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SHORT ARTICLE |
Department of Microbiology, Faculty of Science, Mahidol University, Rama VI Road, Bangkok, Thailand
Corresponding author: Dr S. Ubol (e-mail: scsul{at}mahidol.mucc.ac.th).
Received 4 February 2000; revised version received 10 April 2000; accepted 11 April 2000.
Abstract
A laboratory strain of rabies virus has been reported to induce apoptosis in experimental animals. The present study demonstrated that a bat strain and a primary canine rabies virus isolate also induced apoptosis in vivo. This death process involved reactivation of the caspase gene, Nedd-2, a developmentally down-regulated apoptotic gene. Expression of Nedd-2 was significantly up-regulated in infected adult and suckling mice. Reactivation of Nedd-2 in infected adult mice started at around day 3 and was prominent on day 5. The level of expression was constantly high up to the time that mice showed signs of illness. Expression of Nedd-2 correlated with the appearance of apoptotic nuclei within the infected brain, suggesting that reactivation of a developmentally down-regulated gene, Nedd-2, may be required for apoptotic elimination of cells damaged by infection.
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