Bookflare net enteroviruses omics, molecular biology, and control

A A A A 47 A A 13 A A 61 M A 75 M m 13 a2 v b 52 B M 104 B B M B7 M B9 M B 48 M B 00 M B1 EV RV -B Enteroviruses Omics, Molecular Biology, and Control -C V R RV -A A 68 M A 20 M A 51 A 102 M A A 6103 A 06 A 171 M A 45 M A d 08 M Ad C 35 C 49 C 04 C 19 C 50 C 14 C 48 C 33 C 47 C 40 C 02 C 09 C 46 C 36 C 26 C5 C 371 C C C 42 C 32 C 39 C 13 C 07 C 21 C 003 C C 010 C21 C4 B M B 101 M B 02 M B 35 M B 83 M B 79 M B1 M B 72 M BB 03 B 06 M B 103 M B 37 M B 86 M B 26 M B 004 M B 45 M B 99 M B 27 M B 93 M B 97 M B 84 C 11 C 38 C 05 C 27 C 20 C 34 C 29 C 450 C31 C4 C 215 C 24 C 25 C 18 C 28 C 08 C 31 C 16 C 17 C C Edited by William T Jackson and Carolyn B Coyne Caister Academic Press Enteroviruses Omics, Molecular Biology, and Control https://doi.org/10.21775/9781910190739 Edited by William T Jackson Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA and Carolyn B Coyne Department of Pediatrics, University of Pittsburgh, Pittsburgh, PA, USA Caister Academic Press Copyright © 2018 Caister Academic Press Norfolk, UK www.caister.com British Library Cataloguing-in-Publication Data A catalogue record for this book is available from the British Library ISBN: 978-1-910190-73-9 (paperback) ISBN: 978-1-910190-74-6 (ebook) Description or mention of instrumentation, software, or other products in this book does not imply endorsement by the author or publisher The author and publisher not assume responsibility for the validity of any products or procedures mentioned or described in this book or for the consequences of their use All rights reserved No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission of the publisher No claim to original U.S Government works Cover design adapted from Figure 4.1 Ebooks Ebooks supplied to individuals are single-user only and must not be reproduced, copied, stored in a retrieval system, or distributed by any means, electronic, mechanical, photocopying, email, internet or otherwise Ebooks supplied to academic libraries, corporations, government organizations, public libraries, and school libraries are subject to the terms and conditions specified by the supplier Contents Preface  v Enteroviruses Future Enterovirus Receptors and Entry Hijacking Host Functions for Translation and RNA Replication by Enteroviruses 23 The Omics of Rhinoviruses  51 Viral Population Dynamics and Sequence Space 69 Enterovirus Control of Cytoplasmic RNA Granules 93 The Autophagic Pathway and Enterovirus Infection 113 The Lipid Blueprints of Replicating Viral Genomes 129 Karla Kirkegaard Jacqueline D Corry, Jeffrey M Bergelson and Carolyn B Coyne Sonia Maciejewski and Bert L Semler Ann C Palmenberg Gonzalo Moratorio and Marco Vignuzzi Richard E Lloyd William T Jackson Nihal Altan-Bonnet, Marianita Santiana and Olha Ilnytska Index145 Current Books 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Microbiology: Technology and Applications2015 Full details at www.caister.com Preface The 12 species of the Enteroviruses – enterovirus A–H, enterovirus J, and rhinovirus A–C – are responsible, by many accounts, for more morbidity than any other viruses The diversity of diseases caused by these genetically similar viruses is enormous, from the common cold to hand, foot and mouth disease to more serious diseases including cardiac infection, bulbar paralysis, and encephalitis Despite, or possibly because of, their success as pathogens, these prevalent and successful viruses function as highly efficient machines Their entire genomes are usually under 8000 nucleosides, perhaps the size of two human genes, in a single positive-sense RNA molecule The single open reading frames typically encode a single polyprotein which is produced in the absence of typical 5′ cap signals, through use of an internal ribosome entry site The polyprotein is cleaved, by viral proteases encoded within the polyprotein itself, into the proteins required to facilitate virus replication A subset of these proteins produce a negative sense copy of the genome, which in turn are used to template more positive sense genomes for further translation and, ultimately, packaging in nascent virions The typical end of the cycle is cell lysis and virus release, although not all infections are lytic and virus can be shed throughout the life cycle as naked and enveloped virions Poliovirus, which remains by far the best-studied member of the genus, is on the verge of eradication in the wild Yet much more work remains to be done, as improvements in available poliovirus vaccines will be needed to complete the final challenges of eradication In the meantime, enteroviruses D68 and 71 have emerged as significant public health threats over the last decade, and while the available data from study of other Enteroviruses have jump-started research on these viruses, there are clearly enormous differences between the Enteroviruses, such that nothing can be taken for granted or assumed when studying a new member of the genus In this volume, some of the best researchers in the Enterovirus field take the reader on a tour of the most exciting frontiers in the study of the genus From understanding viral entry into cells, translation of the genome, and RNA–RNA replication, to the dynamic genomics of these viruses, to studies of viral avoidance of host cell defenses and lipid-mediated exit from cells, the topics are cutting-edge and the expertise second