Fundamentals of molecular virology:
Gespeichert in:
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| Format: | Buch |
| Sprache: | English |
| Veröffentlicht: |
Hoboken, NJ
Wiley
2011
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| Ausgabe: | 2. ed. |
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XXV, 500 S., [1] Bl. Ill., graph. Darst. |
| ISBN: | 9780470900598 |
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| 245 | 1 | 0 | |a Fundamentals of molecular virology |c Nicholas H. Acheson |
| 250 | |a 2. ed. | ||
| 264 | 1 | |a Hoboken, NJ |b Wiley |c 2011 | |
| 300 | |a XXV, 500 S., [1] Bl. |b Ill., graph. Darst. | ||
| 336 | |b txt |2 rdacontent | ||
| 337 | |b n |2 rdamedia | ||
| 338 | |b nc |2 rdacarrier | ||
| 650 | 4 | |a Molecular virology | |
| 650 | 4 | |a Viruses |x Reproduction | |
| 650 | 0 | 7 | |a Molekulare Virologie |0 (DE-588)4170393-5 |2 gnd |9 rswk-swf |
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Datensatz im Suchindex
| _version_ | 1804148673226997760 |
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| adam_text | IMAGE 1
B R I EF C O N T E N TS
SECTION I: INTRODUCTION TO VIROLOGY
1. INTRODUCTION TO VIROLOGY 2
NICHOLAS H. ACHESON, MCGILL UNIVERSITY
2. VIRUS STRUCTURE AND ASSEMBLY 18
STEPHEN C. HARRISON, HARVARD UNIVERSITY
3. VIRUS CLASSIFICATION: THE WORLD OF VIRUSES 31
NICHOLAS H. ACHESON, MCGILL UNIVERSITY
4. VIRUS ENTRY 45
ARI HELENIUS, SWISS FEDERAL INSTITUTE OF TECHNOLOGY, ZURICH
SECTION II: VIRUSES OF BACTERIA AND ARCHAEA
5. SINGLE-STRANDED RNA BACTERIOPHAGES 59
JAN VAN DUIN, UNIVERSITY OF LEIDEN
6. MICROVIRUSES 69
BENTLEY FANE, UNIVERSITY OF ARIZONA
7. BACTERIOPHAGE T7 77
WILLIAM C. SUMMERS, YALE UNIVERSITY
8. BACTERIOPHAGE LAMBDA 85
MICHAEL FEISS, UNIVERSITY OF IOWA
9. VIRUSES OF ARCHAEA 97
DAVID PRANGISHVILI, INSTITUT PASTEUR
SECTION III: POSITIVE-STRAND RNA VIRUSES OF EUKARYOTES
1 O. CUCUMBER MOSAIC VIRUS 1 12
PING X*, J. NOBLE RESEARCH INSTITUTE MARILYN J. ROOSINCK, J. NOBLE
RESEARCH INSTITUTE
1 1. PICORNAVIRUSES 1 25
BERT L. SEMLER, UNIVERSITY OF CALIFORNIA, IRVINE
1 2. FLAVIVIRUSES 137
RICHARD KUHN, PURDUE UNIVERSITY
1 3. TOGAVIRUSES 148
MILTON SCHLESINGER, WASHINGTON UNIVERSITY IN ST. LOUIS SONDRA
SCHLESINGER, WASHINGTON UNIVERSITY IN ST. LOUIS REVISED BY: RICHARD
KUHN, PURDUE UNIVERSITY
1 4. CORONAVIRUSES 159
MARK DENISON, VANDERBILT UNIVERSITY MICHELLE M. BECKER, VANDERBILT
UNIVERSITY
SECTION IV: NEGATIVE-STRAND AND DOUBLE-STRANDED RNA VIRUSES OF
EUKARYOTES
1 5. PARAMYXOVIRUSES AND RHABDOVIRUSES 1 75
NICHOLAS H. ACHESON, MCGILL UNIVERSITY DANIEL KOLAKOFSKY, UNIVERSITY OF
GENEVA CHRISTOPHER RICHARDSON, DALHOUSIE UNIVERSITY
REVISED BY: LAURENT ROUX, UNIVERSITY OF GENEVA
1 6. FILOVIRUSES 188
HEINZ FELDMANN, DIVISION OF INTRAMURAL RESEARCH, MAID, NIH HANS-DIETER
KLENK, UNIVERSITY OF MARBURG NICHOLAS H. ACHESON, MCGILL UNIVERSITY
17. BUNYAVIRUSES 200
RICHARD M. ELLIOTT, UNIVERSITY OF ST. ANDREWS
1 8. INFLUENZA VIRUSES 210
DALIUSJ. BRIEDIS, MCGILL UNIVERSITY
1 9. REOVIRUSES 225
TERENCE S. DERMODY, VANDERBILT UNIVERSITY JAMES D. CHAPPELL, VANDERBILT
UNIVERSITY
IMAGE 2
VI BRIEF CONTENTS
SECTION V: SMALL DNA VIRUSES OF EUKARYOTES
20. PARVOVIRUSES 238
PETER BEARD, SWISS INSTITUTE FOR EXPERIMENTAL CANCER RESEARCH
21. POLYOMAVIRUSES 247
NICHOLAS H. ACHESON, MCGILL UNIVERSITY
22. PAPILLOMAVIRUSES 263
GREG MATLASHEWSKI, MCGILL UNIVERSITY REVISED BY: LAWRENCE BANKS,
INTERNATIONAL CENTRE FOR GENETIC ENGINEERING AND BIOTECHNOLOGY, TRIESTE
SECTION VI: LARGER DNA VIRUSES OF EUKARYOTES
23. ADENOVIRUSES 274
PHILIP BRANTON, MCGILL UNIVERSITY RICHARD C. MARCELLUS, MCGILL
UNIVERSITY
24. HERPESVIRUSES 285
BERNARD ROIZMAN, UNIVERSITY OF CHICAGO GABRIELLA CAMPADELLI-FIUME,
UNIVERSITY OF BOLOGNA RICHARD LONGNECKER, NORTHWESTERN UNIVERSITY
25. BACULOVIRUSES 302
ERIC B. CARSTENS, QUEEN S UNIVERSITY
26. POXVIRUSES 312
RICHARD C. CONDIT, UNIVERSITY OF FLORIDA
27. VIRUSES OF ALGAE AND MIMI VIRUS 325
MICHAEL J. ALLEN, PLYMOUTH MARINE LABORATORY WILLIAM H. WILSON, BIGELORO
LABORATORY FOR OCEAN SCIENCES
SECTION VII: VIRUSES THAT USE A REVERSE TRANSCRIPTASE
28. RETROVIRUSES 342
ALAN COCHRANE, UNIVERSITY OF TORONTO
29. HUMAN IMMUNODEFICIENCY VIRUS 354
ALAN COCHRANE, UNIVERSITY OF TORONTO
30. HEPADNAVIRUSES 365
CHRISTOPHER RICHARDSON, DALHOUSIE UNIVERSITY
SECTION VIII: VIROIDS AND PRIONS
3 1. VIROIDS AND HEPATITIS DELTA VIRUS 378
JEAN-PIERRE PERREAULT, UNIVERSITE DE SHERBROOKE MARTIN PELCHAT,
UNIVERSITY OF OTTAWA
32. PRIONS 387
DALIUSJ. BRIEDIS, MCGILL UNIVERSITY
SECTION IX: HOST DEFENSES AGAINST VIRUS INFECTION
33. INTRINSIC CELLULAR DEFENSES AGAINST VIRUS INFECTION 398
KAREN MOSSMAN, MCMASTER UNIVERSITY PIERRE GENIN, UNIVERSITY PARIS
DESCARTES JOHN HISCOTT, MCGILL UNIVERSITY
34. INNATE AND ADAPTIVE IMMUNE RESPONSES TO VIRUS INFECTION 415
MALCOLM G. BAINES, MCGILL UNIVERSITY KAREN MOSSMAN, MCMASTER UNIVERSITY
SECTION X: ANTIVIRAL AGENTS AND VIRUS VECTORS
35. ANTIVIRAL VACCINES 428
BRIAN WARD, MCGILL UNIVERSITY
36. ANTIVIRAL CHEMOTHERAPY 444
DONALD M. COEN, HARVARD UNIVERSITY
37. EUKARYOTIC VIRUS VECTORS 456
RENALD GILBERT, NRC BIOTECHNOLOGY RESEARCH INSTITUTE, MONTREAL BERNARD
MASSIE, NRC BIOTECHNOLOGY RESEARCH INSTITUTE, MONTREAL
IMAGE 3
C O N T E N TS
SECTION I: INTRODUCTION TO VIROLOGY
1. INTRODUCTION TO VIROLOGY 2
THE NATURE OF VIRUSES 3 VIRUSES CONSIST OF A NUCLEIC ACID GENOME
PACKAGED IN A PROTEIN COAT 3 VIRUSES ARE DEPENDENT ON LIVING CELLS FOR
THEIR REPLICATION
VIRUS PARTICLES BREAK DOWN AND RELEASE THEIR GENOMES INSIDE THE CELL 3
VIRUS GENOMES ARE EITHER RNA OR DNA, BUT NOT BOTH 4
WHY STUDY VIRUSES? 4 VIRUSES ARE IMPORTANT DISEASE-CAUSING AGENTS 4
VIRUSES CAN INFECT ALL FORMS OF LIFE 4 VIRUSES ARE THE MOST ABUNDANT
FORM OF LIFE ON EARTH 5
THE STUDY OF VIRUSES HAS LED TO NUMEROUS DISCOVERIES IN MOLECULAR AND
CELL BIOLOGY 5
A BRIEF HISTORY OF VIROLOGY:
TH E STU DY OF VI RUSES 6 THE SCIENTIFIC STUDY OF VIRUSES IS VERY RECENT
6 VIRUSES WERE FIRST DISTINGUISHED FROM OTHER MICROORGANISMS BY
FILTRATION 6
THE CRYSTALLIZATION OF TOBACCO MOSAIC VIRUS CHALLENGED CONVENTIONAL
NOTIONS ABOUT GENES AND THE NATURE OF LIVING ORGANISMS 6 THE PHAGE
GROUP STIMULATED STUDIES OF BACTERIOPHAGES
AND HELPED ESTABLISH THE FIELD OF MOLECULAR BIOLOGY 7 STUDY OF TUMOR
VIRUSES LED TO DISCOVERIES IN MOLECULAR BIOLOGY AND UNDERSTANDING OF THE
NATURE OF CANCER 8
DETECTION AND TITRATION OF VIRUSES MOST VIRUSES WERE FIRST DETECTED AND
STUDIED BY INFECTION OF INTACT ORGANISMS 9 THE PLAQUE ASSAY AROSE FROM
WORK WITH BACTERIOPHAGES 9
EUKARYOTIC CELLS CULTURED IN VITRO HAVE BEEN ADAPTED FOR PLAQUE ASSAYS 9
HEMAGGLUTINATION IS A CONVENIENT AND RAPID ASSAY FOR MANY VIRUSES 10
VIRUS PARTICLES CAN BE SEEN AND COUNTED BY ELECTRON
MICROSCOPY 10 THE RATIO OF PHYSICAL VIRUS PARTICLES TO INFECTIOUS
PARTICLES CAN BE MUCH GREATER THAN 1 11
THE VIRUS REPLICATION CYCLE: AN OVERVIEW 11 THE SINGLE-CYCLE VIRUS
REPLICATION EXPERIMENT 11
AN EXAMPLE OF A VIRUS REPLICATION CYCLE: MOUSE POLYOMAVIRUS 12
14 15
ANALYSIS OF VIRAL MACROMOLECULES REVEALS THE DETAILED PATHWAYS OF VIRUS
REPLICATION 13
STEPS IN THE VIRUS REPLICATION CYCLE 13 1. VIRIONS BIND TO RECEPTORS ON
THE CELL SURFACE 13 2. THE VIRION (OR THE VIRAL GENOME) ENTERS THE CELL
14
3. EARLY VIRAL GENES ARE EXPRESSED: THE BALTIMORE CLASSIFICATION OF
VIRUSES 14 THE SEVEN GROUPS IN THE BALTIMORE CLASSIFICATION SYSTEM 4.
