |
Journal | Archives of virology
(Arch Virol)
Vol. 141
Issue 3-4
Pg. 573-85
( 1996)
ISSN: 0304-8608 [Print] Austria |
PMID | 8645096
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Interleukin-1
- Receptors, Interleukin-1
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Topics |
- Animals
- Brain
(metabolism, pathology, virology)
- Cerebral Cortex
(metabolism)
- Hippocampus
(metabolism)
- Interleukin-1
(biosynthesis)
- Male
- Mice
- Mice, Inbred BALB C
- Rabies
(metabolism)
- Rabies virus
(physiology)
- Receptors, Interleukin-1
(metabolism)
- Virus Replication
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