to none We are proud to bring you a collection of chapters representing the best of the field and our latest understanding of the genus Enterovirus We hope you enjoy reading it as much as we have enjoyed assembling and editing it William T Jackson Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA Carolyn B Coyne Department of Pediatrics, University of Pittsburgh, Pittsburgh, PA, USA Enteroviruses Future Karla Kirkegaard Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA Correspondence: karlak@stanford.edu https://doi.org/10.21775/9781910190739.01 Abstract At a time when poliovirus, the flagship Enterovirus, is on the brink of eradication, and while other Enteroviruses are simultaneously just emerging as serious public health threats, studies focused on the Enteroviruses and other picornaviruses are as important as ever The true nature of cell exit and cell-to-cell movement by these viruses, for example, is only now being elucidated, particularly taking advantage of recent advances in cell modelling of physiologically relevant cell systems Modern genomic techniques are just beginning to allow a population-level understanding of mutation and adaptation in these viruses, and are sure to reveal novel drug targets based on the cis/trans genetics of viral genomic regions Continued understanding of the basic life cycle of these viruses, and of their genomes, will allow novel avenues of vaccine development In the slightly more distant future, infection by Enteroviruses will be rapidly diagnosed and treatments may be tailored by personalized medicine Finally, Enteroviruses are only beginning to be used as tools, particularly as anticancer therapeutics It is impossible to see the future, but as the field moves forward, it is clear that both basic and applied Enterovirus research will remain an important topic for decades to come Introduction It is a privilege to write an introduction to this compendium of cutting-edge Enterovirus research We find ourselves at an interesting time Poliovirus, we hope, is on the brink of eradication, due to the dedicated use of two very effective vaccines, although each has its drawbacks Newly prominent pathogens such as enterovirus 71 and enterovirus D68 are currently causing considerable morbidity and mortality in humans Foot-and-mouth disease virus is somewhat controlled, thanks to the world’s first genetically engineered vaccine, but continues to be a dreaded scourge of livestock because of the rapid spread of even occasional outbreaks An excellent subunit vaccine for hepatitis A has been developed, although its use in areas where hepatitis A is most threatening to human health is limited No vaccines exist for rhinoviruses, coxsackieviruses, or any other Enteroviruses other than those mentioned above No FDA-approved antiviral to any Enterovirus is available Thus, intensive study of Enteroviruses is certainly warranted from the point of view of amelioration of human and 2  | Kirkegaard animal disease Both anticipated developments in vaccination and antivirals will be discussed below From a basic science perspective, we can certainly point to many findings – receptordependent tropism, internal ribosomal entry, RNA-dependent RNA polymerase activity and protease-mediated inhibition of critical cellular proteins, just to mention a few – that have proved ground-breaking in virology and beyond However, given the spectacular and effective focus on hepatitis C virology in recent years, previous claims that Enteroviruses are the best-studied model systems for positive-strand RNA viruses have received a serious challenge Yet, so many interesting questions remain! Curiouser and curiouser One of my favourite memories of any virus meeting is when Vadim Agol came slowly to the podium, appraised the audience and darkly intoned, ‘There are many ways to die’ This Dostoyevskian preface segued into a discussion of poliovirus’s ability to inhibit early innate immune responses, prolonging the life of an infected cell, only to let it die later after the virus has had a chance to replicate It has long been a source of anxiety to me that we did not know exactly why cells infected with any Enterovirus lived or died Now, with the proliferation of cell death mechanisms – apoptotic, necrotic, pyroptotic, necroptotic and autophagic, in which the same signal can also lead to different outcomes in different cell types, and the same cell type under different circumstances – this seems less embarrassing We are understanding more and more about the tissues in which viruses replicate, those through which they spread, and those in which they cause disease Given that these tissues can be very different, much about viral strategy can be learned in the contemplation of which cells live and which cells die The balance of life and death, so important to understanding how viruses spread through tissues, is likely to be influenced by everything we know about the cell biology of infection – from which cells show the strongest inhibition of translation to which cells are polarized and allow viral egress only directionally Pharmaceuticals against specific kinds of cell death, such as TNF inhibitors and necrostatins, are currently available and more are promised due to intensive research on tissue-sparing treatments for neurodegenerative disease Darwinian evolution requires pre-existing diversity Then, successful genomes are selected from that diverse pool