MARC details
| 000 -LEADER |
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41520cam a2200397 i 4500 |
| 001 - CONTROL NUMBER |
| control field |
14552950 |
| 005 - DATE AND TIME OF LATEST TRANSACTION |
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20201025104833.0 |
| 008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION |
| fixed length control field |
060915s2007 njua b 001 0 eng |
| 020 ## - INTERNATIONAL STANDARD BOOK NUMBER |
| International Standard Book Number |
0471351512 (pbk.) |
| 020 ## - INTERNATIONAL STANDARD BOOK NUMBER |
| International Standard Book Number |
9780471351511 (pbk.) |
| 040 ## - CATALOGING SOURCE |
| Original cataloging agency |
DLC |
| Description conventions |
rda |
| Transcribing agency |
DLC |
| Modifying agency |
BAKER |
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C#P |
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YDXCP |
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WAU |
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OCLCA |
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BTCTA |
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NLM |
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UKM |
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DLC |
| Language of cataloging |
eng |
| 082 00 - DEWEY DECIMAL CLASSIFICATION NUMBER |
| Classification number |
616.9101 |
| Edition number |
22 |
| Item number |
A.N.F |
| 100 1# - MAIN ENTRY--PERSONAL NAME |
| Personal name |
Acheson, N. H. |
| 9 (RLIN) |
9114 |
| 245 10 - TITLE STATEMENT |
| Title |
Fundamentals of molecular virology / |
| Statement of responsibility, etc |
Nicholas H. Acheson. |
| 264 #1 - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT) |
| Place of publication, distribution, etc |
Hoboken, NJ : |
| Name of publisher, distributor, etc |
Wiley, |
| Date of publication, distribution, etc |
[2007] |
| 264 #4 - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT) |
| Date of publication, distribution, etc |
copyright 2007 |
| 300 ## - PHYSICAL DESCRIPTION |
| Extent |
xxii, 405 pages : |
| Other physical details |
illustrations ; |
| Dimensions |
28 cm. |
| 336 ## - CONTENT TYPE |
| Content type term |
text |
| Content type code |
txt |
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rdacontent |
| 337 ## - MEDIA TYPE |
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unmediated |
| Media type code |
n |
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rdamedia |
| 338 ## - CARRIER TYPE |
| Carrier type term |
volume |
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nc |
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rdacarrier |
| 504 ## - BIBLIOGRAPHY, ETC. NOTE |
| Bibliography, etc |
Includes bibliographical references and index. |
| 505 0# - FORMATTED CONTENTS NOTE |
| Formatted contents note |
I. INTRODUCTION<br/>1. Introduction to Virology 1<br/>THE NATURE OF VIRUSES 2<br/>Viruses consist of a nucleic acid genome packaged in a<br/>protein coat 2<br/>Viruses are dependent on living cells for their replication 2<br/>Virus particles break down and release their genomes inside<br/>the cell 2<br/>Virus genomes are either RNA or DNA, but not both 2<br/>WHY STUDY VIRUSES? 3<br/>Viruses are important disease-causing agents 3<br/>Viruses can infect all forms of life 3<br/>Viruses are the most abundant form of life on Earth 4<br/>The study of viruses has led to numerous discoveries in<br/>molecular and cell biology 4<br/>A BRIEF HISTORY OF VIROLOGY: THE STUDY OF<br/>VIRUSES 5<br/>The scientific study of viruses is very recent 5<br/>Viruses were first distinguished from other microorganisms<br/>by filtration 5<br/>The crystallization of tobacco mosaic virus challenged<br/>conventional notions about genes and the nature of living<br/>organisms 5<br/>The ?phage group? stimulated studies of bacteriophages and<br/>helped found the field of molecular biology 7<br/>Study of tumor viruses led to discoveries in molecular<br/>biology and understanding of the nature of cancer 7<br/>DETECTION AND TITRATION OF VIRUSES 8<br/>Most viruses were first detected and studied by infection of<br/>intact organisms 8<br/>The plaque assay arose from work with bacteriophages 8<br/>Eukaryotic cells cultured in vitro have been adapted for<br/>plaque assays 8<br/>Hemagglutination is a convenient and rapid assay for many<br/>viruses 9<br/>Virus particles can be seen and counted by electron<br/>microscopy 10<br/>The ratio of physical virus particles to infectious particles can<br/>be much greater than 1 10<br/>THE VIRUS REPLICATION CYCLE:<br/>AN OVERVIEW 10<br/>The single-cycle virus replication experiment 10<br/>An example of a virus replication cycle: mouse<br/>polyomavirus 11<br/>Analysis of viral macromolecules reveals the detailed<br/>pathways of virus replication 12<br/>xiii<br/>STEPS IN THE VIRUS REPLICATION CYCLE 12<br/>1. Virions bind to receptors on the cell surface 12<br/>2. The virion (or the viral genome) enters the cell 12<br/>3. Early viral genes are expressed: the Baltimore classification<br/>of viruses 13<br/>The six groups in the Baltimore classification system 13<br/>4. Early viral proteins direct replication of viral genomes 14<br/>5. Late messenger RNAs are made from newly-replicated<br/>genomes 15<br/>6. Late viral proteins package viral genomes and assemble<br/>virions 15<br/>7. Progeny virions are released from the host cell 15<br/>2. Virus Structure 17<br/>The molecular structure of virus particles 17<br/>How virus structure is studied: viruses come in a variety of<br/>sizes and shapes 18<br/>Small viruses come in simple, symmetrical packages 18<br/>Many virus capsids have icosahedral symmetry 18<br/>Some examples of virions with icosahedral symmetry 21<br/>The concept of quasi equivalence 21<br/>How many subunits can be accomodated on the capsid<br/>surface? 