| Preface |
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xvii | |
| Acknowledgments |
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xix | |
| Author |
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xxi | |
| 1 The Fundamentals Of Molecular And Cellular Virology |
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1 | (18) |
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1.1 Molecular and cellular virology focuses on the molecular interactions that occur when a virus infects a host cell |
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2 | (1) |
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1.2 The discipline of virology can be traced historically to agricultural and medical science |
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3 | (3) |
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1.3 Basic research in virology is critical for molecular biology, both historically and today |
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6 | (2) |
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1.4 Viruses, whether understood as living or not, are the most abundant evolving entities known |
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8 | (1) |
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1.5 Viruses can be defined unambiguously by four traits |
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8 | (2) |
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1.6 Virions are infectious particles minimally made up of nucleic acids and proteins |
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10 | (1) |
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1.7 Viruses can be classified according to the ways they synthesize and use mRNA |
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11 | (1) |
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1.8 Viruses are propagated in the laboratory by mixing them with host cells |
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12 | (2) |
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1.9 Viral sequences are ubiquitous in animal genomes, including the human genome |
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14 | (3) |
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17 | (1) |
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17 | (1) |
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18 | (1) |
| 2 The Virus Replication Cycle |
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19 | (14) |
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2.1 Viruses reproduce through a lytic virus replication cycle |
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20 | (2) |
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2.2 Molecular events during each stage of the virus replication cycle |
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22 | (1) |
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2.3 The influenza virus is a model for replication of an animal virus |
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23 | (1) |
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2.4 The host surface is especially important for attachment, penetration, and uncoating |
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23 | (3) |
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2.5 Viral gene expression and genome replication take advantage of host transcription, translation, and replication features |
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26 | (1) |
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2.6 The host cytoskeleton and membranes are typically crucial during virus assembly |
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27 | (1) |
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2.7 Host-cell surfaces influence the mechanism of virus release |
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27 | (1) |
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2.8 Viruses can also cause long-term infections |
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27 | (2) |
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2.9 Herpesvirus is a model for latent infections |
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29 | (1) |
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2.10 Research in molecular and cellular virology often focuses on the molecular details of each stage of the replication cycle |
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29 | (1) |
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30 | (1) |
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30 | (1) |
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31 | (2) |
| 3 Attachment, Penetration, And Uncoating |
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33 | (44) |
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3.1 Viruses enter the human body through one of six routes |
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33 | (1) |
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3.2 The likelihood of becoming HIV+ depends on the route of transmission and the amount of virus in the infected tissue |
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34 | (1) |
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3.3 Viruses are selective in their host range and tissue tropism |
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35 | (1) |
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3.4 The virion is a genome delivery device |
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36 | (1) |
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3.5 The genomic contents of a virion are irrelevant for attachment, penetration, and uncoating |
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37 | (3) |
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3.6 Animal viruses attach to specific cells and can spread to multiple tissues |
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40 | (1) |
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3.7 Noncovalent intermolecular forces are responsible for attaching to host cells |
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41 | (1) |
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3.8 Most animal virus receptors are glycoproteins |
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42 | (1) |
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3.9 Animal virus receptors can be identified through genetic, biochemical, and immunological approaches |
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43 | (1) |
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3.10 Animal virus receptors can be identified through molecular cloning |
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43 | (1) |
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3.11 Animal virus receptors can be identified through affinity chromatography |
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44 | (1) |
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3.12 Antibodies can be used to identify animal virus receptors |
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45 | (2) |
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3.13 Rhinovirus serves as a model for attachment by animal viruses lacking spikes |
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47 | (3) |
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3.14 Several independent lines of evidence indicate that ICAM-1 is the rhinovirus receptor |
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50 | (1) |
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3.15 Experiments using molecular genetics support the conclusion that ICAM-1 is the rhinovirus receptor |
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50 | (1) |
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3.16 Structural biology experiments support the conclusion that ICAM-1 is the rhinovirus receptor |
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51 | (1) |
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3.17 Bioinformatics comparisons support the conclusion that ICAM-1 is the rhinovirus receptor |
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51 | (1) |
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3.18 Influenza serves as a model for attachment by enveloped viruses |
