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1 Negative Strand RNA Virus

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3 Negative Strand RNA Virus Editor Ming Luo The University of Alabama at Birmingham, USA World Scientific NEW JERSEY LONDON SINGAPORE BEIJING SHANGHAI HONG KONG TAIPEI CHENNAI

4 Published by World Scientific Publishing Co. Pte. Ltd. 5 Toh Tuck Link, Singapore USA office: 27 Warren Street, Suite , Hackensack, NJ UK office: 57 Shelton Street, Covent Garden, London WC2H 9HE British Library Cataloguing-in-Publication Data A catalogue record for this book is available from the British Library. NEGATIVE STRAND RNA VIRUS Copyright 2011 by World Scientific Publishing Co. Pte. Ltd. All rights reserved. This book, or parts thereof, may not be reproduced in any form or by any means, electronic or mechanical, including photocopying, recording or any information storage and retrieval system now known or to be invented, without written permission from the Publisher. For photocopying of material in this volume, please pay a copying fee through the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, USA. In this case permission to photocopy is not required from the publisher. ISBN ISBN Typeset by Stallion Press enquiries@stallionpress.com Printed in Singapore.

5 Contents Foreword vii Chapter 1. Overview of Negative-Strand RNA Viruses 1 Biao He Chapter 2. Rhabdovirus Entry into the Host Cell 15 Aurélie Albertini and Yves Gaudin Chapter 3. Virus Entry: Parainfluenza Viruses 35 Masato Tsurudome Chapter 4. Chapter 5. What Controls the Distinct VSV RNA Synthetic Processes of Replication and Transcription? 63 Gail Williams Wertz, Summer E. Galloway and Djamila Harouaka mrna Capping by Vesicular Stomatitis Virus and Other Related Viruses 79 Tomoaki Ogino and Amiya K. Banerjee Chapter 6. Structural Disorder within the Measles Virus Nucleoprotein and Phosphoprotein: Functional Implications for Transcription and Replication 95 Sonia Longhi v

6 vi Chapter 7. Contents Biochemical and Structural Insights into Vesicular Stomatitis Virus Transcription 127 Amal A. Rahmeh and Sean P. J. Whelan Chapter 8. Transcription of Vesicular Stomatitis Virus RNA Genome 149 Debasis Panda and Asit K. Pattnaik Chapter 9. Assembly of Vesicular Stomatitis Virus 175 Ming Luo, Todd J. Green and Z. Hong Zhou Chapter 10. Paramyxovirus Budding Mechanisms 193 Megan S. Harrison, Takemasa Sakaguchi and Anthony P. Schmitt Chapter 11. Chapter 12. Chapter 13. Virus Host Interaction by Members of the Family Rhabdoviridae and Filoviridae 219 Douglas S. Lyles Paramyxovirus and Rig-Like Helicases: A Complex Molecular Interplay Driving Innate Immunity 243 Denis Gerlier The Molecular and Cellular Biology of Emerging Bunyaviruses 261 John N. Barr Chapter 14. Ebolaviruses: What We Know and Where We Are on Potential Therapeutics 295 Peter Halfmann, Gabriele Neumann and Yoshihiro Kawaoka Index 309

7 Foreword The Negative Strand RNA Viruses are the causative agents of a large number of human and animal diseases. Several of the Negative Strand RNA Viruses have been classified by the United States National Institutes of Allergy and Infectious Diseases as category A, B or C priority pathogens, resulting in increased attention to both research on these viruses as well as to the development of vaccines and antiviral drugs. The Negative Strand RNA Viruses can be divided into those viruses with non-segment genomes (order Mononegavirales) and those viruses with segment RNA genomes. The Mononegavirales include bornavirus, vesicular stomatitis virus (VSV) and rabies virus, Marburg virus and Ebola virus, measles virus, mumps virus, Nipah virus, Hendra virus, canine distemper virus, Sendai virus, Newcastle disease virus, human parainfluenza viruses 1-4, parainfluenza virus 5 (formerly known as simian virus 5), human respiratory syncytial virus and human metapneumovirus. The segmented Negative Strand RNA Viruses include influenza A, B and C viruses, the bunyaviruses and the new and old world arenaviruses. In addition to studies on the mechanism of replication of these viruses and also studies on viral pathogenesis and epidemiology, several of the Negative Strand RNA Viruses have been used as model systems in cell biology, biochemistry and structural biology. The VSV glycoprotein (G) has served as a model to study the cellular exocytic pathway. The VSV RNA polymerase has been studied intensively as a model RNA polymerase. The influenza virus glycoproteins, hemagglutinin (HA) and neuraminidase, were among the earliest glycoproteins to have their structure determined at atomic resolution. The influenza virus HA together with the VSV G protein and parainfluenza virus 5 fusion (F) protein have served as model metastable proteins that undergo on triggering dramatic protein refolding and in doing so mediate the fusion of the viral envelope with a host cell membrane, enabling the viral nucleocapsid to enter the cytoplasm. vii

8 viii Foreword In this book are timely chapters on important topics to elucidate the biology of Negative Strand RNA Viruses. In two chapters the process of entry into the host cell by rhabdoviruses and parainfluenza virus are described. As befitting an important model system, four chapters describe different aspects of transcription and replication of VSV. For parainfluenza viruses the proteins involved in transcription are natively unfolded and this is described together with functional implications for transcription and replication. The assembly and budding of VSV and paramyxoviruses are reviewed together with virus host interactions of VSV and Ebola virus. The innate immune system and the mechanism by which paramyxoviruses counteract this cellular pathway are described. One chapter is devoted to discussing the molecular and cellular biology of emerging bunyaviruses and lastly a chapter describes the current status of potential therapeutics to Ebola virus. All of these chapters bring together a great deal of knowledge about the cellular, structural and molecular biology of Negative Strand RNA Viruses. Despite our current knowledge of Negative Strand RNA Viruses we still have not fully understood the switch between RNA transcription to synthesize mrnas and RNA replication to make anti-genome RNA strands and genomic RNA. The atomic structure of the RNA-dependent RNA polymerase has yet to be determined for any Negative Strand RNA virus. For those viruses that use their receptor binding protein to activate the fusion protein, a molecular description of how binding lowers the energy barrier for the fusion protein to cause virus entry into cells is only understood at a rudimentary level. Similarly, there is only fragmentary knowledge of how host-cell proteins interact with viral proteins to mediate the assembly and budding of most of the Negative Strand RNA Viruses. Although many scientists have made impressive advances in studying the innate immune response to Negative Strand RNA Viruses, there is still much to be learned about this complex cellular pathway. We still lack vaccines to important human pathogens such as respiratory syncytial virus, new and old world arenaviruses (particularly Lassa fever virus) and Ebola virus. Furthermore, anti-viral drugs are currently mostly a mirage on the horizon, the one major success story being inhibitors of influenza A and B virus neuraminidase, such as oseltamivir phosphate. Hopefully, a full understanding of the biology and the atomic structure of proteins for Negative Strand RNA Viruses will aid in devising new vaccines and provide new targets for the development of anti-viral drugs. Robert A. Lamb, Ph.D., Sc.D. Department of Molecular Biosciences Northwestern University