22<br/>Other structures, large and small, display icosahedral<br/>symmetry 23<br/>Many virus capsids are organized as helical tubes 23<br/>Larger viruses come in more complex packages 24<br/>Specific packaging signals direct incorporation of viral<br/>genomes into virions 25<br/>Core proteins may accompany the viral genome inside the<br/>capsid 25<br/>Scaffolding proteins help in virion assembly but are not<br/>incorporated into the mature virion 25<br/>Viral envelopes are made from lipid bilayer membranes 26<br/>Viral glycoproteins are inserted into the lipid membrane to<br/>form the envelope 26<br/>Budding is driven by interactions between viral proteins 27<br/>Assembly and disassembly of virions: the importance of an<br/>irreversible step 27<br/>3. Virus Classification: The World of<br/>Viruses 30<br/>VIRUS CLASSIFICATION 30<br/>Many viruses, infecting virtually all known life forms, have<br/>been discovered 30<br/>Virus classification is based on molecular architecture,<br/>genetic relatedness, and host organism 31<br/>Contents<br/>xiv Contents<br/>Viruses are grouped into species, genera, and families 31<br/>Distinct naming conventions and classification schemes have<br/>developed in different domains of virology 32<br/>MAJOR VIRUS GROUPS 32<br/>Study of the major groups of viruses leads to understanding<br/>of shared characteristics and replication pathways 32<br/>Viruses with single-stranded DNA genomes are small and<br/>have few genes 33<br/>Viruses with double-stranded DNA genomes include the<br/>largest known viruses 34<br/>Most plant viruses and many viruses of vertebrates have<br/>positive-strand RNA genomes 35<br/>All viruses with negative-strand RNA genomes have helical<br/>nucleocapsids and some have fragmented genomes 36<br/>Viruses with double-stranded RNA genomes have<br/>fragmented genomes packaged in capsids with icosahedral<br/>symmetry 37<br/>Viruses with a reverse transcription step in their replication<br/>cycle can have either RNA or DNA genomes 38<br/>Satellite viruses and satellite nucleic acids require a helper<br/>virus to replicate 39<br/>Viroids do not code for proteins, but replicate independently<br/>of other viruses 39<br/>THE EVOLUTIONARY ORIGIN OF VIRUSES 40<br/>The first steps in the development of life on earth: the RNA<br/>world 40<br/>Viroids and RNA viruses may have originated in the RNA<br/>world 40<br/>The transition to the DNA-based world 40<br/>Small and medium-sized DNA viruses could have arisen<br/>as independently-replicating genetic elements<br/>in cells 41<br/>Large DNA viruses could have evolved from cells that<br/>became obligatory intracellular parasites 41<br/>4. Virus Entry 43<br/>How do virions get into eukaryotic cells? 43<br/>Enveloped and nonenveloped viruses have distinct<br/>penetration strategies 44<br/>Some viruses can pass directly from cell to cell 44<br/>A variety of cell surface proteins can serve as specific virus<br/>receptors 45<br/>Receptors interact with viral glycoproteins, surface<br/>protrusions, or ?canyons? in the surface of the virion 45<br/>Many viruses enter the cell via receptor-mediated<br/>endocytosis 45<br/>Passage from endosomes to the cytosol is often triggered by<br/>low pH 47<br/>Membrane fusion is mediated by specific viral ?fusion<br/>proteins? 47<br/>Fusion proteins undergo major conformational changes that<br/>lead to membrane fusion 48<br/>Nonenveloped viruses penetrate by membrane lysis or pore<br/>formation 49<br/>Virions and capsids are transported within the cell in vesicles<br/>or on microtubules 49<br/>Import of viral genomes into the nucleus 50<br/> |
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The many ways in which viral genomes are uncoated and<br/>released 50<br/>5. Single-Stranded RNA Bacteriophages 53<br/>The discovery of RNA phages stimulated research into<br/>messenger RNA function and RNA replication 53<br/>RNA phages are among the simplest known organisms 54<br/>Two genera of RNA phages have subtle differences 54<br/>RNA phages bind to the F-pilus and use it to insert their<br/>RNA into the cell 55<br/>Phage RNA is translated and replicated in a regulated<br/>fashion 55<br/>RNA secondary structure controls translation of lysis and<br/>replicase genes 56<br/>Ribosomes translating the coat gene disrupt secondary<br/>structure, allowing replicase translation 57<br/>Ribosomes terminating coat translation can reinitiate at the<br/>lysis gene start site 57<br/>Replication versus translation: competition for the same<br/>RNA template 58<br/>Genome replication requires four host cell proteins plus the<br/>replicase 58<br/>A host ribosomal protein directs polymerase to the coat start<br/>site 59<br/>Polymerase skips the first A residue but adds a terminal A to<br/>the minus strand copy 59<br/>Synthesis of plus strands is less complex and more efficient<br/>than that of minus strands 59<br/>The start site for synthesis of maturation protein is normally<br/>inaccessible to ribosomes 61<br/>Synthesis of maturation protein is controlled by delayed<br/>RNA folding 61<br/>Assembly and release of virions 62<br/>6 Bacteriophage _X 174 63<br/>_X174: a tiny virus with a big impact 63<br/>Overlapping reading frames allow efficient use of a small<br/>genome 64<br/>_X174 binds to glucose residues in lipopolysaccharide on the<br/>cell surface 65<br/>_X174 delivers its genome into the cell through spikes on the<br/>capsid surface 66<br/>Stage I DNA replication generates double-stranded<br/>replicative form DNA 66<br/>Gene expression is controlled by the strength of promoters<br/>and transcriptional terminators 66<br/>Replicative form DNAs are amplified via a rolling circle<br/>mechanism 67<br/>Summary of viral DNA replication mechanisms 67<br/>Procapsids are assembled by the use of scaffolding proteins<br/>67<br/>Contents xv<br/>Scaffolding proteins have a flexible structure 68<br/>Single-stranded genomes are packaged into procapsids as<br/>they are synthesized 68<br/>Role of the J protein in DNA packaging 69<br/>Cell lysis caused by E protein leads to release of phage 69<br/>Did all icosahedral ssDNA virus families evolve from a<br/>common ancestor? 