EARLY VIRAL PROTEINS DIRECT REPLICATION OF VIRAL GENOMES
5. LATE MESSENGER RNAS ARE MADE FROM NEWLY REPLICATED GENOMES 15 6. LATE
VIRAL PROTEINS PACKAGE VIRAL GENOMES AND ASSEMBLE VIRIONS 16
7. PROGENY VIRIONS ARE RELEASED FROM THE HOST CELL 16
2. VIRUS STRUCTURE AND ASSEMBLY 18
BASIC CONCEPTS OF VIRUS STRUCTURE 18 VIRUS STRUCTURE IS STUDIED BY
ELECTRON MICROSCOPY AND X-RAY DIFFRACTION 19
MANY VIRUSES COME IN SIMPLE, SYMMETRICAL PACKAGES 19
CAPSIDS WITH ICOSAHEDRAL SYMMETRY 21 SOME EXAMPLES OF VIRIONS WITH
ICOSAHEDRAL SYMMETRY THE CONCEPT OF QUASI-EQUIVALENCE 21 LARGER VIRUSES
COME IN MORE COMPLEX PACKAGES 2 3
CAPSIDS WITH HELICAL SYMMETRY 25
VIRAL ENVELOPES 26 VIRAL ENVELOPES ARE MADE FROM LIPID BILAYER MEMBRANES
26 VIRAL GLYCOPROTEINS ARE INSERTED INTO THE LIPID MEMBRANE TO FORM THE
ENVELOPE 2 7
PACKAGING OF GENOMES AND VIRION ASSEMBLY 28 MULTIPLE MODES OF CAPSID
ASSEMBLY 2 8
SPECIFIC PACKAGING SIGNALS DIRECT INCORPORATION OF VIRAL GENOMES INTO
VIRIONS 2 8 CORE PROTEINS MAY ACCOMPANY THE VIRAL GENOME INSIDE THE
CAPSID 28 FORMATION OF VIRAL ENVELOPES BY BUDDING IS DRIVEN BY
INTERACTIONS BETWEEN VIRAL PROTEINS 2 8
DISASSEMBLY OF VIRIONS: THE DELIVERY OF VIRAL GENOMES TO THE HOST CELL
29 VIRIONS ARE PRIMED TO ENTER CELLS AND RELEASE THEIR GENOME 29
VII
IMAGE 4
VIII CONTENTS
3. VIRUS CLASSIFICATION: THE WORLD OF VIRUSES 31 VIRUS CLASSIFICATION 31
MANY DIFFERENT VIRUSES INFECTING A WIDE VARIETY
OF ORGANISMS HAVE BEEN DISCOVERED 31 VIRUS CLASSIFICATION IS BASED ON
MOLECULAR ARCHITECTURE, GENETIC RELATEDNESS, AND HOST ORGANISM 3 1
VIRUSES ARE GROUPED INTO SPECIES, GENERA, AND FAMILIES 32
DISTINCT NAMING CONVENTIONS AND CLASSIFICATION SCHEMES HAVE DEVELOPED IN
DIFFERENT DOMAINS OF VIROLOGY 33
MAJOR VIRUS GROUPS 33 STUDY OF THE MAJOR GROUPS OF VIRUSES LEADS TO
UNDERSTANDING OF SHARED CHARACTERISTICS AND REPLICATION PATHWAYS 3 3
VIRUSES WITH SINGLE-STRANDED DNA GENOMES ARE SMALL AND
HAVE FEW GENES 34 VIRUSES WITH DOUBLE-STRANDED DNA GENOMES INCLUDE THE
LARGEST KNOWN VIRUSES 3 5 MOST PLANT VIRUSES AND MANY VIRUSES OF
VERTEBRATES HAVE
POSITIVE-STRAND RNA GENOMES 35 VIRUSES WITH NEGATIVE-STRAND RNA GENOMES
HAVE HELICAL NUCLEOCAPSIDS; SOME HAVE FRAGMENTED GENOMES 38 VIRUSES WITH
DOUBLE-STRANDED RNA GENOMES HAVE
FRAGMENTED GENOMES AND CAPSIDS WITH ICOSAHEDRAL SYMMETRY 3 8 VIRUSES
WITH A REVERSE TRANSCRIPTION STEP IN THEIR REPLICATION CYCLE CAN HAVE
EITHER RNA OR DNA GENOMES 39
SATELLITE VIRUSES AND SATELLITE NUCLEIC ACIDS REQUIRE A HELPER VIRUS TO
REPLICATE 40 VIROIDS DO NOT CODE FOR PROTEINS, BUT REPLICATE
INDEPENDENTLY OF OTHER VIRUSES 40
THE EVOLUTIONARY ORIGIN OF VIRUSES 40 THE FIRST STEPS IN THE DEVELOPMENT
OF LIFE ON EARTH: THE RNA WORLD 40
VIROIDS AND RNA VIRUSES MAY HAVE ORIGINATED IN THE RNA WORLD 41 THE
TRANSITION TO THE DNA-BASED WORLD 42 RETROVIRUSES COULD HAVE ORIGINATED
DURING THE
TRANSITION TO DNA-BASED CELLS 43 SMALL- AND MEDIUM-SIZED DNA VIRUSES
COULD HAVE ARISEN AS INDEPENDENTLY REPLICATING GENETIC
ELEMENTS IN CELLS 43 LARGE DNA VIRUSES COULD HAVE EVOLVED FROM CELLULAR
FORMS THAT BECAME OBLIGATORY
INTRACELLULAR PARASITES 43 THESE ARGUMENTS ABOUT THE ORIGIN OF VIRUSES
ARE ONLY SPECULATIONS 44
4. VIRUS ENTRY 45
HOW DO VIRIONS GET INTO CELLS? 45 ENVELOPED AND NON-ENVELOPED VIRUSES
HAVE DISTINCT PENETRATION STRATEGIES 46 SOME VIRUSES CAN PASS DIRECTLY
FROM CELL TO CELL 46
A VARIETY OF CELL SURFACE PROTEINS CAN SERVE AS SPECIFIC VIRUS RECEPTORS
47 RECEPTORS INTERACT WITH VIRAL GLYCOPROTEINS, SURFACE PROTRUSIONS, OR
CANYONS ON THE SURFACE OF THE VIRION 48 MANY VIRUSES ENTER THE CELL
VIA RECEPTOR-MEDIATED
ENDOCYTOSIS 48 PASSAGE FROM ENDOSOMES TO THE CYTOSOL IS OFTEN TRIGGERED
BY LOW PH 49 MEMBRANE FUSION IS MEDIATED BY SPECIFIC VIRAL FUSION
PROTEINS 50 FUSION PROTEINS UNDERGO MAJOR CONFORMATIONAL CHANGES THAT
LEAD TO MEMBRANE FUSION 50 NON-ENVELOPED VIRUSES PENETRATE BY MEMBRANE
LYSIS OR
PORE FORMATION 51 VIRIONS AND CAPSIDS ARE TRANSPORTED WITHIN THE CELL IN
VESICLES OR ON MICROTUBULES 52 IMPORT OF VIRAL GENOMES INTO THE NUCLEUS
52 THE MANY WAYS IN WHICH VIRAL GENOMES ARE
UNCOATED AND RELEASED 54
SECTION II: VIRUSES OF BACTERIA AND ARCHAEA
5. SINGLE-STRANDED RNA BACTERIOPHAGES 59 THE DISCOVERY OF RNA PHAGES
STIMULATED RESEARCH INTO MESSENGER RNA FUNCTION AND
RNA REPLICATION 59 RNA PHAGES ARE AMONG THE SIMPLEST KNOWN ORGANISMS 59
TWO GENERA OF RNA PHAGES HAVE SUBTLE DIFFERENCES 60 RNA PHAGES BIND TO
THE F-PILUS AND USE IT TO INSERT THEIR
RNA INTO THE CELL 60 PHAGE RNA IS TRANSLATED AND REPLICATED IN A
REGULATED FASHION 61 RNA SECONDARY STRUCTURE CONTROLS TRANSLATION OF
LYSIS AND
REPLICASE GENES 61 RIBOSOMES TRANSLATING THE COAT GENE DISRUPT SECONDARY
STRUCTURE, ALLOWING REPLICASE TRANSLATION 62 RIBOSOMES TERMINATING COAT
TRANSLATION CAN REINITIATE AT THE
LYSIS GENE START SITE 63 REPLICATION VERSUS TRANSLATION: COMPETITION FOR
THE SAME RNA TEMPLATE 64 GENOME REPLICATION REQUIRES FOUR HOST CELL
PROTEINS
PLUS THE REPLICASE 64 A HOST RIBOSOMAL PROTEIN DIRECTS POLYMERASE TO THE
COAT START SITE 65 POLYMERASE SKIPS THE FIRST A RESIDUE BUT ADDS A
TERMINAL
