[Frontiers in Bioscience 14, 2181-2192, January 1, 2009]

Apoptotic signaling cascades operating in poliovirus-infected cells

Bruno Blondel1, Arnaud Autret1, Cynthia Brisac1, Sandra Martin-Latil1, Laurence Mousson1, Isabelle Pelletier1, Jerome Estaquier2, Florence Colbere-Garapin1

1Biologie des Virus Enteriques, Institut Pasteur, 28 rue du Docteur Roux, 75724 Paris cedex 15, France, 2INSERM U841, 94010 Creteil, France

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Poliovirus
3.1. Structure of the virion
3.2. Poliovirus receptor
3.3. Viral cycle
3.4. Effect of poliovirus replication on the host cell
4. Pathogenesis of poliomyelitis and post-polio syndrome
5. Poliovirus and apoptosis
5.1. Poliovirus-induced apoptosis in nerve cells in vivo and ex vivo.
5.2. Poliovirus-induced apoptosis in non-neuronal cells in vitro
5.3. CD155 and apoptosis
5.4. Poliovirus induces simultaneously the JNK-mediated cell death and the PI3K/Akt suvival pathways in neuroblastoma cells
5.4.1. Poliovirus induces Bax-dependent cell death mediated by c-Jun NH2-terminal kinase
5.4.2. Early PI3K/Akt survival pathways activation limits poliovirus-induced JNK-mediated cell death in neuroblastoma cells
6. Concluding remarks
7. Acknowledgements
8. References

1. ABSTRACT

The flaccid paralyses characteristic of poliomyelitis are a direct consequence of the infection of motor neurons with poliovirus (PV). In PV-infected mice, motor neurons die by apoptosis. However, the mechanisms by which PV induces cell death in neurons remain unclear. Analyses of the apoptotic pathways induced by PV infection in several cell lines have demonstrated that mitochondria play a key role in PV-induced apoptosis. Furthermore, mitochondrial dysfunction results from an imbalance between pro- and anti-apoptotic pathways. We present here an overview of the many studies of PV-induced apoptosis carried out in recent years and discuss the contribution of these studies to our understanding of poliomyelitis.