69<br/>7. Bacteriophage T7 71<br/>T7: a model phage for DNA replication, transcription, and<br/>RNA processing 71<br/>T7 genes are organized into three groups based on<br/>transcription and gene function 72<br/>Entry of T7 DNA into the cytoplasm is powered by<br/>transcription 73<br/>Transcription of class II and III genes requires a novel<br/>T7-coded RNA polymerase 73<br/>Class II genes code for enzymes involved in T7 DNA<br/>replication 74<br/>T7 RNAs are cleaved by host cell ribonuclease III to smaller,<br/>stable mRNAs 74<br/>Regulation of class III gene expression 74<br/>DNA replication starts at a unique internal origin and is<br/>primed by T7 RNA polymerase 75<br/>Large DNA concatemers are formed during replication 76<br/>Concatemers are processed and packaged into preformed<br/>proheads 76<br/>Special features of the T7 family of phages 76<br/>8. Bacteriophage Lambda: A Piñata of<br/>Paradigms 79<br/>In the beginning . . . 80<br/>Uptake of _DNA depends on cellular proteins involved in<br/>sugar transport 80<br/>The _lytic transcription program is controlled by<br/>termination and antitermination of RNA synthesis at<br/>specific sites on the genome 81<br/>The CI repressor blocks expression of the lytic program by<br/>regulating three nearby promoters: PL, PR, and PRM 82<br/>Cleavage of CI repressor in cells with damaged DNA leads to<br/>prophage induction 83<br/>The Cro repressor suppresses CI synthesis and regulates<br/>early gene transcription 83<br/>Making the decision: Go lytic or lysogenize? 83<br/>A quick review 85<br/>Breaking and entering: The insertion of _DNA into the<br/>bacterial chromosome 85<br/>The great escape: The liberation of _DNA from the<br/>bacterial chromosome 86<br/>Int synthesis is controlled by retroregulation 86<br/>_DNA Replication is directed by O and P, but carried out<br/>by host cell proteins 87<br/>Assembly of _heads involves chaperone and scaffolding<br/>proteins 87<br/>DNA is inserted into preformed proheads by an ATPdependent<br/>mechanism 87<br/>Host cell lysis 88<br/>9. Parvoviruses 89<br/>Parvoviruses have very small virions and a linear, singlestranded<br/>DNA genome 89<br/>Parvoviruses replicate in cells that are going through the cell<br/>cycle 90<br/>Discovery of mammalian parvoviruses 90<br/>Parvoviruses have one of the simplest known virion<br/>structures 91<br/>Parvoviruses have very few genes 91<br/>Single-stranded parvovirus DNAs have unusual terminal<br/>structures 92<br/>Uncoating of parvovirus virions takes place in the nucleus<br/>and is cell-specific 92<br/>DNA replication begins by extension of the 3_ end of the<br/>terminal hairpin 93<br/>The DNA ?end replication? problem 93<br/>Steps in DNA replication 93<br/>Non-structural proteins are multifunctional 95<br/>Adenovirus functions that help AAV replication 96<br/>In the absence of helper virus, AAV DNA can integrate into<br/>the cell genome 96<br/>Parvovirus pathogenesis: the example of B19 virus 96<br/>10. Polyomaviruses 98<br/>Mouse polyomavirus was discovered as a tumor-producing<br/>infectious agent 98<br/>Simian virus 40 was found as a contaminant of Salk<br/>poliovirus vaccine 99<br/>Polyomaviruses are models for studying DNA virus<br/>replication and tumorigenesis 99<br/>Polyomavirus capsids are constructed from pentamers of the<br/>major capsid protein 99<br/>The circular DNA genome is packaged with cellular<br/>histones 100<br/>Circular DNA becomes supercoiled upon removal of<br/>histones 100<br/> |
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Supercoiled DNA can be separated from relaxed or linear<br/>DNA molecules 101<br/>Polyomavirus genes are organized in two divergent<br/>transcription units 102<br/>Virions enter cells in caveolae and are transported to the<br/>nucleus 102<br/>The viral minichromosome is transcribed by cellular RNA<br/>polymerase II 103<br/>Four early mRNAs are made by differential splicing of a<br/>common transcript 104<br/>T antigens share common N-terminal sequences but have<br/>different C-terminal sequences 105<br/>T antigens bring resting cells into the DNA synthesis (S)<br/>phase of the cell cycle 105<br/>xvi Contents<br/>Small T antigen inhibits protein phosphatase 2A and induces<br/>cell cycling 105<br/>Middle T antigen stimulates protein tyrosine kinases that<br/>signal cell proliferation and division 105<br/>Large T antigen activates or suppresses transcription of<br/>cellular genes by binding to a number of important cellular<br/>regulatory proteins 107<br/>Large T antigen hexamers bind to the origin of DNA<br/>replication and locally unwind the two DNA strands 108<br/>Large T antigen hexamers assemble cellular DNA synthesis<br/>machinery to initiate viral DNA replication 110<br/>High levels of late transcripts are made after DNA<br/>replication begins 111<br/>Three late mRNAs are made by alternative splicing 112<br/>How do polyomaviruses transform cells in vitro and cause<br/>tumors in vivo? 112<br/>11. Papillomaviruses 114<br/>Papillomaviruses cause warts and other skin and mucosal<br/>lesions 114<br/>Oncogenic human papillomaviruses are a major cause of<br/>genital tract cancers 115<br/>Papillomaviruses are not easily grown in cell culture 115<br/>Papillomavirus genomes are circular, double-stranded<br/>DNA 116<br/>The infectious cycle follows differentiation of epithelial<br/>cells 116<br/>Viral mRNAs are made from two promoters and two<br/>polyadenylation signals 117<br/>Viral E1 and E2 proteins bind to the replication origin and<br/>direct initiation of DNA replication 118<br/>Viral E7 protein interacts with cell cycle regulatory proteins,<br/>particularly Rb 118<br/>Viral E6 protein controls the level of cellular p53<br/>protein 120<br/>Synergism between E6 and E7 and the