Absence of the p55 Kd TNF-alpha receptor promotes survival in rabies virus acute encephalitis. View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2000-01

AUTHORS

S Camelo, M Lafage, M Lafon

ABSTRACT

We investigated the role played by inflammation in acute encephalitis following infection with a neurotropic virus by comparing the disease caused by the CVS strain of rabies virus in C57BL/6 and mice deficient for the p55 Kd TNF-alpha receptor (p55TNFR-/-). Morbidity (weight loss and paralysis) and mortality of infected mice were associated with viral propagation, cytokine (IL-6, IL-10, TNF-alpha and IFN-gamma) production, induction of apoptosis and infiltration of inflammatory cells. Mortality occurred later in p55TNFR-/- (than in C57BL/6 mice. In contrast, morbidity and the number of cells undergoing apoptosis were similar in C57BL/6 and p55TNFR-/- mice.) This suggests that morbidity and mortality are independently regulated and that the death of the animal was not due to CNS apoptosis. Delayed mortality correlated with: a reduction in viral load on day 9 p.i., an increase in IFN-gamma and IL-10 concentrations and a reduction in inflammatory cell infiltration in the CNS. Thus, these data indicate that CVS infection elicits an inflammatory response within the CNS and suggest that cytokines signaling via the p55 Kd TNF-alpha receptor is deleterious for the survival of the host. These results strongly suggest that, the modulation of TNF-alpha and upregulation of IFN-gamma would be a powerful anti-virus strategy in cases of viral encephalitis. More... »

PAGES

507-18

Identifiers

URI

http://scigraph.springernature.com/pub.10.3109/13550280009091951

DOI

http://dx.doi.org/10.3109/13550280009091951

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1070985838

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11175323


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