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52 | (1) |
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3.19 The influenza HA spike protein binds to sialic acids |
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53 | (2) |
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3.20 The second stage of the virus replication cycle includes both penetration and uncoating and, if necessary, transport to the nucleus |
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55 | (1) |
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3.21 Viruses subvert the two major eukaryotic mechanisms for internalizing particles |
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56 | (1) |
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3.22 Many viruses subvert receptor-mediated endocytosis for penetration |
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56 | (1) |
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3.23 Herpesvirus penetrates the cell through phagocytosis |
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57 | (1) |
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3.24 Common methods for determining the mode of viral penetration include use of drugs and RNA interference |
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58 | (1) |
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3.25 The virion is a metastable particle primed for uncoating once irreversible attachment and penetration have occurred |
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59 | (1) |
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3.26 Picornaviruses are naked viruses that release their genomic contents through pore formation |
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60 | (1) |
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3.27 Some enveloped viruses use membrane fusion with the outside surface of the cell for penetration |
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60 | (1) |
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3.28 Vesicle fusion in neuroscience is a model for viral membrane fusion |
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61 | (2) |
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3.29 HIV provides a model of membrane fusion triggered by a cascade of protein-protein interactions |
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63 | (1) |
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3.30 Influenza provides a model for viral envelope fusion triggered by acidification of an endocytic vesicle |
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64 | (1) |
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3.31 The destination for the virus genome may be the cytoplasm or the nucleus |
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65 | (1) |
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3.32 Subversion of the cellular cytoskeleton is critical for uncoating |
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65 | (1) |
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3.33 Viruses that enter an intact nucleus must manipulate gated nuclear pores |
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66 | (1) |
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3.34 Viruses introduce their genomes into the nucleus in a variety of ways |
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67 | (1) |
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3.35 Adenovirus provides a model for uncoating that delivers the viral genome into the nucleus |
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68 | (1) |
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3.36 The unusual uncoating stages of reoviruses and poxviruses leave the virions partially intact in the cytoplasm |
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69 | (2) |
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3.37 Viruses that penetrate plant cells face plant-specific barriers to infection |
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71 | (1) |
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3.38 Plant viruses are often transmitted by biting arthropod vectors |
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72 | (1) |
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73 | (1) |
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74 | (1) |
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74 | (3) |
| 4 Gene Expression And Genome Replication In Model Bacteriophages |
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77 | (48) |
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4.1 Bacterial host cell transcription is catalyzed by a multisubunit machine that catalyzes initiation, elongation, and termination |
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78 | (2) |
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4.2 Bacterial host cell and bacteriophage mRNA are typically polycistronic |
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80 | (1) |
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4.3 Transcription and translation in bacterial host cells and bacteriophages are nearly simultaneous because of the proximity of ribosomes and chromosomes |
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81 | (1) |
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4.4 Bacterial translation initiation, elongation, and termination are controlled by translation factors |
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81 | (2) |
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4.5 Bacteriophages, like all viruses, encode structural and nonstructural proteins |
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83 | (1) |
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4.6 The T7 bacteriophage has naked, complex virions and a large double- stranded DNA genome |
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84 | (1) |
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4.7 Bacteriophage T7 encodes 55 proteins in genes that are physically grouped together by function |
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85 | (1) |
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4.8 Bacteriophage T7 proteins are expressed in three major waves |
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85 | (1) |
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4.9 The functions of bacteriophage proteins often correlate with the timing of their expression |
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86 | (1) |
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4.10 Bacteriophage T7 gene expression is highly regulated at the level of transcription initiation |
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87 | (1) |
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4.11 Bacterial host chromosome replication is regulated by the DnaA protein and occurs via a theta intermediate |
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88 | (2) |
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4.12 Many bacterial proteins are needed to catalyze chromosome replication |
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90 | (2) |
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4.13 Although many bacteriophages have linear dsDNA genomes, bacterial hosts cannot replicate the ends of linear DNA |
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92 | (1) |
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4.14 T7 bacteriophage genome replication is catalyzed by one of the simplest known replication machines |
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93 | (3) |
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4.15 The λ bacteriophage has naked, complex virions and a large double- stranded DNA genome |
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96 | (1) |
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4.16 Bacteriophage λ can cause lytic or long- term infections |
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96 | (2) |
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4.17 There are three waves of gene expression during lytic λ replication |
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98 | (1) |