A TO THE MINUS-STRAND COPY 65 SYNTHESIS OF PLUS-STRANDS IS LESS COMPLEX
AND MORE EFFICIENT THAN THAT OF MINUS-STRANDS 65 THE START SITE FOR
SYNTHESIS OF MATURATION PROTEIN IS
NORMALLY INACCESSIBLE TO RIBOSOMES 65 SYNTHESIS OF MATURATION PROTEIN IS
CONTROLLED BY DELAYED RNA FOLDING 66 ASSEMBLY AND RELEASE OF VIRIONS 67
J
IMAGE 5
CONTENTS IX
6. MICROVIRUSES 69
TPX174: A TINY VIRUS WITH A BIG IMPACT 69 OVERLAPPING READING FRAMES
ALLOW EFFICIENT USE OF A SMALL GENOME 70 TPX174 BINDS TO GLUCOSE
RESIDUES IN LIPOPOLYSACCHARIDE
ON THE CELL SURFACE 70 TPX174 DELIVERS ITS GENOME INTO THE CELL THROUGH
SPIKES ON THE CAPSID SURFACE 71 STAGE I DNA REPLICATION GENERATES
DOUBLE-STRANDED
REPLICATIVE FORM DNA 72 GENE EXPRESSION IS CONTROLLED BY THE STRENGTH OF
PROMOTERS AND TRANSCRIPTIONAL TERMINATORS 72 REPLICATIVE FORM DNAS ARE
AMPLIFIED VIA A ROLLING CIRCLE
MECHANISM 72 SUMMARY OF VIRAL DNA REPLICATION MECHANISMS 73 PROCAPSIDS
ARE ASSEMBLED BY THE USE OF SCAFFOLDING PROTEINS 73
SCAFFOLDING PROTEINS HAVE A FLEXIBLE STRUCTURE 74 SINGLE-STRANDED
GENOMES ARE PACKAGED INTO PROCAPSIDS AS THEY ARE SYNTHESIZED 74 ROLE OF
THE J PROTEIN IN DNA PACKAGING 75
CELL LYSIS CAUSED BY E PROTEIN LEADS TO RELEASE OF PHAGE 75 DID ALL
ICOSAHEDRAL SSDNA VIRUS FAMILIES EVOLVE FROM A COMMON ANCESTOR? 75
7. BACTERIOPHAGE T7 77
T7: A MODEL PHAGE FOR DNA REPLICATION, TRANSCRIPTION, AND RNA PROCESSING
77 T7 GENES ARE ORGANIZED INTO THREE GROUPS BASED ON TRANSCRIPTION AND
GENE FUNCTION 78
ENTRY OF T7 DNA INTO THE CYTOPLASM IS POWERED BY TRANSCRIPTION 79
TRANSCRIPTION OF CLASS II AND III GENES REQUIRES A NOVEL T7-CODED RNA
POLYMERASE 79
CLASS II GENES CODE FOR ENZYMES INVOLVED IN T7 DNA REPLICATION 80 T7
RNAS ARE CLEAVED BY HOST CELL RIBONUCLEASE III TO SMALLER, STABLE INRNAS
80
CLASS III GENE EXPRESSION IS REGULATED BY DELAYED ENTRY AND BY PROMOTER
STRENGTH 80 DNA REPLICATION STARTS AT A UNIQUE INTERNAL ORIGIN AND IS
PRIMED BY T7 RNA POLYMERASE 80 LARGE DNA CONCATEMERS ARE FORMED
DURING REPLICATION 81 CONCATEMER PROCESSING DEPENDS ON TRANSCRIPTION BY
T7 RNA POLYMERASE AND OCCURS DURING DNA PACKAGING INTO PREFORMED
PROHEADS 82
SPECIAL FEATURES OF THE T7 FAMILY OF PHAGES 82
8. BACTERIOPHAGE LAMBDA 85
ROOTS... 85
PHAGE ADSORPTION AND DNA ENTRY DEPEND ON CELLULAR PROTEINS INVOLVED IN
SUGAR TRANSPORT 86
THE X LYTIC TRANSCRIPTION PROGRAM IS CONTROLLED BY TERMINATION AND
ANTITERMINATION OF RNA SYNTHESIS AT SPECIFIC SITES ON THE GENOME 87
THE CI REPRESSOR BLOCKS EXPRESSION OF THE LYTIC PROGRAM BY REGULATING
THREE NEARBY PROMOTERS: P ] , P R ,ANDP RV , 88 CLEAVAGE OF CI REPRESSOR
IN CELLS WITH DAMAGED DNA
LEADS TO PROPHAGE INDUCTION 89 THE CRO REPRESSOR SUPPRESSES CI SYNTHESIS
AND REGULATES EARLY GENE TRANSCRIPTION 89 MAKING THE DECISION: GO LYTIC
OR LYSOGENIZE? 90
A QUICK REVIEW 90 BREAKING AND ENTERING: THE INSERTION OF X PROPHAGE DNA
INTO THE BACTERIAL CHROMOSOME 90 EXCISION OF DNA FROM THE BACTERIAL
CHROMOSOME 92 INT SYNTHESIS IS CONTROLLED BY RETROREGULATION 93
X DNA REPLICATION IS DIRECTED BY O AND P, BUT CARRIED OUT BY HOST CELL
PROTEINS 93 ASSEMBLY OF X HEADS INVOLVES CHAPERONES AND SCAFFOLDING
PROTEINS 93
DNA IS INSERTED INTO PREFORMED PROHEADS BY AN ATP-DEPENDENT MECHANISM 94
HOST CELL LYSIS 94
9. VIRUSES OF ARCHAEA 97
ARCHAEA, THE THIRD DOMAIN OF LIFE 97 VIRUSES OF ARCHAEA HAVE DIVERSE AND
UNUSUAL MORPHOLOGIES 99
FUSELLOVIRIDAE ARE TEMPERATE VIRUSES THAT PRODUCE VIRIONS WITHOUT
KILLING THE HOST CELL 99 GENOMES OF FUSELLOVIRUSES ARE POSITIVELY
SUPERCOILED 101 TRANSCRIPTION OF SSV-1 DNA IS TEMPORALLY CONTROLLED 101
FILAMENTOUS ENVELOPED VIRUSES OF THE LIPOTHRIXVIRIDAE COME IN MANY
LENGTHS 102 A DROPLET-SHAPED VIRUS IS THE ONLY KNOWN MEMBER OF THE
GUTTAVIRIDAE (FROM THE LATIN GTITTA, DROPLET ) 103 ACIDIANIIS
BOTTLE-SHAPED VIRUS (ABV): ITS NAME
SAYS IT ALL! 103 THE GENOME OF PYROBACULUM SPHERICAL VIRUS HAS NEARLY
ALL OPEN READING FRAMES ENCODED ON ONE DNA STRAND 104 VIRUSES IN THE
FAMILY RUDIVIRIDAE (FROM THE LATIN RUDIS,
SMALL ROD ) ARE NON-ENVELOPED, HELICAL RODS 105 RUDIVIRUSES ESCAPE FROM
THE CELL BY MEANS OF UNIQUE PYRAMIDAL STRUCTURES 106 ACIDIANUS
TWO-TAILED VIRUS (ATV) HAS A VIRION WITH TAILS THAT
SPONTANEOUSLY ELONGATE 106 INFECTION WITH ATV AT HIGH TEMPERATURES LEADS
TO LYSOGENY 106 TWO RELATED VIRUSES OF HYPERHALOPHILES RESEMBLE
FUSELLOVIRUSES BY MORPHOLOGY BUT NOT BY GENETICS 108 TWO UNUSUAL VIRUSES
WITH ICOSAHEDRAL CAPSIDS AND PROMINENT
SPIKES 108 A VIRUS WITH A SINGLE-STRANDED DNA GENOME IS CLOSELY RELATED
TO A VIRUS WITH A DOUBLE-STRANDED DNA GENOME 108 COMPARATIVE GENOMICS OF
ARCHAEAL VIRUSES 109
CONCLUSION 1 10
IMAGE 6
XII CONTENTS
EBOLA VIRUS USES RNA EDITING TO MAKE TWO GLYCOPROTEINS FROM THE SAME
GENE 194 DO THE SECRETED GLYCOPROTEINS PLAY A ROLE IN VIRUS
PATHOGENESIS? 195 MINOR NUCLEOCAPSID PROTEIN VP30 ACTIVATES VIRAL MRNA
SYNTHESIS IN EBOLA VIRUS 195 MATRIX PROTEIN VP40 DIRECTS BUDDING AND
FORMATION OF FILAMENTOUS PARTICLES 195 MOST FILOVIRUS OUTBREAKS HAVE
OCCURRED IN EQUATORIAL
AFRICA 196 FILOVIRUS INFECTIONS ARE TRANSMITTED TO HUMANS FROM AN
UNKNOWN ANIMAL ORIGIN 197 SPREAD OF FILOVIRUS INFECTIONS AMONG HUMANS IS