predisposition to<br/>cancer 121<br/>Cells transformed by papillomaviruses express E6 and E7<br/>gene products from integrated viral DNA 121<br/>Future prospects for diagnosis and treatment of diseases<br/>caused by papillomaviruses 121<br/>12. Adenoviruses 123<br/>Adenoviruses cause respiratory and enteric infections in<br/>humans 124<br/>Adenoviruses can be oncogenic, but not in humans 124<br/>Virions have icosahedral symmetry and are studded with<br/>knobbed fibers 124<br/>Fibers make contact with cellular receptor proteins to initiate<br/>infection 124<br/>Expression of adenovirus genes is controlled at the level of<br/>transcription 126<br/>E1A proteins are the kingpins of the adenovirus growth<br/>cycle 127<br/>E1A proteins bind to the retinoblastoma protein and activate<br/>E2F, a cellular transcription factor 127<br/>E1A proteins also activate other cellular transcription<br/>factors 128<br/>E1A proteins indirectly induce apoptosis by activation of<br/>cellular p53 protein 128<br/>E1B proteins suppress E1A-induced apoptosis, allowing viral<br/>replication to proceed 128<br/>The preterminal protein primes DNA synthesis carried out<br/>by viral DNA polymerase 129<br/>Single-stranded DNA is circularized via the inverted<br/>terminal repeat 130<br/>The major late promoter is activated after DNA replication<br/>begins 131<br/>Five different poly(A) sites and alternative splicing generate<br/>multiple late mRNAs 131<br/>The tripartite leader ensures efficient transport of late<br/>mRNAs to the cytoplasm 132<br/>The tripartite leader directs efficient translation of late<br/>adenovirus proteins 132<br/>Adenoviruses kill cells by apoptosis, aiding virus release 132<br/>Cell transformation and oncogenesis by human<br/>adenoviruses 132<br/>13. Herpes Simplex Virus 134<br/>Herpesviruses are important human pathogens 135<br/>Most herpesviruses can establish latent infections 135<br/>Herpes simplex virus genomes contain both unique and<br/>repeated sequence elements 135<br/>Nomenclature of herpes simplex virus genes and<br/>proteins 137<br/>The icosahedral capsid is enclosed in an envelope along with<br/>tegument proteins 137<br/>Entry by fusion is mediated by envelope glycoproteins<br/>and may occur at the plasma membrane or in<br/>endosomes 138<br/>Viral genes are sequentially expressed during the replication<br/>cycle 138<br/>Tegument proteins interact with cellular machinery to<br/>activate viral gene expression and to degrade cellular<br/>messenger RNAs 139<br/>Immediate early ( _) genes regulate expression of other<br/>herpesvirus genes 140<br/>_gene products set the stage for viral DNA replication 140<br/>Herpesvirus begins with bidirectional DNA replication 141<br/>Rolling-circle replication subsequently produces multimeric<br/>concatemers of viral DNA 141<br/>DNA replication leads to activation of _1 and _2 genes 142<br/>Viral nucleocapsids are assembled on a scaffold in the<br/>nucleus 143<br/>Envelopment and egress: three possible routes 143<br/>Many viral genes are involved in blocking host responses to<br/>infection 143<br/>The establishment and maintenance of virus latency 145<br/>Latency-associated transcripts include stable introns 145<br/>Contents xvii<br/>14. Baculoviruses 147<br/>Insect viruses were first discovered as pathogens of<br/>silkworms 148<br/>Baculoviruses are used for pest control and to express<br/>eukaryotic proteins 148<br/>Baculoviruses produce two kinds of particles: ?budded? and<br/>?occlusion-derived? virions 149<br/>Baculoviruses have large, circular DNA genomes and encode<br/>many proteins 150<br/>Insects are infected by ingesting occlusion bodies; infection<br/>spreads within the insect via budded virions 151<br/>Viral proteins are expressed in a timed cascade regulated at<br/>the transcription level 152<br/>Immediate early gene products control expression of early<br/>genes 152<br/>Early gene products regulate DNA replication, late<br/>transcription, and apoptosis 153<br/>Late genes are transcribed by a novel virus-coded RNA<br/>polymerase 153<br/>Baculoviruses are widely used to express foreign<br/>proteins 156<br/>15. Poxviruses 157<br/>Smallpox was a debilitating and fatal worldwide disease 158<br/>Variolation led to vaccination, which has eradicated smallpox<br/>worldwide 158<br/>Poxviruses remain a subject of intense research interest 159<br/>Linear vaccinia virus genomes have covalently sealed hairpin<br/>ends and lack introns 159<br/>Two forms of vaccinia virions have different roles in<br/>spreading infection 160<br/>Poxviruses replicate in the cytoplasm 162<br/>Poxvirus genes are expressed in a regulated transcriptional<br/>cascade controlled by viral transcription factors 162<br/>Virus-coded enzymes packaged in the core carry out early<br/>RNA synthesis and processing 162<br/>Enzymes that direct DNA replication are encoded by early<br/>mRNAs 163<br/>Poxviruses produce large concatemeric DNA molecules that<br/>are resolved into monomers 164<br/>Postreplicative mRNAs have 5_ end poly(A) extensions and 3_<br/>end heterogeneity 164<br/>Mature virions are formed within virus ?factories? 