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Journal of Virology, January 2003, p. 790-798, Vol. 77, No. 1
0022-538X/03/$08.00+0 DOI: 10.1128/JVI.77.1.790-798.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Unité de Neurovirologie et Régénération du Système Nerveux, Institut Pasteur, 75724 Paris cedex 15,1 Laboratoire de Génétique et Biologie Cellulaire, CNRS UPRES-A 8087, Université de Versailles/Saint-Quentin, 78035 Versailles, France2
Received 8 May 2002/ Accepted 24 September 2002
Poliovirus (PV) can establish persistent infections in human neuroblastoma IMR-32 cells. We previously showed that during persistent infection, specific mutations were selected in the first extracellular domain of the PV receptor (CD155) of these cells (N. Pavio, T. Couderc, S. Girard, J. Y. Sgro, B. Blondel, and F. Colbère-Garapin, Virology 274:331-342, 2000). These mutations included the Ala 67
Thr substitution, corresponding to a previously described allelic form of the PV receptor. The mutated CD155Thr67 and the nonmutated IMR-32 CD155 (CD155IMR) were expressed independently in murine LM cells lacking the CD155 gene. Following infection of the cells with PV, we analyzed the death of cells expressing these two forms of CD155. Levels of DNA fragmentation, caspase activity, and cytochrome c release were lower in LM-CD155Thr67 cells than in LM-CD155IMR cells. Thus, the level of apoptosis was lower in cells expressing mutated CD155 selected during persistent PV infection in IMR-32 than in cells expressing the wild-type receptor.
* Corresponding author. Mailing address: Unité de Neurovirologie et Régénération du Système Nerveux, Institut Pasteur, 28 rue du Docteur Roux, 75724 Paris cedex 15, France. Phone: (33) 1.45.68.87.62. Fax: (33) 1.40.61.34.21. E-mail: bblondel{at}pasteur.fr.
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