LIMITED TO
CLOSE CONTACTS 197 PATHOGENESIS OF FILOVIRUS INFECTIONS 197 CLINICAL
FEATURES OF INFECTION 198
1 7. BUNYAVIRUSES 200
MOST BUNYAVIRUSES ARE TRANSMITTED BY ARTHROPOD VECTORS, INCLUDING
MOSQUITOES AND TICKS 200 SOME BUNYAVIRUSES CAUSE SEVERE HEMORRHAGIC
FEVER, RESPIRATORY DISEASE, OR ENCEPHALITIS 201 BUNYAVIRUSES ENCAPSIDATE
A SEGMENTED RNA GENOME IN A
SIMPLE ENVELOPED PARTICLE 202 BUNYAVIRUS PROTEIN CODING STRATEGIES:
NEGATIVE-STRAND AND AMBISENSE RNAS 203 L RNA CODES FOR VIRAL RNA
POLYMERASE 203 M RNA CODES FOR VIRION ENVELOPE GLYCOPROTEINS 203
S RNA CODES FOR NUCLEOCAPSID PROTEIN AND A NONSTRUCTURAL PROTEIN 204
AFTER ATTACHMENT VIA VIRION GLYCOPROTEINS, BUNYAVIRUSES ENTER THE CELL
BY ENDOCYTOSIS 204
BUNYAVIRUS MRNA SYNTHESIS IS PRIMED BY THE CAPPED 5 ENDS OF CELLULAR
MRNAS 204 COUPLED TRANSLATION AND TRANSCRIPTION MAY PREVENT PREMATURE
TERMINATION OF MRNAS 206
GENOME REPLICATION BEGINS ONCE SUFFICIENT N PROTEIN IS MADE 206 VIRUS
ASSEMBLY TAKES PLACE AT GOLGI MEMBRANES 206 EVOLUTIONARY POTENTIAL OF
BUNYAVIRUSES VIA GENOME
REASSORTMENT 207
18. INFLUENZA VIRUSES 210
INFLUENZA VIRUSES CAUSE SERIOUS ACUTE DISEASE IN HUMANS, AND OCCASIONAL
PANDEMICS 210 INFLUENZA VIRUS INFECTIONS OF THE RESPIRATORY TRACT CAN
LEAD TO SECONDARY BACTERIAL INFECTIONS 211
ORTHOMYXOVIRUSES ARE NEGATIVE-STRAND RNA VIRUSES WITH SEGMENTED GENOMES
211 EIGHT INFLUENZA VIRUS GENOME SEGMENTS CODE FOR A TOTAL OF 11
DIFFERENT VIRAL PROTEINS 2 12
HEMAGGLUTININ PROTEIN BINDS TO CELL RECEPTORS AND MEDIATES FUSION OF THE
ENVELOPE WITH THE ENDOSOMAL MEMBRANE 214 M2 IS AN ION CHANNEL THAT
FACILITATES RELEASE OF NUCLEOCAPSIDS FROM THE VIRION 214
NUCLEOCAPSIDS ENTER THE NUCLEUS, WHERE MRNA SYNTHESIS AND RNA
REPLICATION OCCUR 215 CAPPED 5 ENDS OF CELLULAR PREMESSENGER RNAS ARE
USED AS PRIMERS FOR SYNTHESIS OF VIRAL MRNAS 215 VIRAL MRNAS TERMINATE
IN POLY(A) TAILS GENERATED BY
STUTTERING TRANSCRIPTION 216 TWO INFLUENZA A MRNAS UNDERGO ALTERNATIVE
SPLICING IN THE NUCLEUS 216 GENOME REPLICATION BEGINS WHEN NEWLY
SYNTHESIZED NP
PROTEIN ENTERS THE NUCLEUS 217 NUCLEOCAPSIDS ARE EXPORTED FROM THE
NUCLEUS IN A COMPLEX WITH MATRIX PROTEIN AND NS2 218 THE NS1 PROTEIN
INTERFERES WITH POLYADENYLATION OF CELLULAR
MRNAS 218 THE NS1 PROTEIN ALSO SUPPRESSES A VARIETY OF HOST CELL
ANTIVIRAL RESPONSE PATHWAYS 219 PB1-F2 MAY CONTRIBUTE TO SUPPRESSION OF
THE HOST IMMUNE
RESPONSE 219 VIRAL ENVELOPE PROTEINS ASSEMBLE IN THE PLASMA INEMBRANE
AND DIRECT BUDDING OF VIRIONS 219 NEURAMINIDASE CLEAVES SIALIC ACID, THE
CELLULAR RECEPTOR THAT
BINDS TO HA 220 INFLUENZA VIRUS STRAINS VARY IN BOTH TRANSMISSIBILITY
AND PATHOGENICITY 220 GENETIC VARIABILITY GENERATES NEW VIRUS STRAINS
THAT CAN CAUSE
PANDEMICS 220 THE 1918 PANDEMIC INFLUENZA A VIRUS WAS PROBABLY NOT A
REASSORTANT VIRUS 221 GENOME SEQUENCES FROM SOME PREVIOUS INFLUENZA A
VIRUS
STRAINS CONFIRM THE ANTIGENIC SHIFT HYPOTHESIS 221 HIGHLY PATHOGENIC
AVIAN INFLUENZA A H5N1 STRAINS IN POULTRY FARMS ARE A POTENTIAL THREAT
BUT ARE POORLY TRANSMITTED AMONG HUMANS 221 A NEW PANDEMIC STRAIN OF
INFLUENZA A VIRUS AROSE BY GENETIC
SHIFT AND SPREAD WORLDWIDE IN 2009 222
19. REOVIRUSES 225
REOVIRUSES WERE THE FIRST DOUBLE-STRANDED RNA VIRUSES DISCOVERED 225
SOME MEMBERS OF THE REOVIRIDAE ARE IMPORTANT PATHOGENS 226 REOVIRIDAE
HAVE SEGMENTED GENOMES MADE OF DOUBLE-
STRANDED RNA 226 REOVIRUS VIRIONS CONTAIN CONCENTRIC LAYERS OF CAPSID
PROTEINS 227 THE ATTACHMENT PROTEIN BINDS TO ONE OR TWO CELLULAR
RECEPTORS 228 DURING ENTRY, THE OUTER CAPSID IS STRIPPED FROM VIRIONS
AND THE CORE IS RELEASED INTO THE CYTOPLASM 229 ENZYMES IN THE VIRAL
CORE SYNTHESIZE AND CAP MESSENGER
RNAS 230 TRANSLATION OF REOVIRUS MRNAS IS REGULATED 231 INTERFERON AND
PKR: EFFECTS ON VIRAL AND CELLULAR PROTEIN SYNTHESIS 231
SYNTHESIS OF PROGENY DOUBLE-STRANDED GENOMES OCCURS WITHIN SUBVIRAL
PARTICLES 232
IMAGE 7
CONTENTS XIII
REOVIRUSES INDUCE APOPTOSIS VIA ACTIVATION OF INNATE IMMUNE
RESPONSE TRANSCRIPTION FACTORS N F - KB AND IRF-3 233 STUDIES OF
REOVIRUS PATHOGENESIS IN MICE 234
SECTION V: SMALL DNA VIRUSES OF EUKARYOTES
20. PARVOVIRUSES 238
PARVOVIRUSES HAVE VERY SMALL VIRIONS AND A LINEAR, SINGLE-STRANDED DNA
GENOME 238 PARVOVIRUSES REPLICATE IN CELLS THAT ARE GOING THROUGH THE
CELL CYCLE 239 DISCOVERY OF MAMMALIAN PARVOVIRUSES 2 3 9 PARVOVIRUSES
HAVE ONE OF THE SIMPLEST-KNOWN VIRION
STRUCTURES 239 PARVOVIRUSES HAVE VERY FEW GENES 239 SINGLE-STRANDED
PARVOVIRUS DNAS HAVE UNUSUAL
TERMINAL STRUCTURES 240 UNCOATING OF PARVOVIRUS VIRIONS TAKES PLACE IN
THE NUCLEUS AND IS CELL-SPECIFIC 240 DNA REPLICATION BEGINS BY EXTENSION
OF THE 3 END
OF THE TERMINAL HAIRPIN 241 THE DNA END REPLICATION PROBLEM 241 STEPS
IN DNA REPLICATION 243 NONSTRUCTURAL PROTEINS ARE MULTIFUNCTIONAL 243
ADENOVIRUS FUNCTIONS THAT HELP REPLICATION OF
ADENO-ASSOCIATED VIRUS 244 IN THE ABSENCE OF HELPER VIRUS,
ADENO-ASSOCIATED VIRUS DNA CAN INTEGRATE INTO THE CELL GENOME 244
PARVOVIRUS PATHOGENESIS: THE EXAMPLE OF B19 VIRUS 244
21. POLYOMAVIRUSES 247
MOUSE POLYOMAVIRUS WAS DISCOVERED AS A TUMOR-PRODUCING INFECTIOUS AGENT