165<br/>Extracellular virions are extruded through the plasma<br/>membrane by actin tails 166<br/>Poxviruses make several proteins that target host immune<br/>defenses 167<br/>16. Picornaviruses 169<br/>Picornaviruses cause a variety of human and animal diseases<br/>including poliomyelitis and the common cold 170<br/>Poliovirus: a model picornavirus for vaccine development<br/>and studies of replication 170<br/>Picornavirus virions bind to cellular receptors via depressions<br/>or loop regions on their surface 171<br/>Genome RNA may pass through pores formed in cell<br/>membranes by capsid proteins 171<br/>Translation initiates on picornavirus RNAs by a novel<br/>internal ribosome entry mechanism 172<br/>Essential features of picornavirus IRES elements 173<br/>Interaction of picornavirus IRES elements with host cell<br/>proteins 175<br/>Picornavirus proteins are made as a single precursor polyprotein<br/>that is autocatalytically cleaved by viral proteinases 176<br/>Picornaviruses make a variety of proteinases that cleave the<br/>polyprotein and some cellular proteins 176<br/>Replication of picornavirus RNAs is initiated in a<br/>multiprotein complex bound to proliferated cellular<br/>vesicles 176<br/>RNA synthesis is primed by VPg covalently bound to uridine<br/>residues 177<br/>Virion assembly involves cleavage of VP0 to VP2 plus<br/>VP4 178<br/>Inhibition of host cell macromolecular functions 179<br/>17. Flaviviruses 181<br/>Flaviviruses cause several important human diseases 182<br/>Yellow fever is a devastating human disease transmitted by<br/>mosquitoes 182<br/>A live, attenuated yellow fever virus vaccine is available and<br/>widely used 183<br/>Hepatitis C virus: a recently discovered member of the<br/>Flaviviridae 183<br/>The flavivirus virion contains an icosahedral nucleocapsid<br/>wrapped in a tightly fitted envelope 183<br/>Flavivirus E protein directs both binding to receptors and<br/>membrane fusion 184<br/>Flaviviruses enter the cell by pH-dependent fusion 185<br/>Flavivirus genome organization resembles that of<br/>picornaviruses 185<br/>The polyprotein is processed by both viral and cellular<br/>proteinases 186<br/>Nonstructural proteins organize protein processing, viral<br/>RNA replication, and capping 187<br/>Flavivirus RNA synthesis is carried out on membranes in<br/>the cytoplasm 188<br/>Virus assembly also takes place at intracellular<br/>membranes 189<br/>18. Togaviruses 191<br/>Most togaviruses are arthropod borne, transmitted between<br/>vertebrate hosts by mosquitoes 192<br/>Togavirus virions contain a nucleocapsid with icosahedral<br/>symmetry wrapped in an envelope of the same<br/>symmetry 192<br/>Togaviruses enter cells by low pH-induced fusion inside<br/>endosome vesicles 193<br/>xviii Contents<br/>Nonstructural proteins are made as a polyprotein that is<br/>cleaved by a viral protease 193<br/>Partly-cleaved nonstructural proteins catalyze synthesis of<br/>full-length antigenome RNA 194<br/>Replication and transcription: synthesis of genome and<br/>subgenomic RNAs 196<br/>Structural proteins are cleaved during translation and<br/>directed to different cellular locations 196<br/>Assembly of virions and egress at the plasma membrane 197<br/>Effects of mutations in viral proteins on cytopathic<br/>effects and on pathogenesis 198<br/>Alphaviruses have been modified to serve as vectors for<br/>the expression of heterologous proteins 199<br/>Alphavirus vectors have multiple potential uses 199<br/> |
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19. CORONAVIRUSES 201<br/>Coronaviruses cause common colds in humans and important<br/>veterinary diseases 202<br/>A newly emerged coronavirus caused a worldwide epidemic<br/>of severe acute respiratory syndrome (SARS) 202<br/>The SARS coronavirus may have passed from animals to<br/>humans via direct contact 202<br/>Coronaviruses have large, single-stranded, positive sense<br/>RNA genomes 203<br/>Coronaviruses fall into three groups based on genome<br/>sequences 203<br/>Coronaviruses have enveloped virions containing helical<br/>nucleocapsids 204<br/>Coronavirus virions contain multiple envelope proteins 204<br/>Coronavirus spike proteins bind to a variety cellular<br/>receptors 205<br/>The virus envelope fuses with the plasma membrane or an<br/>endosomal membrane 206<br/>The replicase gene is translated from genome RNA into a<br/>polyprotein that is processed by viral proteinases 206<br/>RNA polymerase, RNA helicase, and RNA modifying<br/>enzymes are coded by the replicase gene 207<br/>Replication complexes are associated with cytoplasmic<br/>membranes 207<br/>Genome replication proceeds via a full-length negativestrand<br/>intermediate 208<br/>Transcription produces a nested set of subgenomic<br/>mRNAs 208<br/>Subgenomic mRNAs are most likely transcribed from<br/>subgenomic negative-sense RNA templates 208<br/>The alternative model of discontinuous transcription of<br/>antigenome RNA is unlikely to be correct 209<br/>Assembly of virions takes place at intracellular membrane<br/>structures 211<br/>Adaptability of Coronaviruses 212<br/>20. Paramyxoviruses and Rhabdoviruses 214<br/>The mononegaviruses: a group of related negative-strand<br/>RNA viruses 215<br/>Rabies is a fatal human encephalitis caused by a<br/>rhabdovirus 215<br/>Measles is a serious childhood disease caused by a<br/>paramyxovirus 215<br/>Paramyxovirus and rhabdovirus virions have distinct<br/>morphologies 216<br/>Viral envelope proteins are responsible for receptor binding<br/>and fusion with cellular membranes 217<br/>Genome RNA is contained within helical nucleocapsids 218<br/>Paramyxoviruses enter the cell by fusion with the plasma<br/>membrane at neutral pH 218<br/>Gene order is conserved among different paramyxoviruses<br/>and rhabdoviruses 219<br/>Viral messenger RNAs are synthesized by an RNA<br/>polymerase packaged in the virion 220<br/>Viral RNA polymerase initiates transcription exclusively at<br/>the 3? end of the viral genome 220<br/>The promoter for plus-strand RNA synthesis consists of two<br/>sequence elements separated by one turn of the<br/>ribonucleoprotein helix 220<br/>mRNAs are synthesized sequentially from the 3? to the 5? end<br/>of the genome RNA 222<br/>The P/C/V gene codes for several proteins by using<br/>alternative translational starts and by mRNA<br/>?editing? 