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4.18 The λ control region is responsible for early gene expression because of its promoters and the Cro and N proteins it encodes |
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99 | (1) |
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4.19 The λ N antitermination protein controls the onset of delayed-early gene expression |
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99 | (1) |
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4.20 The λ Q antitermination protein and Cro repressor protein control the switch to late gene expression |
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100 | (1) |
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4.21 Bacteriophages T7 and λ both have three waves of gene expression but the molecular mechanisms controlling them differ |
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100 | (1) |
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4.22 Bacteriophage λ genome replication occurs in two stages, through two different intermediates |
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101 | (1) |
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4.23 Lambda genome replication requires phage proteins O and P and many subverted host proteins |
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102 | (1) |
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4.24 The abundance of host DnaA protein relative to the amount of phage DNA controls the switch to rolling-circle replication |
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102 | (1) |
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4.25 There are billions of other bacteriophages that regulate gene expression in various ways |
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103 | (1) |
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4.26 Some bacteriophages have ssDNA, dsDNA, or (+) ssRNA genomes |
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104 | (1) |
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4.27 The replication cycles of ssDNA bacteriophages always include formation of a double-stranded replicative form |
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104 | (1) |
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4.28 Bacteriophage Φχ174 is of historical importance |
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105 | (1) |
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4.29 Bacteriophage Φχ174 has extremely overlapping protein-coding sequences |
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105 | (1) |
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4.30 Bacteriophage Φχ174 proteins are expressed in different amounts |
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106 | (1) |
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4.31 A combination of mRNA levels and differential translation accounts for levels of bacteriophage Φχ174 protein expression |
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107 | (1) |
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4.32 Bacteriophage M13 genome replication is catalyzed by host proteins and occurs via a replicative form |
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108 | (2) |
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4.33 Bacteriophage MS2 is a (+) ssRNA virus that encodes four proteins |
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110 | (1) |
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4.34 Bacteriophage MS2 protein abundance is controlled by secondary structure in the genome |
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111 | (3) |
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4.35 Bacteriophage RdRp enzymes subvert abundant host proteins to create an efficient replicase complex |
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114 | (1) |
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4.36 Bacteriophage proteins are common laboratory tools |
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115 | (6) |
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121 | (1) |
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122 | (1) |
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123 | (2) |
| 5 Gene Expression And Genome Replication In The Positive-Strand RNA Viruses |
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125 | (38) |
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5.1 Class IV virus replication cycles have common gene expression and genome replication strategies |
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126 | (1) |
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5.2 Terminal features of eukaryotic mRNA are essential for translation |
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127 | (1) |
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5.3 Monopartite Class IV (+) strand RNA viruses express multiple proteins from a single genome |
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128 | (1) |
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5.4 Picornaviruses are models for the simplest (+) strand RNA viruses |
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128 | (2) |
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5.5 Class IV viruses such as poliovirus encode one or more polyproteins |
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130 | (2) |
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5.6 Class IV viruses such as poliovirus use proteolysis to release small proteins from viral polyproteins |
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132 | (2) |
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5.7 Translation of Class IV virus genomes occurs despite the lack of a 5' cap |
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134 | (2) |
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5.8 Class IV virus genome replication occurs inside a virus replication compartment |
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136 | (1) |
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5.9 The picornavirus 3Dpol is an RdRp and synthesizes a protein-based primer |
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137 | (1) |
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5.10 Structural features of the viral genome are essential for replication of Class IV viral genomes |
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137 | (1) |
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5.11 Picornavirus genome replication occurs in four phases |
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138 | (3) |
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5.12 Flaviviruses are models for simple enveloped (+) strand RNA viruses |
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141 | (1) |
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5.13 The linear (+) strand RNA flavivirus genomes have unusual termini |
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141 | (1) |
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5.14 Enveloped HCV encodes 10 proteins including several with transmembrane segments |
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142 | (1) |
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5.15 Togaviruses are small enveloped viruses with replication cycles more complex than those of the flaviviruses |
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143 | (2) |
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5.16 Four different togavirus polyproteins are found inside infected cells |
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145 | (1) |
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5.17 Different molecular events predominate early and late during togavirus infection |
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146 | (1) |
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5.18 Translation of togavirus sgRNA requires use of the downstream hairpin loop |
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147 | (1) |
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5.19 Suppression of translation termination is necessary for production of the nonstructural p1234 Sindbis virus polyprotein |
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148 | (1) |