247 SIMIAN VIRUS 40 WAS FOUND AS A CONTAMINANT OF SALK POLIOVIRUS
VACCINE 247 HUMAN POLYOMAVIRUSES ARE WIDESPREAD BUT CAUSE DISEASE
ONLY RARELY 248 POLYOMAVIRUSES ARE MODELS FOR STUDYING DNA VIRUS
REPLICATION AND TUMORIGENESIS 248 POLYOMAVIRUS CAPSIDS ARE CONSTRUCTED
FROM PENTAMERS OF THE
MAJOR CAPSID PROTEIN 248 THE CIRCULAR DNA GENOME IS PACKAGED WITH
CELLULAR HISTONES 249 CIRCULAR DNA BECOMES SUPERCOILED UPON REMOVAL
OF HISTONES 249 SUPERCOILED DNA CAN BE SEPARATED FROM RELAXED OR LINEAR
DNA MOLECULES 250 POLYOMAVIRUS GENES ARE ORGANIZED IN TWO DIVERGENT
TRANSCRIPTION UNITS 250 VIRIONS ENTER CELLS IN CAVEOLAE AND ARE
TRANSPORTED TO THE NUCLEUS 2 51 THE VIRAL MINICHROMOSOME IS TRANSCRIBED
BY CELLULAR RNA
POLYMERASE II 252
FOUR EARLY MRNAS ARE MADE BY DIFFERENTIAL SPLICING OF A COMMON
TRANSCRIPT 253 T ANTIGENS SHARE COMMON N-TERMINAL SEQUENCES BUT HAVE
DIFFERENT C-TERMINAL SEQUENCES 254
T ANTIGENS BRING RESTING CELLS INTO THE DNA SYNTHESIS (S) PHASE OF THE
CELL CYCLE 254 SMALL T ANTIGEN INHIBITS PROTEIN PHOSPHATASE 2A AND
INDUCES CELL CYCLING 254 MIDDLE T ANTIGEN STIMULATES PROTEIN TYROSINE
KINASES THAT
SIGNAL CELL PROLIFERATION AND DIVISION 255 LARGE T ANTIGEN ACTIVATES OR
SUPPRESSES TRANSCRIPTION OF CELLULAR GENES BY BINDING TO A NUMBER OF
IMPORTANT CELLULAR
REGULATORY PROTEINS 255 LARGE T ANTIGEN HEXAMERS BIND TO THE ORIGIN OF
DNA REPLICATION AND LOCALLY UNWIND THE TWO DNA STRANDS 257 LARGE T
ANTIGEN ASSEMBLES THE CELLULAR DNA SYNTHESIS
MACHINERY TO INITIATE VIRAL DNA REPLICATION 257 HIGH LEVELS OF LATE
TRANSCRIPTS ARE MADE AFTER DNA REPLICATION BEGINS 259 THREE LATE MRNAS
ARE MADE BY ALTERNATIVE SPLICING 260
HOW DO POLYOMAVIRUSES TRANSFORM CELLS IN VITRO AND CAUSE TUMORS IN VIVO}
260 ONLY NON-PERMISSIVE CELLS CAN BE TRANSFORMED 261 TRANSFORMED CELLS
INTEGRATE VIRAL DNA INTO THE CELL
CHROMOSOME 261
22. PAPILLOMAVIRUSES 263
PAPILLOMAVIRUSES CAUSE WARTS AND OTHER SKIN AND MUCOSAL LESIONS 263
ONCOGENIC HUMAN PAPILLOMAVIRUSES ARE A MAJOR CAUSE OF GENITAL TRACT
CANCERS 264 PAPILLOMAVIRUSES ARE NOT EASILY GROWN IN CELL CULTURE 264
PAPILLOMAVIRUS GENOMES ARE CIRCULAR, DOUBLE-STRANDED DNA 264 THE
INFECTIOUS CYCLE FOLLOWS DIFFERENTIATION OF EPITHELIAL CELLS 265 VIRAL
MRNAS ARE MADE FROM TWO PROMOTERS AND TWO
POLYADENYLATION SIGNALS 266 VIRAL EL AND E2 PROTEINS BIND TO THE
REPLICATION ORIGIN AND DIRECT INITIATION OF DNA REPLICATION 267 VIRAL E7
PROTEIN INTERACTS WITH CELL-CYCLE REGULATORY PROTEINS,
PARTICULARLY RB 267 VIRAL E6 PROTEIN CONTROLS THE LEVEL OF CELLULAR P53
PROTEIN 268 SYNERGISM BETWEEN E6 AND E7 AND THE PREDISPOSITION
TO CANCER 269 CELLS TRANSFORMED BY PAPILLOMAVIRUSES EXPRESS E6 AND E7
GENE PRODUCTS FROM INTEGRATED VIRAL DNA 270 FUTURE PROSPECTS FOR
DIAGNOSIS AND TREATMENT OF DISEASES
CAUSED BY PAPILLOMAVIRUSES 270
SECTION VI: LARGER DNA VIRUSES OF EUKARYOTES
23. ADENOVIRUSES 274
ADENOVIRUSES CAUSE RESPIRATORY AND ENTERIC INFECTIONS IN HUMANS 274
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XIV CONTENTS
ADENOVIRUSES CAN BE ONCOGENIC, BUT DO NOT CAUSE CANCER IN HUMANS 274
VIRIONS HAVE ICOSAHEDRAL SYMMETRY AND ARE STUDDED WITH KNOBBED FIBERS
275
FIBERS MAKE CONTACT WITH CELLULAR RECEPTOR PROTEINS TO INITIATE
INFECTION 276 EXPRESSION OF ADENOVIRUS GENES IS CONTROLLED AT THE LEVEL
OF TRANSCRIPTION 276 EL A PROTEINS ARE THE KINGPINS OF THE ADENOVIRUS
GROWTH CYCLE 277 E1A PROTEINS BIND TO THE RETINOBLASTOMA PROTEIN AND
ACTIVATE E2F, A CELLULAR TRANSCRIPTION FACTOR 277 EL A PROTEINS ALSO
ACTIVATE OTHER CELLULAR
TRANSCRIPTION FACTORS 278 EL A PROTEINS INDIRECTLY INDUCE APOPTOSIS BY
ACTIVATION OF CELLULAR P53 PROTEIN 279 E1B PROTEINS SUPPRESS ELA-INDUCED
APOPTOSIS AND TARGET
KEY PROTEINS FOR DEGRADATION, ALLOWING VIRUS REPLICATION TO PROCEED 279
THE PRETERMINAL PROTEIN PRIMES DNA SYNTHESIS CARRIED OUT BY VIRAL DNA
POLYMERASE 280
SINGLE-STRANDED DNA IS CIRCULARIZED VIA THE INVERTED TERMINAL REPEAT 2
80 T HE MAJOR LATE PROMOTER IS ACTIVATED AFTER DNA REPLICATION BEGINS 2
81
FIVE DIFFERENT POLY(A) SITES AND ALTERNATIVE SPLICING GENERATE MULTIPLE
LATE MRNAS 281 THE TRIPARTITE LEADER ENSURES EFFICIENT TRANSPORT OF LATE
MRNAS TO THE CYTOPLASM 2 81
THE TRIPARTITE LEADER DIRECTS EFFICIENT TRANSLATION OF LATE ADENOVIRUS
PROTEINS 282 ADENOVIRUS-INDUCED CELL KILLING 283 CELL TRANSFORMATION AND
ONCOGENESIS BY HUMAN
ADENOVIRUSES 283
24. HERPESVIRUSES 285
HERPESVIRUSES ARE IMPORTANT HUMAN PATHOGENS 285 MOST HERPESVIRUSES CAN
ESTABLISH LATENT INFECTIONS 286
HERPES SIMPLEX VIRUS 286 HERPES SIMPLEX VIRUS GENOMES CONTAIN BOTH
UNIQUE AND REPEATED SEQUENCE ELEMENTS 286 NOMENCLATURE OF HERPES SIMPLEX
VIRUS GENES
AND PROTEINS 288 THE ICOSAHEDRAL CAPSID IS ENCLOSED IN AN ENVELOPE ALONG
WITH TEGUMENT PROTEINS 288 ENTRY BY FUSION IS MEDIATED BY ENVELOPE
GLYCOPROTEINS AND
MAY OCCUR AT THE PLASMA MEMBRANE OR IN ENDOSOMES 288 VIRAL GENES ARE
SEQUENTIALLY EXPRESSED DURING THE REPLICATION CYCLE 289 TEGUMENT
PROTEINS INTERACT WITH CELLULAR MACHINERY TO
ACTIVATE VIRAL GENE EXPRESSION AND TO DEGRADE CELLULAR MESSENGER RNAS
289 IMMEDIATE EARLY (A) GENES REGULATE EXPRESSION OF OTHER HERPESVIRUS
GENES 291