223<br/>Functions of P, C and V proteins 224<br/>N protein levels control the switch from transcription to<br/>genome replication 224<br/>Virions are assembled at the plasma membrane 224<br/>21. Filoviruses 226<br/>Marburg and Ebola viruses: sporadically emerging viruses<br/>that cause severe, often fatal disease 227<br/>Filoviruses are related to paramyxoviruses and<br/>rhabdoviruses 228<br/>Filoviruses cause hemorrhagic fever 228<br/>Filovirus genomes contain seven genes in a conserved<br/>order 228<br/>Filovirus transcription, replication and assembly 230<br/>Cloned cDNA copies of viral mRNAs and viral genome<br/>RNA are used for study of filoviruses 230<br/>Multi-plasmid transfection systems allow recovery of<br/>infectious filoviruses 230<br/>Filovirus glycoprotein mediates both receptor-binding and<br/>entry by fusion 231<br/>Ebola virus uses RNA editing to make two glycoproteins<br/>from the same gene 232<br/>Does the secreted glycoprotein play a role in virus<br/>pathogenesis? 232<br/>Minor nucleocapsid proteinVP30 activates viral mRNA<br/>synthesis in Ebola virus 233<br/>Matrix protein VP40 directs budding and formation of<br/>filamentous particles 234<br/>Most filovirus outbreaks have occurred in equatorial<br/>Africa 234<br/>Contents xix<br/>Filovirus infections are transmitted to humans from an<br/>unknown animal origin 235<br/>Spread of filovirus infections among humans is limited to<br/>close contacts 235<br/>Pathogenesis of filovirus infections 236<br/>Clinical features of infection 236<br/>22. Bunyaviruses 238<br/>Most bunyaviruses are transmitted by arthropod vectors,<br/>including mosquitoes and ticks 239<br/>Some bunyaviruses cause severe hemorrhagic fever,<br/>respiratory disease, or encephalitis 240<br/>Bunyaviruses encapsidate a segmented RNA genome in a<br/>simple enveloped particle 240<br/>Bunyavirus protein coding strategies: negative-strand and<br/>ambisense RNAs 240<br/>L RNA codes for viral RNA polymerase 241<br/>M RNA codes for virion envelope glycoproteins 242<br/>S RNA codes for nucleocapsid protein and a nonstructural<br/>protein 243<br/>After attachment via the virion glycoproteins, bunyaviruses<br/>enter the cell by endocytosis 243<br/>Bunyavirus mRNA synthesis is primed by the capped 5? ends<br/>of cellular mRNAs 243<br/>Coupled translation and transcription may prevent<br/>premature termination of mRNAs 244<br/>Genome replication begins once sufficient N protein is<br/>made 244<br/>Virus assembly takes place at Golgi membranes 245<br/>Evolutionary potential of bunyaviruses via genome<br/>reassortment 246<br/>23. Orthomyxoviruses 248<br/>Influenza viruses cause serious acute disease in humans, and<br/>occasional pandemics 249<br/>Influenza virus infections of the respiratory tract can lead to<br/>secondary bacterial infections 249<br/>Orthomyxoviruses are negative-strand RNA viruses with<br/>segmented genomes 249<br/>Eight influenza virus genome segments code for a total of ten<br/>different viral proteins 251<br/>Hemagglutinin protein binds to cell receptors and<br/>mediates fusion of the envelope with the endosomal<br/>membrane 252<br/>M2 is an ion channel that facilitates release of nucleocapsids<br/>from the virion 252<br/>Nucleocapsids enter the nucleus, where mRNA synthesis and<br/>RNA replication occur 253<br/>Capped 5_ ends of cellular pre-messenger RNAs are used as<br/>primers for synthesis of viral mRNAs 254<br/>Viral mRNAs terminate in poly(A) tails generated by<br/>?stuttering? transcription 255<br/>Two influenza A mRNAs undergo alternative splicing in the<br/>nucleus 255<br/>Genome replication begins when newly synthesized NP<br/>protein enters the nucleus 255<br/>Nucleocapsids are exported from the nucleus in a complex<br/>with matrix protein and NS2 256<br/>The NS1 protein interferes with polyadenylation of cellular<br/>mRNAs 256<br/>NS1 also inhibits activation of PKR, an important antiviral<br/>pathway induced by interferon 257<br/>Viral envelope proteins assemble in the plasma membrane<br/>and direct budding of virions 257<br/>Neuraminidase cleaves sialic acid, the cellular receptor that<br/>binds to HA 257<br/>Influenza virus strains vary in both transmissibility and<br/>pathogenicity 257<br/>Genetic variability generates new virus strains that can cause<br/>pandemics 258<br/>The 1918 pandemic influenza A virus was probably not a<br/>reassortant virus 258<br/>Genome sequences from some previous influenza A virus<br/>strains confirm the antigenic shift hypothesis 258<br/>Highly pathogenic influenza A strains in poultry farms could<br/>lead to a new pandemic 259<br/>24. Reoviruses 261<br/>Reoviruses were the first double-stranded RNA viruses<br/>discovered 262<br/>Some members of the Reoviridae are important<br/>pathogens 262<br/>Reoviridae have segmented genomes made of doublestranded<br/>RNA 262<br/>Reovirus virions contain concentric layers of capsid<br/>proteins 263<br/>The attachment protein binds to one or two cellular<br/>receptors 265<br/>During entry, the outer capsid is stripped from virions and<br/>the core is released into the cytoplasm 265<br/>Enzymes in the viral core synthesize and cap messenger<br/>RNAs 266<br/>Translation of reovirus mRNAs is regulated 267<br/>Interferon and PKR: effects on viral and cellular protein<br/>synthesis 267<br/>Synthesis of progeny double-stranded genomes occurs within<br/>subviral particles 268<br/>Reoviruses induce apoptosis via activation of transcription<br/>factor NF- _B 269<br/>Studies of reovirus pathogenesis in mice 270<br/>25. Retroviruses 272<br/>Retroviruses have a unique replication cycle based<br/>on reverse transcription and integration of their<br/>genomes 273<br/>Viral proteins derived from the gag, pol and env genes are<br/>incorporated in virions 273<br/>Retroviruses enter cells by the fusion pathway 274<br/>xx Contents<br/>Viral RNA is converted into a double-stranded DNA copy by<br/>reverse transcription 275<br/>A copy of proviral DNA is integrated into the cellular<br/>genome at a random site 277<br/>Sequence elements in the long terminal repeats direct<br/>transcription and polyadenylation by host cell<br/>enzymes 277<br/>Differential splicing generates multiple mRNAs 279<br/>The Gag/Pol polyprotein is made by suppression of<br/>termination and use of