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5.20 Sindbis virus uses an unusual mechanism to encode the TF protein |
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149 | (1) |
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5.21 A programmed -1 ribosome frameshift is needed to produce the togavirus TF protein |
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150 | (1) |
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5.22 The picornaviruses, flaviviruses, and togaviruses illustrate many common properties among (+) strand RNA viruses |
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151 | (1) |
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5.23 Coronaviruses have long (+) strand RNA genomes and novel mechanisms of gene expression and genome replication |
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152 | (1) |
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5.24 Coronaviruses have enveloped spherical virions and encode conserved and species-specific accessory proteins |
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152 | (1) |
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5.25 Coronaviruses express a nested set of sgRNAs with leader and TRS sequences |
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153 | (2) |
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5.26 Coronaviruses use a discontinuous mechanism for synthesis of replicative forms |
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155 | (1) |
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5.27 Most coronavirus sgRNA is translated into a single protein |
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156 | (1) |
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5.28 Coronaviruses use a leaky scanning mechanism to synthesize proteins from overlapping sequences |
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156 | (1) |
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5.29 Coronaviruses may proofread RNA during synthesis |
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157 | (2) |
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5.30 Plants can also be infected by Class IV RNA viruses |
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159 | (1) |
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5.31 Comparing Class IV viruses reveals common themes with variations |
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160 | (1) |
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161 | (1) |
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161 | (1) |
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162 | (1) |
| 6 Gene Expression And Genome Replication In The Negative-Strand RNA Viruses |
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163 | (22) |
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6.1 Study of two historically infamous Class V viruses, rabies and influenza, were instrumental in the development of molecular and cellular virology |
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163 | (1) |
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6.2 The mononegavirus replication cycle includes primary and secondary transcription catalyzed by the viral RdRp |
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164 | (2) |
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6.3 Rhabdoviruses have linear (-) RNA genomes and encode five proteins |
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166 | (1) |
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6.4 Rhabdoviruses produce five mRNAs with 5' caps and polyadenylated 3' tails through a start-stop mechanism |
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167 | (2) |
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6.5 Rhabdovirus genome replication occurs through the use of a complete antigenome cRNP as a template |
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169 | (1) |
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6.6 The paramyxoviruses are mononegaviruses that use RNA editing for gene expression |
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170 | (3) |
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6.7 Filoviruses are filamentous mononegaviruses that encode seven to nine proteins |
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173 | (2) |
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6.8 The filovirus VP30 protein, not found in other mononegaviruses, is required for transcription |
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175 | (1) |
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6.9 Influenza is an example of an orthomyxovirus |
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175 | (1) |
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6.10 Of the 17 influenza A proteins, 9 are found in the virion |
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176 | (1) |
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6.11 Orthomyxovirus nucleic acid synthesis occurs in the host cell nucleus, not in the cytoplasm |
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177 | (1) |
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6.12 The first step of transcription by influenza virus is cap snatching |
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178 | (1) |
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6.13 An influenza cRNP intermediate is used as the template for genome replication |
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179 | (2) |
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6.14 Arenavirus RNA genomes are ambisense |
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181 | (1) |
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6.15 Expression of the four arenavirus proteins reflects the ambisense nature of the genome |
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182 | (1) |
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183 | (1) |
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184 | (1) |
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184 | (1) |
| 7 Gene Expression And Genome Replication In The Double-Stranded RNA Viruses |
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185 | (8) |
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7.1 The rotavirus replication cycle includes primary transcription, genome replication, and secondary transcription inside partially intact capsids in the host cytoplasm |
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186 | (1) |
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7.2 Rotavirus A has a naked capsid with three protein layers enclosing 11 segments of dsRNA |
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186 | (2) |
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7.3 Rotavirus A encodes 13 proteins |
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188 | (1) |
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7.4 Synthesis of rotavirus nucleic acids occurs in a fenestrated double-layered particle |
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188 | (1) |
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7.5 Translation of rotavirus mRNA requires NSP3 and occurs in viroplasm formed by NSP2 and NSP5 |
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189 | (2) |
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7.6 Rotavirus genome replication precedes secondary transcription |
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191 | (1) |
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191 | (1) |
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191 | (1) |
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192 | (1) |
| 8 Gene Expression And Genome Replication In The Double-Stranded DNA Viruses |
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193 | (48) |
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8.1 DNA viruses can cause productive lytic infections, cellular transformation, or latent infections |
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194 | (1) |
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8.2 Most Class I animal viruses rely on host transcription machinery for gene expression |