* GENE PRODUCTS ENABLE VIRAL DNA REPLICATION 291
DNA REPLICATION INITIALLY PROCEEDS IN A BIDIRECTIONAL FASHION FROM A
REPLICATION ORIGIN 291 ROLLING CIRCLE REPLICATION SUBSEQUENTLY PRODUCES
MULTIMERIC CONCATEMERS OF VIRAL DNA 292
DNA REPLICATION LEADS TO ACTIVATION OF ^ AND Y 2 GENES 292 VIRAL
NUCLEOCAPSIDS ARE ASSEMBLED ON A SCAFFOLD IN THE NUCLEUS 293 ENVELOPMENT
AND EGRESS: THREE POSSIBLE ROUTES 294
MANY VIRAL GENES ARE INVOLVED IN BLOCKING HOST RESPONSES TO INFECTION
295 HERPES SIMPLEX VIRUS ESTABLISHES LATENT INFECTION IN NEURONS 296
LATENCY-ASSOCIATED TRANSCRIPTS INCLUDE STABLE INTRONS 296
EPSTEIN-BARR VIRUS 296 EPSTEIN-BARR VIRUS WAS DISCOVERED IN LYMPHOMAS IN
AFRICAN CHILDREN 296 EPSTEIN-BARR VIRUS INFECTS MUCOSAL EPITHELIAL CELLS
AND
B-LYMPHOCYTES 297 EPSTEIN-BARR VIRUS EXPRESSES A LIMITED SET OF PROTEINS
IN LATENTLY INFECTED B LYMPHOCYTES 298 EPSTEIN-BARR VIRUS NUCLEAR
ANTIGENS DIRECT LIMITED
REPLICATION OF THE VIRAL GENOME AND ACTIVATE VIRAL AND CELLULAR GENES
299 LATENT MEMBRANE PROTEINS MIMIC RECEPTORS ON B LYMPHOCYTES 299
SMALL, UNTRANSLATED VIRAL RNAS EXPRESSED DURING LATENT INFECTIONS TARGET
HOST DEFENSE MECHANISMS 300
25. BACULOVIRUSES 302
INSECT VIRUSES WERE FIRST DISCOVERED AS PATHOGENS OF SILKWORMS 302
BACULOVIRUSES ARE USED FOR PEST CONTROL AND TO EXPRESS EUKARYOTIC
PROTEINS 303 BACULOVIRUS VIRIONS CONTAIN AN ELONGATED NUCLEOCAPSID 303
BACULOVIRUSES PRODUCE TWO KINDS OF PARTICLES: BUDDED AND
OCCLUSION-DERIVED VIRIONS 304 BACULOVIRUSES HAVE LARGE, CIRCULAR DNA
GENOMES AND ENCODE MANY PROTEINS 305 INSECTS ARE INFECTED BY INGESTING
OCCLUSION BODIES; INFECTION
SPREADS WITHIN THE INSECT VIA BUDDED VIRIONS 306 VIRAL PROTEINS ARE
EXPRESSED IN A TIMED CASCADE REGULATED AT THE TRANSCRIPTION LEVEL 306
IMMEDIATE EARLY GENE PRODUCTS CONTROL EXPRESSION OF EARLY
GENES 307 EARLY GENE PRODUCTS REGULATE DNA REPLICATION, LATE
TRANSCRIPTION, AND APOPTOSIS 307 LATE GENES ARE TRANSCRIBED BY A NOVEL
VIRUS-CODED RNA
POLYMERASE 308 BACULOVIRUSES ARE WIDELY USED TO EXPRESS FOREIGN PROTEINS
3 08
26. POXVIRUSES 312
SMALLPOX WAS A DEBILITATING AND FATAL WORLDWIDE DISEASE 312 VARIOLATION
LED TO VACCINATION, WHICH HAS ERADICATED SMALLPOX WORLDWIDE 313
POXVIRUSES REMAIN A SUBJECT OF INTENSE RESEARCH INTEREST 313
IMAGE 9
CONTENTS XV
LINEAR VACCINIA VIRUS GENOMES HAVE COVALENTLY SEALED HAIRPIN ENDS AND
LACK INTRONS 314 TWO FORMS OF VACCINIA VIRIONS HAVE DIFFERENT ROLES IN
SPREADING INFECTION 3 15
POXVIRUSES REPLICATE IN THE CYTOPLASM 316 POXVIRUS GENES ARE EXPRESSED
IN A REGULATED TRANSCRIPTIONAL CASCADE CONTROLLED BY VIRAL TRANSCRIPTION
FACTORS 317 VIRUS-CODED ENZYMES PACKAGED IN THE CORE CARRY OUT EARLY
RNA SYNTHESIS AND PROCESSING 3 18 ENZYMES THAT DIRECT DNA REPLICATION
ARE ENCODED BY EARLY MRNAS 318 POXVIRUSES PRODUCE LARGE CONCATEMERIC DNA
MOLECULES THAT
ARE RESOLVED INTO MONOMERS 3 18 POSTREPLICATIVE MRNAS HAVE 5 END
POLY(A) EXTENSIONS AND 3 END HETEROGENEITY 319 MATURE VIRIONS ARE
FORMED WITHIN VIRUS FACTORIES 320
EXTRACELLULAR VIRIONS ARE EXTRUDED THROUGH THE PLASMA MEMBRANE BY ACTIN
TAILS 321 POXVIRUSES MAKE SEVERAL PROTEINS THAT TARGET HOST DEFENSES
AGAINST INVADING PATHOGENS 321
27. VIRUSES OF ALGAE AND MIMIVIRUS 325
AQUATIC ENVIRONMENTS HARBOR LARGE VIRUSES 3 2 5 PHYCODNAVIRUSES ARE
DIVERSE AND PROBABLY ANCIENT 326 PHYCODNAVIROLOGY: A FIELD IN ITS
INFANCY 326 CONSERVED STRUCTURE, DIVERSE COMPOSITION 327
CHLOROVIRUSES 327 KNOWN CHLOROVIRUSES REPLICATE IN CHLORELLA ISOLATED
FROM SYMBIOTIC HOSTS 327 THE LINEAR GENOMES OF CHLOROVIRUSES CONTAIN
HUNDREDS OF GENES,
AND EACH VIRUS SPECIES ENCODES SOME UNIQUE PROTEINS 327 CHLOROVIRUS
CAPSIDS ARE CONSTRUCTED FROM MANY CAPSOMERS AND HAVE A UNIQUE SPIKE 328
VIRUS ENTRY BEGINS BY BINDING TO AND DEGRADATION OF THE HOST
CELL WALL 329 TRANSCRIPTION OF VIRAL GENES IS TEMPORALLY CONTROLLED AND
PROBABLY OCCURS IN THE CELL NUCLEUS 329 PROGENY VIRIONS ARE ASSEMBLED IN
THE CYTOPLASM 329
SMALL AND EFFICIENT PROTEINS 3 30 A VIRUS FAMILY WITH A PENCHANT FOR
SUGAR METABOLISM:
HYALURONAN AND CHITIN 330
COCCOLITHOVIRUSES 331 VIRUSES THAT CONTROL THE WEATHER 331 MANY GENES
LOOKING FOR A FUNCTION 332 EXPRESSION OF COCCOLITHOVIRUS GENES IS
TEMPORALLY
REGULATED 332 CHESHIRE CAT DYNAMICS: SEX TO AVOID VIRUS INFECTION 3 3 3
SURVIVAL OF THE FATTEST: THE GIANT COCCOLITHOVIRUS GENOME
ENCODES SPHINGOLIPID BIOSYNTHESIS 3 3 3
PRASINOVIRUSES 334 SMALL HOST, BIG VIRUS 334 VIRAL GENOMES CONTAIN
MULTIPLE GENES FOR CAPSID PROTEINS 3 34 IT WORKS BOTH WAYS 334
NOT MUCH ROOM FOR MANEUVER 335
P H A E O VI R U S ES 335 SEAWEED VIRUSES 3 3 5 PHAEOVIRUSES HAVE A
TEMPERATE LIFE CYCLE AND INTEGRATE THEIR GENOMES INTO THE HOST 3 3 5
PRYMNESIOVIRUSES AND RAPHIDOVIRUSES 335 THE LESSER-KNOWN PHYCODNAVIRIDAE
3 3 5
MIMIVIRUS 336 THE WORLD S LARGEST KNOWN VIRUS 336 MIMIVIRUS IS
UNQUESTIONABLY A VIRUS 3 3 6 WHY SUCH A LARGE GENOME? 3 3 7 MIMIVIRUS
HAS A UNIQUE MECHANISM FOR RELEASING ITS CORE 3 3 7 VIRUS REPLICATION
OCCURS EXCLUSIVELY IN THE CYTOPLASM 3 3 7
GENOME REPLICATION 338 GENES CODING FOR TRANSLATION FACTORS AND DNA
REPAIR ENZYMES 338 ANCESTORS OF MIMIVIRUS MAY HAVE TRANSFERRED GENES
