[Frontiers in Bioscience 16, 608-618, January 1, 2011]

Modulation of programmed cell death pathways by the hepatitis C virus

Jude Juventus Aweya1,2, Yee-Joo Tan 1,2

1Collaborative Anti-Viral Research Group, Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), Singapore. 2Department of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Contribution of structural proteins to apoptosis regulation
3.1. Core
3.1.1. Effects of core on extrinsic apoptotic pathways
3.1.2. Effects of core on intrinsic apoptotic pathways
3.1.3. Effects of core on other cellular pathways that contribute to apoptosis regulation
3.1.4. Effects of alternate reading frame proteins on apoptosis
3.2. E1 and E2
4. Contribution of non-structural proteins to apoptosis regulation
4.1. p7
4.2. NS2
4.3. NS3
4.4. NS4A
4.5. NS5A
4.6. NS5B
5. Apoptosis during infection by recombinant HCVcc
6. Involvement of other cell death pathways
7. Future studies
8. Acknowledgements
9. References

1. ABSTRACT

Hepatitis C virus (HCV), a positive stranded RNA virus of the family Flaviviridae, is the major cause of non-A, non-B hepatitis worldwide. The HCV genome encodes a precursor polyprotein of ~ 3,000 amino acids that is processed co-translationally and post-translationally to give rise to viral structural and non-structural proteins. Nearly all of these viral proteins have been shown to modulate cell death via various mechanisms. In addition, studies using the replicon and recombinant HCV cell culture systems have yield important insights into the modulation of programmed cell death by HCV replication. Here, we summarize current knowledge on the modulation of apoptosis and other programmed cell death pathways by the HCV in these cell culture systems.