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194 | (1) |
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8.3 Eukaryotic transcription is affected by the state of the chromatin |
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195 | (1) |
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8.4 Eukaryotic capping, splicing, and polyadenylation occur co-transcriptionally |
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196 | (3) |
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8.5 Polyomaviruses are small DNA viruses with early and late gene expression |
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199 | (1) |
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8.6 The SV40 polyomavirus encodes seven proteins in only 5,243 bp of DNA |
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200 | (1) |
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8.7 The synthesis of mRNA in SV40 is controlled by the noncoding control region |
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201 | (1) |
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8.8 Late SV40 transcription is regulated by both host and viral proteins |
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202 | (2) |
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8.9 Most Baltimore Class I viruses including polyomaviruses manipulate the eukaryotic cell cycle |
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204 | (2) |
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8.10 Most Class I viruses prevent or delay cellular apoptosis |
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206 | (1) |
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8.11 SV40 forces the host cell to express S phase genes and uses large T antigen and host proteins for genome replication |
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207 | (1) |
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8.12 SV40 genome replication requires viral and host proteins to form active DNA replication forks |
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208 | (1) |
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8.13 The papillomavirus replication cycle is tied closely to the differentiation status of its host cell |
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209 | (2) |
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8.14 Human papillomaviruses encode about 13 proteins that are translated from polycistronic mRNA |
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211 | (2) |
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8.15 The long control region of HPV regulates papillomavirus transcription in which pre-mRNA is subjected to alternative splicing |
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213 | (1) |
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8.16 Leaky scanning, internal ribosome entry sites, and translation re-initiation lead to the expression of papillomavirus proteins from polycistronic mRNA |
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213 | (2) |
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8.17 DNA replication in papillomaviruses is linked to host cell differentiation status |
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215 | (1) |
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8.18 Papillomaviruses use early proteins to manipulate the host cell cycle and apoptosis |
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216 | (1) |
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8.19 Comparing the small DNA viruses reveals similar economy in coding capacity but different mechanisms for gene expression, manipulating the host cell cycle, and DNA replication |
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216 | (1) |
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8.20 Adenoviruses are large dsDNA viruses with three waves of gene expression |
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217 | (1) |
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8.21 Adenoviruses have large naked spherical capsids with prominent spikes and large linear dsDNA genomes |
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217 | (1) |
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8.22 Adenoviruses encode early, delayed- early, and late proteins |
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218 | (2) |
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8.23 The large E1A protein is important for regulating the adenovirus cascade of gene expression |
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220 | (1) |
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8.24 Splicing of pre-mRNA was first discovered through studying adenovirus gene expression |
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220 | (1) |
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8.25 Both host cells and adenovirus rely on alternative splicing to encode multiple proteins using the same DNA sequence |
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221 | (1) |
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8.26 Regulated alternative splicing of a late adenovirus transcript relies on cis-acting regulatory sequences, on the E4-ORF4 viral protein, and on host splicing machinery |
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222 | (2) |
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8.27 Adenovirus shuts off translation of host mRNA, while ensuring translation of its own late mRNAs through a ribosome- shunting mechanism |
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224 | (1) |
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8.28 DNA replication in adenovirus requires three viral proteins even though the genome is replicated in the host cell nucleus |
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225 | (3) |
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8.29 Herpesviruses have very large enveloped virions and large linear dsDNA genomes |
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228 | (1) |
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8.30 Lytic herpesvirus replication involves a cascade with several waves of gene expression |
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228 | (1) |
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8.31 Groups of herpes simplex virus 1 proteins have functions relating to the timing of their expression |
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229 | (1) |
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8.32 Waves of gene expression in herpesviruses are controlled by transcription activation and chromatin remodeling |
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230 | (1) |
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8.33 Herpesvirus genome replication results in concatamers |
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231 | (1) |
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8.34 Poxviruses are extremely large dsDNA viruses that replicate in the host cytoplasm |
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231 | (2) |
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8.35 Many vaccinia virus proteins are associated with the virion itself |
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233 | (1) |
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8.36 Vaccinia RNA polymerase transcribes genes in three waves using different transcription activators |
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233 | (3) |
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8.37 Vaccinia genome replication requires the unusual ends of the genome sequence |
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236 | (2) |
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8.38 The synthetic demands on the host cell make vaccinia a possible anticancer treatment |
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238 | (1) |
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238 | (1) |
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239 | (1) |
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240 | (1) |
| 9 Gene Expression And Genome Replication In The Single-Stranded DNA Viruses |
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241 | (10) |