FROM
BACTERIA TO EUKARYOTES 339 CONCLUSION 340
SECTION VII: VIRUSES THAT USE A REVERSE TRANSCRIPTASE
28. RETROVIRUSES 342
RETROVIRUSES HAVE A UNIQUE REPLICATION CYCLE BASED ON REVERSE
TRANSCRIPTION AND INTEGRATION OF THEIR GENOMES 342 VIRAL PROTEINS
DERIVED FROM THE GAG, POL, AND ENV GENES ARE INCORPORATED IN VIRIONS 343
RETROVIRUSES ENTER CELLS BY THE FUSION PATHWAY 344 VIRAL RNA IS
CONVERTED INTO A DOUBLE-STRANDED DNA COPY BY REVERSE TRANSCRIPTION 345 A
COPY OF PROVIRAL DNA IS INTEGRATED INTO THE CELLULAR
GENOME AT A RANDOM SITE 347 SEQUENCE ELEMENTS IN THE LONG TERMINAL
REPEATS DIRECT TRANSCRIPTION AND POLYADENYLATION BY HOST CELL
ENZYMES 348 DIFFERENTIAL SPLICING GENERATES MULTIPLE MRNAS 348 THE
GAG/POL POLYPROTEIN IS MADE BY SUPPRESSION OF TERMINATION AND USE OF
ALTERNATIVE READING FRAMES 348 VIRIONS MATURE INTO INFECTIOUS PARTICLES
AFTER BUDDING
FROM THE PLASMA MEMBRANE 349 ACUTE TRANSFORMING RETROVIRUSES EXPRESS
MUTATED FORMS OF CELLULAR GROWTH SIGNALING PROTEINS 350 RETROVIRUSES
LACKING ONCOGENES CAN TRANSFORM CELLS BY
INSERTION OF PROVIRAL DNA NEAR A PROTO-ONCOGENE 3 51
29. HUMAN IMMUNODEFICIENCY VIRUS 354
HUMAN IMMUNODEFICIENCY VIRUS TYPE 1 (HIV-1) AND ACQUIRED
IMMUNODEFICIENCY SYNDROME (AIDS) 355 HIV-1 WAS PROBABLY TRANSMITTED TO
HUMANS FROM CHIMPANZEES INFECTED WITH SIVCPZ 3 5 5 HIV-1 INFECTION LEADS
TO A PROGRESSIVE LOSS OF CELLULAR
IMMUNITY AND INCREASED SUSCEPTIBILITY TO OPPORTUNISTIC INFECTIONS 355
IMAGE 10
XVI CONTENTS
ANTIVIRAL DRUGS CAN CONTROL HIV-1 INFECTION AND PREVENT DISEASE
PROGRESSION, BUT AN EFFECTIVE VACCINE HAS YET TO BE DEVELOPED 356 HIV-1
IS A COMPLEX RETROVIRUS 3 57 HIV-1 TARGETS CELLS OF THE IMMUNE SYSTEM BY
RECOGNIZING
CD4 ANTIGEN AND CHEMOKINE RECEPTORS 357 VIRUS MUTANTS ARISE RAPIDLY
BECAUSE OF ERRORS GENERATED DURING REVERSE TRANSCRIPTION 3 5 8 UNLIKE
OTHER RETROVIRUSES, HIV-1 DIRECTS TRANSPORT OF PROVIRAL
DNA INTO THE CELL NUCLEUS 359 LATENT INFECTION COMPLICATES THE
ELIMINATION OF HIV-1 359 THE TAT PROTEIN INCREASES HIV-1 TRANSCRIPTION
BY STIMULATING ELONGATION BY RNA POLYMERASE II 360 THE REV PROTEIN
MEDIATES CYTOPLASMIC TRANSPORT OF VIRAL
MRNAS THAT CODE FOR HIV-1 STRUCTURAL PROTEINS 360 TOGETHER, THE TAT AND
REV PROTEINS STRONGLY UPREGULATE VIRAL PROTEIN EXPRESSION 3 61 THE VIF
PROTEIN INCREASES VIRION INFECTIVITY BY COUNTERACTING
A CELLULAR DEOXCYTIDINE DEAMINASE 361 THE VPR PROTEIN ENHANCES HIV-1
REPLICATION AT MULTIPLE LEVELS 362 THE VPU PROTEIN ENHANCES RELEASE OF
PROGENY VIRIONS FROM
INFECTED CELLS 362 THE NEF PROTEIN IS AN IMPORTANT MEDIATOR OF
PATHOGENESIS 362
30. HEPADNAVIRUSES 365
AT LEAST SEVEN DISTINCT VIRUSES CAUSE HUMAN HEPATITIS 365 THE DISCOVERY
OF HEPATITIS B VIRUS 366 DANE PARTICLES ARE INFECTIOUS VIRIONS; ABUNDANT
NON-INFECTIOUS PARTICLES LACK NUCLEOCAPSIDS 366
THE VIRAL GENOME IS A CIRCULAR, PARTLY SINGLE-STRANDED DNA WITH
OVERLAPPING READING FRAMES 367 NUCLEOCAPSIDS ENTER THE CYTOPLASM VIA
FUSION AND ARE TRANSPORTED TO THE NUCLEUS 367 TRANSCRIPTION OF VIRAL DNA
GIVES RISE TO SEVERAL
MRNAS AND A PREGENOME RNA 368 THE ROLES OF HEPATITIS B VIRUS PROTEINS
369 THE PREGENOME RNA IS PACKAGED BY INTERACTION WITH POLYMERASE AND
CORE PROTEINS 371
GENOME REPLICATION OCCURS VIA REVERSE TRANSCRIPTION OF PREGENOME RNA 372
VIRIONS ARE FORMED BY BUDDING IN THE ENDOPLASMIC RETICULUM 3 7 3
HEPATITIS B VIRUS CAN CAUSE CHRONIC OR ACUTE HEPATITIS,
CIRRHOSIS, AND LIVER CANCER 374 HEPATITIS B VIRUS IS TRANSMITTED BY
BLOOD TRANSFUSIONS, CONTAMINATED NEEDLES, AND UNPROTECTED SEX 374 A
RECOMBINANT VACCINE IS AVAILABLE 375 ANTIVIRAL DRUG TREATMENT HAS REAL
SUCCESS 375
SECTION VIM: VIROIDS AND PRIONS
31. VIROIDS AND HEPATITIS DELTA VIRUS 378 VIROIDS ARE SMALL, CIRCULAR
RNAS THAT DO NOT ENCODE PROTEINS 379
THE TWO FAMILIES OF VIROIDS HAVE DISTINCT PROPERTIES 379
VIROIDS REPLICATE VIA LINEAR MULTIMERIC RNA INTERMEDIATES 380 THREE
ENZYMATIC ACTIVITIES ARE NEEDED FOR VIROID REPLICATION 380
HOW DO VIROIDS CAUSE DISEASE? 382 INTERACTION OF VIROID RNA WITH
CELLULAR RNAS OR PROTEINS MAY DISRUPT CELL METABOLISM 382 RNA
INTERFERENCE COULD DETERMINE VIROID PATHOGENICITY AND
CROSS-PROTECTION 382 CIRCULAR PLANT SATELLITE RNAS RESEMBLE VIROIDS BUT
ARE ENCAPSIDATED 383 HEPATITIS DELTA VIRUS IS A HUMAN VIROID-LIKE
SATELLITE VIRUS 383 HEPATITIS DELTA VIRUS MAY USE TWO DIFFERENT CELLULAR
RNA
POLYMERASES TO REPLICATE 383 RNA EDITING GENERATES TWO FORMS OF
HEPATITIS DELTA ANTIGEN 384 CONCLUSION: VIROIDS MAY BE A LINK TO THE
ANCIENT
RNA WORLD 384
32. PRIONS 387
PRIONS ARE PROTEINS THAT CAUSE FATAL BRAIN DISEASES 387 PRION DISEASES
WERE FIRST DETECTED IN DOMESTIC RUMINANTS 388 BOVINE SPONGIFORM
ENCEPHALOPATHY ( MAD COW DISEASE )
DEVELOPED IN BRITAIN AND APPARENTLY SPREAD TO HUMANS 388 HUMAN PRION
DISEASES CAN BE EITHER INHERITED OR TRANSMITTED 388 THE INFECTIOUS AGENT
OF PRION DISEASES CONTAINS PROTEIN BUT
NO DETECTABLE NUCLEIC ACID 389 PRP SC IS ENCODED BY A HOST CELL GENE 390
DIFFERENCES BETWEEN PRP C AND PRP ST 390 THE PRION HYPOTHESIS: FORMATION
OF INFECTIOUS AND
PATHOGENIC PRIONS FROM NORMAL PRP C 391 IS THE PRION HYPOTHESIS CORRECT?