alternative reading frames 279<br/>Virions mature into infectious particles after budding from<br/>the plasma membrane 280<br/>Acute transforming retroviruses express mutated forms of<br/>cellular growth signalling proteins 281<br/>Retroviruses lacking oncogenes can transform cells by<br/>insertion of proviral DNA near a proto-oncogene 282<br/>26. Human Immunodeficiency Virus<br/>Type 1 284<br/>Human immunodeficiency virus type 1 (HIV-1) and acquired<br/>immunodeficiency syndrome 285<br/>HIV-1 infection leads to a progressive loss of cellular<br/>immunity and increased susceptibility to opportunistic<br/>infections 285<br/>HIV-1 is a complex retrovirus 287<br/>HIV-1 targets cells of the immune system by recognizing<br/>CD4 antigen and chemokine receptors 287<br/>Virus mutants arise rapidly because of errors generated<br/>during reverse transcription 288<br/>Unlike other retroviruses, HIV-1 directs transport of proviral<br/>DNA into the cell nucleus 288<br/>Latent infection complicates the elimination of<br/>HIV-1 289<br/>The Tat protein increases HIV-1 transcription by<br/>stimulating elongation by RNA polymerase II 289<br/>The Rev protein mediates cytoplasmic transport of viral<br/>mRNAs that code for HIV-1 structural proteins 290<br/>Together, the Tat and Rev proteins strongly upregulate viral<br/>protein expression 291<br/>The Vif protein increases virion infectivity by counteracting<br/>a cellular deoxcytidine deaminase 291<br/>The Vpr protein enables the preintegration complex to be<br/>transported to the nucleus 291<br/>The Vpu protein enhances release of progeny virions from<br/>infected cells 291<br/>The Nef protein is an important mediator of<br/>pathogenesis 292<br/>27. Human T-Cell Leukemia Virus<br/>Type 1 294<br/>Discovery of the first human retrovirus 294<br/>Like lentiviruses, HTLV-1 codes for regulatory proteins by<br/>producing doubly-spliced mRNAs 295<br/>HTLV-1 Rex regulates polyadenylation, splicing, and<br/>nuclear export of viral RNAs 296<br/>HTLV-1 Tax regulates transcription of viral and cellular<br/>genes 297<br/>Cell transformation by HTLV-I is mediated by Tax 299<br/>The interleukin-2?autocrine loop stimulates T-cell<br/>proliferation 299<br/>Activation of the Jak-Stat pathway by p12I mimics<br/>interleukin-2 stimulation 299<br/> |
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Cell Cycle Progression: p16INK4A and cyclin-dependent<br/>kinases 300<br/>The mitotic spindle checkpoint and MAD1 300<br/>Downregulation of p53 activity by Tax allows T cell<br/>proliferation 301<br/>Diseases caused by HTLV-1 develop slowly and can be<br/>severe 301<br/>Coinfection by HIV-1 and HTLV-1 is an emerging<br/>problem 302<br/>Antiviral therapy of disease caused by HTLV-1 has not met<br/>with great success 302<br/>28. Hepadnaviruses 303<br/>At least seven distinct viruses cause human hepatitis 304<br/>The discovery of hepatitis B virus 304<br/>Dane particles are infectious virions; abundant noninfectious<br/>particles lack nucleocapsids 305<br/>The viral genome is a circular, partly single-stranded DNA<br/>with overlapping reading frames 305<br/>Nucleocapsids enter the cytoplasm via fusion and are<br/>transported to the nucleus 305<br/>Transcription of viral DNA gives rise to several mRNAs and<br/>a pregenome RNA 307<br/>The roles of hepatitis B virus proteins 308<br/>The pregenome RNA is packaged by interaction with<br/>polymerase and core proteins 309<br/>Genome replication occurs via reverse transcription of<br/>pregenome RNA 309<br/>Virions are formed by budding in the endoplasmic<br/>reticulum 311<br/>Hepatitis B virus can cause chronic or acute hepatitis,<br/>cirrhosis, and liver cancer 312<br/>Hepatits B virus is transmitted by blood transfusions,<br/>contaminated needles, and unprotected sex 313<br/>A recombinant vaccine is available 313<br/>Antiviral drug treatment has real but limited success 313<br/>29 Viroids and Hepatitis Delta Virus 315<br/>Viroids are small, circular RNAs that do not encode<br/>proteins 316<br/>Group A and group B viroids have distinct properties 316<br/>Viroids replicate via linear multimeric RNA intermediates 317<br/>Three enzymatic activities are needed for viroid<br/>replication 317<br/>Contents xxi<br/>How do viroids cause disease? 318<br/>Interaction of viroid RNA with cellular RNAs or proteins<br/>may disrupt cell metabolism 318<br/>Plant satellite RNAs resemble viroids but are<br/>encapsidated 320<br/>Hepatitis delta virus is a human viroid-like satellite<br/>virus 320<br/>Hepatitis delta virus may use two different cellular RNA<br/>polymerases to replicate 320<br/>RNA editing generates two forms of hepatitis delta<br/>antigen 322<br/>Conclusion: viroids may be a link to the ancient RNA<br/>world 322<br/>30. Prions 323<br/>Prions are proteins that cause fatal brain diseases 323<br/>Prion diseases were first detected in domestic<br/>ruminants 324<br/>Human prion diseases can be either inherited or<br/>transmitted 324<br/>The infectious agent of prion diseases contains protein but<br/>no detectable nucleic acid 325<br/>PrPSc is encoded by a host cell gene 325<br/>Differences between PrPC and PrPSc 326<br/>The prion hypothesis: formation of infectious and<br/>pathogenic prions from normal PrPC 326<br/>Is the prion hypothesis correct? 