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9.1 The ssDNA viruses express their genes and replicate their genomes in the nucleus |
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242 | (1) |
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9.2 Circoviruses are tiny ssDNA viruses with circular genomes |
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242 | (1) |
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9.3 Although their genomes are shorter than an average human gene, circoviruses encode at least four proteins |
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243 | (1) |
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9.4 Both host and viral proteins are needed for circovirus genome replication |
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244 | (1) |
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9.5 Parvoviruses are tiny ssDNA viruses with linear genomes having hairpins at both ends |
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245 | (1) |
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9.6 The model parvovirus MVM encodes six proteins using alternative splicing |
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245 | (1) |
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9.7 The model parvovirus MVM uses a rolling-hairpin mechanism for genome replication |
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246 | (2) |
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248 | (1) |
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248 | (1) |
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249 | (2) |
| 10 Gene Expression And Genome Replication In The Retroviruses And Hepadnaviruses |
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251 | (26) |
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10.1 Viral reverse transcriptases have polymerase and RNase H activity |
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254 | (1) |
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10.2 Retroviruses are enveloped and have RNA genomes yet express their proteins from dsDNA |
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254 | (1) |
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10.3 Reverse transcription occurs during transport of the retroviral nucleic acid to the nucleus, through a discontinuous mechanism |
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255 | (1) |
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10.4 Retroviral integrase inserts the viral cDNA into a chromosome, forming proviral DNA that can be transcribed by host Pol II |
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256 | (3) |
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10.5 All retroviruses express eight essential proteins, whereas some such as HIV encode species-specific accessory proteins |
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259 | (1) |
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10.6 The retroviral LTR sequences interact with host proteins to regulate transcription |
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259 | (1) |
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10.7 The compact retroviral genome is used economically to encode many proteins through the use of polyproteins, alternative splicing, and translation of polycistronic mRNA |
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260 | (4) |
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10.8 The HIV-1 accessory protein TAT is essential for viral gene expression |
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264 | (1) |
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10.9 The HIV-1 accessory protein Rev is essential for exporting some viral mRNA from the nucleus |
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265 | (1) |
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10.10 Retrovirus genome replication is accomplished by host Pol II |
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265 | (1) |
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10.11 HIV-1 is a candidate gene therapy vector for diseases that involve the immune cells normally targeted by HIV |
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266 | (1) |
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10.12 Hepadnaviruses are enveloped and have genomes containing both DNA and RNA in an unusual arrangement |
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267 | (1) |
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10.13 Hepadnaviruses use reverse transcription to amplify their genomes |
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268 | (1) |
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10.14 The cccDNA of HBV is not perfectly identical to the DNA in the infecting virion |
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269 | (1) |
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10.15 The tiny HBV genome encodes eight proteins through alternative splicing, overlapping coding sequences, and alternative start codons |
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269 | (1) |
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10.16 HBV genome replication relies upon an elaborate reverse transcriptase mechanism |
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270 | (4) |
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274 | (1) |
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275 | (1) |
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275 | (2) |
| 11 Assembly, Release, And Maturation |
|
277 | (24) |
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11.1 The last stages of the virus replication cycle are assembly, release, and maturation |
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278 | (1) |
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11.2 Unlike cells, viruses assemble from their constituent parts |
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278 | (2) |
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11.3 Virions more structurally complex than TMV also reproduce by assembly, not by division |
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280 | (1) |
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11.4 Typical sites of assembly in eukaryotic viruses include the cytoplasm, plasma membrane, and nucleus |
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281 | (1) |
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11.5 Eukaryotic virus assembly must take cellular protein localization into account |
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282 | (1) |
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11.6 Capsids and nucleocapsids associate with genomes using one of two general strategies |
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283 | (1) |
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11.7 Assembly of some viruses depends on DNA replication to provide the energy to fill the icosahedral heads |
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283 | (1) |
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11.8 Assembly of some viruses depends on a packaging motor to fill the icosahedral heads |
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284 | (2) |
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11.9 Negative RNA viruses provide a model for concerted nucleocapsid assembly |
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286 | (1) |
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11.10 To assemble, some viruses require assistance from proteins not found in the virion |
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287 | (1) |
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11.11 Viruses acquire envelopes through one of two pathways |
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287 | (1) |
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11.12 The helical vRNPs of influenza virus assemble first, followed by envelope acquisition at the plasma membrane |
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288 | (2) |
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11.13 Some viruses require maturation reactions during release in order to form infectious virions |