392 PATHOLOGY AND DIAGNOSIS OF PRION DISEASES 392 PROTEINS OF YEAST AND
OTHER FUNGI CAN FORM SELF-PROPAGATING
STATES RESEMBLING PRIONS 393 GENETICS OF PRION DISEASES: MUTATIONS IN
THE PRION GENE CAN INCREASE OCCURRENCE OF DISEASE 393 PRION DISEASES ARE
NOT USUALLY TRANSMITTED AMONG DIFFERENT
SPECIES 393 STRAIN VARIATION AND CROSSING OF THE SPECIES BARRIER 394 THE
NATURE OF THE PRION INFECTIOUS AGENT 394
SECTION IX: HOST DEFENSES AGAINST VIRUS INFECTION
33. INTRINSIC CELLULAR DEFENSES AGAINST VIRUS INFECTION 398 INTRODUCTION
399 DETECTION OF VIRUS INFECTION BY
HOST CELLS 399 HOST CELLS SENSE VIRUS INFECTION WITH TOLL-LIKE RECEPTORS
AND A VARIETY OF OTHER MOLECULAR DETECTION SYSTEMS 399 SEVERAL TOLL-LIKE
RECEPTORS RECOGNIZE VIRAL NUCLEIC ACIDS 400
I
IMAGE 11
XVIII CONTENTS
NEW DEVELOPMENTS IN ANTIVIRAL VACCINES 437 NEW APPROACHES TO VACCINE
DEVELOPMENT SHOW GREAT PROMISE 437 NEW ADJUVANTS ARE BEING DEVELOPED 437
NEW DELIVERY SYSTEMS FOR VIRAL ANTIGENS 437 VACCINATION WITH DEFINED
PROTEINS 43 7 USE OF LIVE VIRUSES WITH DEFINED ATTENUATION
CHARACTERISTICS 438 USE OF LIVE VECTORS AND CHIMERIC VIRUSES 439
VACCINES THAT CAN BREAK TOLERANCE 439 THE CHANGING VACCINE PARADIGM 439
ADVERSE EVENTS AND ETHICAL ISSUES 439 VACCINE-ASSOCIATED ADVERSE EVENTS
439 ETHICAL ISSUES IN THE USE OF ANTIVIRAL VACCINES 441
36. ANTIVIRAL CHEMOTHERAPY 444
THE DISCOVERY AND WIDESPREAD USE OF ANTIVIRAL COMPOUNDS BEGAN RELATIVELY
RECENTLY 444 ANTIVIRAL DRUGS ARE USEFUL FOR DISCOVERIES IN BASIC
RESEARCH ON VIRUSES 445 HOW ARE ANTIVIRAL DRUGS OBTAINED? 445 ANTIVIRAL
DRUGS ARE TARGETED TO SPECIFIC STEPS OF VIRUS
INFECTION 445 DRUGS PREVENTING ATTACHMENT AND ENTRY OF VIRIONS 446
AMANTADINE BLOCKS ION CHANNELS AND INHIBITS UNCOATING OF INFLUENZA
VIRIONS 447 NUCLEOSIDE ANALOGUES TARGET VIRAL DNA POLYMERASES 447
ACYCLOVIR IS SELECTIVELY PHOSPHORYLATED BY HERPESVIRUS
THYMIDINE KINASES 448 ACYCLOVIR IS PREFERENTIALLY INCORPORATED BY
HERPESVIRUS DNA POLYMERASES 449 CYTOMEGALOVIRUS ENCODES A PROTEIN KINASE
THAT
PHOSPHORYLATES GANCICLOVIR 450 HIV-1 REVERSE TRANSCRIPTASE
PREFERENTIALLY INCORPORATES AZIDOTHYMIDINE INTO DNA, LEADING TO CHAIN
TERMINATION 450 NON-NUCLEOSIDE INHIBITORS SELECTIVELY TARGET VIRAL
REPLICATION ENZYMES 451 PROTEASE INHIBITORS CAN INTERFERE WITH VIRUS
ASSEMBLY AND MATURATION 452 RITONAVIR: A SUCCESSFUL PROTEASE INHIBITOR
OF HIV-1
THAT WAS DEVELOPED BY RATIONAL INETHODS 452 NEURAMINIDASE INHIBITORS
INHIBIT RELEASE AND SPREAD OF INFLUENZA VIRUS 453 ANTIVIRAL CHEMOTHERAPY
SHOWS PROMISE FOR THE FUTURE 453
37. EUKARYOTIC VIRUS VECTORS 456
MANY VIRUSES CAN BE ENGINEERED TO DELIVER AND EXPRESS SPECIFIC GENES 456
VIRUS VECTORS ARE USED TO PRODUCE HIGH LEVELS OF SPECIFIC PROTEINS IN
CULTURED CELLS 457 GENE THERAPY IS AN EXPANDING APPLICATION OF VIRUS
VECTORS 458 VIRUS VECTORS ARE PRODUCED BY TRANSFECTION OF CELLS WITH
PLASMIDS CONTAINING DELETED GENOMES 458 VIRUS VECTORS ARE ENGINEERED TO
PRODUCE OPTIMAL LEVELS OF GENE PRODUCTS 459
ADENOVIRUS VECTORS 460 ADENOVIRUS VECTORS ARE WIDELY USED IN STUDIES OF
GENE TRANSFER AND ANTITUMOR THERAPY 460
REPLICATION-DEFECTIVE ADENOVIRUS VECTORS ARE PROPAGATED IN COMPLEMENTING
CELL LINES 460 REPLICATION-COMPETENT ADENOVIRUS VECTORS ARE USEFUL TOOLS
IN ANTITUMOR THERAPY 461 ADVANTAGES AND LIMITATIONS OF ADENOVIRUS
VECTORS 461
RETROVIRUS VECTORS 462 RETROVIRUS VECTORS INCORPORATE TRANSGENES INTO
THE CELL CHROMOSOME 462 PACKAGING CELL LINES EXPRESS RETROVIRUS
ENZYMATIC AND
STRUCTURAL PROTEINS 462 STRATEGIES FOR CONTROLLING TRANSGENE
TRANSCRIPTION 463 LENTIVIRUS VECTORS ARE USED FOR GENE DELIVERY TO
NON-DIVIDING CELLS 463 PRODUCTION OF LENTIVIRUS VECTORS REQUIRES
ADDITIONAL V-ACTING SEQUENCES 463 APPLICATIONS OF RETROVIRUS VECTORS:
TREATMENT OF
BLOOD DISORDERS 464 APPLICATIONS OF RETROVIRUS VECTORS: TREATMENT OF
NEUROLOGICAL DISORDERS 465 ADVANTAGES AND LIMITATIONS OF RETROVIRUS
VECTORS 465
ADENO-ASSOCIATED VIRUS VECTORS 465 ADENO-ASSOCIATED VIRUS VECTORS CAN
INSERT TRANSGENES INTO A SPECIFIC CHROMOSOMAL LOCUS 465
PRODUCTION OF AAV VECTORS USUALLY REQUIRES A HELPER VIRUS 466 CLINICAL
TRIALS USING ADENO-ASSOCIATED VIRUS VECTORS 467 ADVANTAGES AND
LIMITATIONS OF AAV VECTORS 467
GLOSSARY 471
CREDITS 484
NAME INDEX 489
SUBJECT INDEX 491
I
|
| any_adam_object | 1 |
| author | Acheson, Nicholas H. |
| author_GND | (DE-588)172990238 |
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| author_role | aut |
| author_sort | Acheson, Nicholas H. |
| author_variant | n h a nh nha |
| building | Verbundindex |
| bvnumber | BV039761064 |
| classification_rvk | WF 3000 XD 7000 |
| ctrlnum | (OCoLC)697768676 (DE-599)HBZHT017042796 |
| dewey-full | 616.9/101 |
| dewey-hundreds | 600 - Technology (Applied sciences) |
| dewey-ones | 616 - Diseases |
| dewey-raw | 616.9/101 |
| dewey-search | 616.9/101 |
| dewey-sort | 3616.9 3101 |
| dewey-tens | 610 - Medicine and health |
| discipline | Biologie Medizin |
| edition | 2. ed. |
| format | Book |
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| id | DE-604.BV039761064 |
| illustrated | Illustrated |
| indexdate | 2024-07-10T00:10:52Z |
| institution | BVB |
| isbn | 9780470900598 |
| language | English |
| oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-024622259 |
| oclc_num | 697768676 |
| open_access_boolean | |
| owner | DE-578 DE-20 DE-11 |
| owner_facet | DE-578 DE-20 DE-11 |
| physical | XXV, 500 S., [1] Bl. Ill., graph. Darst. |
| publishDate | 2011 |
| publishDateSearch | 2011 |
| publishDateSort | 2011 |
| publisher | Wiley |
| record_format | marc |
| spelling | Acheson, Nicholas H. Verfasser (DE-588)172990238 aut Fundamentals of molecular virology Nicholas H. Acheson 2. ed. Hoboken, NJ Wiley 2011 XXV, 500 S., [1] Bl. Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Molecular virology Viruses Reproduction Molekulare Virologie (DE-588)4170393-5 gnd rswk-swf Molekulare Virologie (DE-588)4170393-5 s DE-604 SWB Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=024622259&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Acheson, Nicholas H. Fundamentals of molecular virology Molecular virology Viruses Reproduction Molekulare Virologie (DE-588)4170393-5 gnd |
| subject_GND | (DE-588)4170393-5 |
| title | Fundamentals of molecular virology |
| title_auth | Fundamentals of molecular virology |
| title_exact_search | Fundamentals of molecular virology |
| title_full | Fundamentals of molecular virology Nicholas H. Acheson |
| title_fullStr | Fundamentals of molecular virology Nicholas H. Acheson |
| title_full_unstemmed | Fundamentals of molecular virology Nicholas H. Acheson |
| title_short | Fundamentals of molecular virology |
| title_sort | fundamentals of molecular virology |
| topic | Molecular virology Viruses Reproduction Molekulare Virologie (DE-588)4170393-5 gnd |
| topic_facet | Molecular virology Viruses Reproduction Molekulare Virologie |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=024622259&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
| work_keys_str_mv | AT achesonnicholash fundamentalsofmolecularvirology |