Affiliation:
1. Unité de Neurovirologie et Régénération du Système Nerveux, Institut Pasteur, 75724 Paris cedex 15
2. Laboratoire de Génétique et Biologie Cellulaire, CNRS UPRES-A 8087, Université de Versailles/Saint-Quentin, 78035 Versailles, France
Abstract
ABSTRACT
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 CD155
Thr67
and the nonmutated IMR-32 CD155 (CD155
IMR
) 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-CD155
Thr67
cells than in LM-CD155
IMR
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.
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
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