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290 | (1) |
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11.14 Assembly of HIV occurs at the plasma membrane |
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290 | (1) |
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11.15 Inhibition of HIV-1 maturation provides a classic example of structure-function research in medicine |
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291 | (2) |
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11.16 Release from bacterial cells usually occurs by lysis |
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293 | (2) |
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11.17 Release from animal cells can occur by lysis |
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295 | (1) |
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11.18 Release from animal cells can occur by budding |
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296 | (2) |
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11.19 Release from plant cells often occurs through biting arthropods |
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298 | (1) |
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298 | (1) |
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299 | (1) |
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299 | (2) |
| 12 Virus-Host Interactions During Lytic Growth |
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301 | (16) |
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12.1 All viruses subvert translation |
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302 | (1) |
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12.2 Bacteriophages subvert translation indirectly |
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302 | (2) |
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12.3 Animal viruses have many strategies to block translation of host mRNA |
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304 | (2) |
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12.4 Animal viruses cause structural changes in host cells referred to as cytopathic effects |
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306 | (1) |
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12.5 Viruses affect host cell apoptosis |
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306 | (2) |
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12.6 Some viruses delay apoptosis in order to complete their replication cycles before the host cell dies |
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308 | (1) |
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12.7 Some viruses subvert apoptosis in order to complete their replication cycles |
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309 | (1) |
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12.8 Viruses use the ubiquitin system to their advantage |
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309 | (2) |
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12.9 Viruses can block or subvert the cellular autophagy system |
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311 | (1) |
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12.10 Viruses subvert or co-opt the misfolded protein response triggered in the endoplasmic reticulum |
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312 | (1) |
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12.11 Viruses modify internal membranes in order to create virus replication compartments |
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312 | (3) |
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315 | (1) |
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315 | (1) |
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316 | (1) |
| 13 Persistent Viral Infections |
|
317 | (28) |
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13.1 Some bacteriophages are temperate and can persist as genomes integrated into their hosts' chromosomes |
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318 | (1) |
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13.2 Bacteriophage λ serves as a model for latency |
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318 | (2) |
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13.3 The amount of stable CII protein in the cell determines whether the phage genome becomes a prophage |
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320 | (1) |
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13.4 Activation of PRE', PI', and PantiQ by CII results in lysogeny |
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320 | (2) |
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13.5 Stress triggers an exit from lysogeny |
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322 | (1) |
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13.6 Some lysogens provide their bacterial hosts with virulence genes |
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323 | (1) |
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13.7 Prophages affect the survival of their bacterial hosts |
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324 | (2) |
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13.8 Persistent infections in humans include those with ongoing lytic replication and latent infections |
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326 | (1) |
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13.9 Human immunodeficiency virus causes persistent infections |
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326 | (1) |
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13.10 Human herpesvirus 1 is a model for latent infections |
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327 | (2) |
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13.11 Oncogenic viruses cause cancer through persistent infections |
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329 | (1) |
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13.12 DNA viruses transform cells with oncoproteins that affect the cell cycle and apoptosis |
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330 | (1) |
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13.13 HPV oncoproteins E6 and E7 cause transformation |
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331 | (1) |
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13.14 HPV E6 and E7 overexpression occurs when the virus genome recombines with a host chromosome |
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332 | (1) |
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13.15 Merkel cell polyomavirus is also associated with human cancers |
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332 | (1) |
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13.16 Epstein-Barr virus is an oncogenic herpesvirus |
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332 | (2) |
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13.17 Latency-associated viral proteins are responsible for Epstein-Barr virus- induced oncogenesis |
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334 | (1) |
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13.18 The Kaposi's sarcoma herpesvirus also causes persistent oncogenic infections |
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335 | (1) |
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13.19 Hepatocellular carcinoma is caused by persistent lytic viral infections |
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336 | (1) |
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13.20 Retroviruses have two mechanisms by which they can cause cancer |
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337 | (2) |
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13.21 Viral oncoproteins can be used to immortalize primary cell cultures |
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339 | (1) |
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13.22 The human virome is largely uncharacterized but likely has effects on human physiology |
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340 | (1) |
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341 | (1) |
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341 | (1) |