Thus, the initial postulates of ‘adaptive mutation’, in which the exertion of selective pressures could increase mutation rate, at first seemed frighteningly Lamarckian Could selection pressure itself actually create mutations? Yes, it turns out, because the exertion of selective pressure can induce stress responses in many bacteria Part of the bacterial stress response is an increase in mutation frequency, which will then increase the likelihood that some individuals within the threatened population will survive the selective pressure Could the concept of adaptive mutation be relevant to Enterovirus infection? The incredible power of deep sequencing approaches will continue to elucidate this and other fascinating transmission genetic problems in Enterovirus biology Whether a virus population can survive selection pressure, such as spread to a different tissue in the same host, in the presence of an antiviral compound or increasing concentrations of antibodies depends on many factors First, there is the intrinsic mutation rate based on polymerase fidelity We not actually know this number for any Enterovirus polymerase in the context of an infected cell What is measured in the many elegant experiments Enteroviruses Future |  to define the intracellular quasispecies is the cumulative mutation frequency after several intracellular cycles of RNA synthesis, and the structure of the intracellular generations will greatly influence the cumulative mutation rate For example, if each positive strand generated one negative strand, and each negative strand templated 50 positive strands, only six templated replicative events, or RNA generations, would be required to generate more than 1000 intracellular positive strands Thus, the cumulative error rate will be six times the intrinsic error rate If, on the other hand, each negative strand generated only five positive strands, ten RNA generations would be required to generate more than 1000 intracellular positive strands It is therefore predicted that selection pressures that inhibit positive-strand synthesis might actually increase the cumulative error rate, a form of adaptive mutation that will be interesting to test and could be important for cell-to-cell spread and response to treatments This also brings up the general question whether errors and recombination events occur with fixed probability in a Poisson distribution It is possible that there are RNA replication complexes that are more recombinogenic than others It will be very interesting, now that single-molecule sequencing is available and error-proofed to determine the error rates and recombination frequencies of individual RNA replication complexes Perhaps RNA replication complexes associated with different host factors or assembled on different organelles, or with different ratios of processed polymerase to catalytically inactive precursors, will manifest different amounts of fidelity or processivity It would make sense, evolutionarily, to have some sober and some deranged RNA replication complexes When attending a party, for example, it is often a good idea to bring a boisterous friend Her antics will increase your contacts and allow your inclusion in after-party activities but, the next day, you not actually have to be like her In short, as our sequencing abilities become more and more focused, we are likely to find several levels to viral diversity Viral eradication and control by vaccination Thus far in human history, three viruses have been eradicated: smallpox (in 1978), poliovirus serotype (in 1999) and rinderpest (in 2011) We all fervently hope that the hard-fought campaign to eradicate the remaining two strains of poliovirus will be successful, and soon As of this writing, the only established endemicity is of serotype poliovirus in Pakistan, Afghanistan and Nigeria However, wild-type strains of both serotypes and continue to circulate in several countries, including recent environmental sampling in Israel To the extent that basic science informs and interprets the current eradication campaign, it is interesting to consider what we can learn from this in the management and treatment of other human maladies The complexities of our reliance on the Sabin vaccine to prevent poliovirus was made especially explicit by experiments of Phil Minor and his colleagues, beginning in the 1980s, in the ‘nappies’ of healthy children, including offspring, were monitored immediately after administration of the trivalent Sabin vaccine Within one day, it was possible to observe selection for nucleotide changes that conferred neurovirulence This finding rationalized what had been discovered empirically during the vaccination campaign: that use of live attenuated massive vaccination coverage was needed to ensure that everyone was actually vaccinated with attenuated virus, rather than second hand from a vaccinee Without the availability of infectious cDNA clones of types 1, and poliovirus, and the mouse models .. .Enteroviruses Omics, Molecular Biology, and Control https://doi.org/10.21775/9781910190739 Edited by William T Jackson Department of Microbiology and Immunology, University of Maryland School... coli: Evolution, Omics, Detection and Control 2018 Postgraduate Handbook: A Comprehensive Guide for PhD and Master's Students and their Supervisors2018 Molecular Biology of Kinetoplastid Parasites2018... 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