327<br/>Pathology and diagnosis of prion diseases 330<br/>Genetics of prion diseases 330<br/>Prion diseases are not usually transmitted among different<br/>species 330<br/>Strain variation and crossing of the species barrier 331<br/>The nature of the prion infectious agent 331<br/>31. Interferons 333<br/>Virus-infected cells secrete interferons, which protect nearby<br/>cells against virus infection 334<br/>Interferons are a first line of host defense against viruses but<br/>therapeutic use has been limited 334<br/>Interferons _, _, and _are made by different cells and have<br/>distinct functions 335<br/>Transcription of interferon genes is activated by virus<br/>infection or double-stranded RNA 335<br/>Transcriptional activation occurs by binding of transcription<br/>factors to interferon gene enhancers 335<br/>Interferon signal transduction is carried out via the Jak-Stat<br/>pathway 337<br/>Antiviral activities induced by interferon 338<br/>Interferons have diverse effects on the immune system 340<br/>The adaptive immune system 340<br/>Interferons stimulate antigen processing and<br/>presentation 342<br/>Interferon and the development of CD4-positive helper<br/>T-cells 342<br/>The role of interferon in macrophage activation and cellular<br/>immunity 343<br/>Effects of interferons on antibody production 343<br/>Interferons regulate cell growth and apoptosis 343<br/>Viruses have developed numerous strategies to evade the<br/>interferon response 343<br/>Conclusion: interferons are a first line of defense against<br/>virus infection 344<br/>32 Antiviral Chemotherapy 346<br/>The discovery and widespread use of antiviral compounds<br/>began only recently 346<br/>Importance of antiviral drugs for basic science 347<br/>How are antiviral drugs obtained? 347<br/>Targeting drugs to specific steps of virus infection 347<br/>Capsid-binding drugs prevent attachment and entry of<br/>virions 348<br/>Amantadine blocks ion channels and inhibits uncoating of<br/>influenza virions 349<br/>Nucleoside analogues target viral DNA polymerases 349<br/>Acyclovir is selectively phosphorylated by herpesvirus<br/>thymidine kinases 350<br/>Acyclovir is preferentially incorporated by herpesvirus DNA<br/>polymerases 351<br/>Cytomegalovirus encodes a protein kinase that<br/>phosphorylates ganciclovir 351<br/>HIV-1 reverse transcriptase preferentially incorporates<br/>azidothymidine into DNA, leading to chain<br/>termination 354<br/>Nonnucleoside inhibitors selectively target viral replication<br/>enzymes 354<br/>Protease inhibitors can interfere with virus assembly and<br/>maturation 354<br/>Ritonavir: a successful protease inhibitor of HIV-1 that was<br/>developed by rational methods 354<br/>Neuraminidase inhibitors suppress release and spread of<br/>influenza virus 355<br/>Antiviral chemotherapy shows promise for the<br/>future 357<br/>33. Eukaryotic Virus Vectors 358<br/>Many viruses can be engineered to deliver and express<br/>specific genes 358<br/>Virus vectors are used to produce high levels of specific<br/>proteins in cultured cells 359<br/>Gene therapy is an expanding application of virus<br/>vectors 360<br/>Virus vectors are produced by transfection of cells with<br/>plasmids containing deleted genomes 360<br/>Virus vectors are engineered to produce optimal levels of<br/>gene products 361<br/>xxii Contents<br/>ADENOVIRUS VECTORS 362<br/>Adenovirus vectors are widely used in studies of gene transfer<br/>and antitumor therapy 362<br/>Replication-defective adenovirus vectors are propagated in<br/>complementing cell lines 362<br/>Replication-competent adenovirus vectors are useful tools in<br/>antitumor therapy 363<br/>Advantages and limitations of adenovirus vectors 363<br/>RETROVIRUS VECTORS 364<br/>Retrovirus vectors incorporate transgenes into the cell<br/>chromosome 364<br/>Packaging cell lines express retrovirus enzymatic and<br/>structural proteins 364<br/>Strategies for controlling transgene transcription 364<br/>Lentivirus vectors are used for gene delivery to nondividing<br/>cells 365<br/>Production of lentivirus vectors requires additional cis-acting<br/>sequences 366<br/>Applications of retrovirus vectors: treatment of blood<br/>disorders 367<br/>Advantages and limitations of retrovirus vectors 367<br/>ADENO-ASSOCIATED VIRUS VECTORS 367<br/>Adeno-associated virus vectors can insert transgenes into a<br/>specific chromosomal locus 367<br/>Production of AAV vectors usually requires a helper<br/>virus 367<br/>Applications of adeno-associated virus vectors: treatment of<br/>hemophilia 368<br/>Advantages and limitations of AAV vectors 368<br/>34. Viral Vaccines 370<br/>A brief history of viral vaccines 371<br/>Early vaccine technology was crude but effective 372<br/>Embryonated chicken eggs and cell culture played major<br/>roles in recent vaccine development 373<br/>Major categories of viral vaccines 373<br/>Advantages and drawbacks of vaccine types 374<br/>How do viral vaccines work? 375<br/>The role of the immune system in fighting viral<br/>infections 375<br/>Some vaccines target mainly antibody production; others<br/>target the cellular immune response 376<br/>New approaches to vaccine development show great<br/>promise 376<br/>The changing vaccine paradigm 378<br/>Vaccine-associated adverse events 378<br/>Ethical issues in the use of viral vaccines 380 |
| 650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM |
| Topical term or geographic name as entry element |
Molecular virology. |
| 650 12 - SUBJECT ADDED ENTRY--TOPICAL TERM |
| Topical term or geographic name as entry element |
Viruses. |
| 650 22 - SUBJECT ADDED ENTRY--TOPICAL TERM |
| Topical term or geographic name as entry element |
Viral Physiology. |
| 856 41 - ELECTRONIC LOCATION AND ACCESS |
| Materials specified |
Table of contents only |
| Uniform Resource Identifier |
<a href="http://www.loc.gov/catdir/toc/ecip071/2006030744.html">http://www.loc.gov/catdir/toc/ecip071/2006030744.html</a> |
| 856 42 - ELECTRONIC LOCATION AND ACCESS |
| Materials specified |
Publisher description |
| Uniform Resource Identifier |
<a href="http://www.loc.gov/catdir/enhancements/fy0740/2006030744-d.html">http://www.loc.gov/catdir/enhancements/fy0740/2006030744-d.html</a> |
| 906 ## - LOCAL DATA ELEMENT F, LDF (RLIN) |
| a |
7 |
| b |
cbc |
| c |
orignew |
| d |
1 |
| e |
ecip |
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20 |
| g |
y-gencatlg |
| 942 ## - ADDED ENTRY ELEMENTS (KOHA) |
| Source of classification or shelving scheme |
Dewey Decimal Classification |
| Koha item type |
Books |