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342 | (3) |
| 14 Viral Evasion Of Innate Host Defenses |
|
345 | (20) |
|
14.1 Restriction enzymes are a component of innate immunity to bacteriophages |
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|
346 | (3) |
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14.2 Bacteriophages have counterdefenses against restriction-modification systems |
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349 | (1) |
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14.3 Human innate immune defenses operate on many levels |
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349 | (1) |
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14.4 The human innate immune system is triggered by pattern recognition |
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349 | (2) |
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14.5 Innate immune responses include cytokine secretion |
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351 | (1) |
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14.6 Interferon causes the antiviral state |
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|
351 | (2) |
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14.7 Some viruses can evade the interferon response |
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|
353 | (4) |
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14.8 Neutrophils are active during an innate immune response against viruses |
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|
357 | (1) |
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14.9 Viruses manipulate immune system communication to evade the net response |
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357 | (1) |
|
14.10 Inflammation is the hallmark of an innate immune response |
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358 | (1) |
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14.11 In order to be recognized as healthy, all cells present endogenous antigens in MHC-I molecules |
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358 | (1) |
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14.12 Cells infected by viruses produce and display viral antigens in MHC-I |
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|
359 | (1) |
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14.13 Viruses have strategies to evade MHC-I presentation of viral antigens |
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360 | (1) |
|
14.14 Natural killer cells attack cells with reduced MHC-I display |
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360 | (1) |
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14.15 The complement system targets enveloped viruses and cells infected by them |
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|
361 | (1) |
|
14.16 Some viruses can evade the complement system |
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362 | (1) |
|
14.17 Viral evasion strategies depend on the coding capacity of the virus |
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|
362 | (1) |
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14.18 In vertebrates, if an innate immune reaction does not clear an infection, adaptive immunity comes into play |
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362 | (1) |
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363 | (1) |
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364 | (1) |
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364 | (1) |
| 15 Viral Evasion Of Adaptive Host Defenses |
|
365 | (24) |
|
15.1 CRISPR-Cas is an adaptive immune response found in bacteria |
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|
366 | (4) |
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15.2 Some bacteriophages can evade or subvert the CRISPR-Cas system |
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|
370 | (1) |
|
15.3 The human adaptive immune response includes cell-mediated and humoral immunity |
|
|
371 | (1) |
|
15.4 The human adaptive immune response has specificity because it responds to epitopes |
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|
371 | (1) |
|
15.5 Professional antigen-presenting cells degrade exogenous antigens and display epitopes in MHC-II molecules |
|
|
372 | (1) |
|
15.6 Some viruses evade MHC-II presentation |
|
|
373 | (2) |
|
15.7 Lymphocytes that control viral infections have many properties in common |
|
|
375 | (1) |
|
15.8 CD4+ helper T lymphocytes interact with viral epitopes displayed in MHC-II molecules |
|
|
375 | (2) |
|
15.9 Antibodies are soluble B-cell receptors that bind to extracellular antigens such as virions |
|
|
377 | (1) |
|
15.10 During an antiviral response, B cells differentiate to produce higher- affinity antibodies |
|
|
378 | (1) |
|
15.11 Viruses have strategies to evade or subvert the antibody response |
|
|
379 | (1) |
|
15.12 CD8+ cytotoxic T lymphocytes are crucial for controlling viral infections |
|
|
380 | (1) |
|
15.13 Some viruses can evade the CTL response |
|
|
381 | (1) |
|
15.14 Viruses that cause persistent infections evade immune clearance for a long period of time |
|
|
382 | (1) |
|
15.15 The immune response to influenza serves is a comprehensive model for antiviral immune responses in general |
|
|
383 | (3) |
|
15.16 Influenza provides a model for how a lytic virus evades both innate and adaptive immunity long enough to replicate |
|
|
386 | (1) |
|
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|
387 | (1) |
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|
|
388 | (1) |
|
|
|
388 | (1) |
| 16 Medical Applications Of Molecular And Cellular Virology |
|
389 | (30) |
|
16.1 Vaccines are critical components of an effective public health system |
|
|
390 | (1) |
|
16.2 Attenuated vaccines are highly immunogenic because they can still replicate |
|
|
391 | (1) |
|
16.3 Inactivated vaccines are composed of nonreplicating virions |
|
|
392 | (1) |
|
16.4 Subunit vaccines are composed of selected antigenic proteins |
|
|
393 | (1) |
|
16.5 Although seasonal influenza vaccines are useful, a universal flu vaccine is highly sought after |
|
|
394 | (2) |
|
16.6 Preventative HIV vaccines are in development |
|
|
396 | (2) |
|
16.7 Extreme antigenic variation is a problem for developing an HIV vaccine |
|
|
398 | (1) |
|
16.8 An effective HIV vaccine may require stimulating a strong CTL response |
|
|
398 | (1) |
|
16.9 Antiviral drugs target proteins unique to viruses and essential for their replication cycle |
|
|
399 | (2) |
|
16.10 Many antiviral drugs are nucleoside or nucleotide structural analogs that target the active site of viral polymerases |
|
|
401 | (1) |
|
16.11 Drugs to treat influenza target the uncoating and release stages of viral replication |
|
|
402 | (1) |
|
16.12 Drugs to treat hepatitis C virus target the viral polymerase |
|
|
403 | (1) |
|
16.13 Drugs to treat HIV target many stages of the virus replication cycle |
|
|
404 | (2) |
|
16.14 Viral evolution occurs in response to selective pressure from antiviral drugs |
|
|
406 | (1) |
|
16.15 It might be possible to develop bacteriophage therapy to treat people with antibiotic-resistant bacterial infections |
|
|
407 | (1) |
|
16.16 Engineered viruses could in principle be used for gene therapy to treat cancer and other conditions |
|
|
408 | (2) |
|
16.17 Gene therapy and oncolytic virus treatments currently in use |
|
|
410 | (5) |
|
16.18 Therapeutic applications of CRISPR-Cas technology |
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|
415 | (1) |
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|
416 | (1) |
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|
417 | (1) |
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|
418 | (1) |
| 17 Viral Diversity, Origins, And Evolution |
|
419 | (30) |
|
17.1 The viral world is extremely diverse |
|
|
420 | (1) |
|
17.2 Satellite viruses and nucleic acids require co-infection with a virus to spread |
|
|
421 | (2) |
|
17.3 Viroids are infectious RNA molecules found in plants |
|
|
423 | (1) |
|
17.4 Transposons and introns are subviral entities |
|
|
423 | (2) |
|
17.5 Viruses have ancient origins |
|
|
425 | (1) |
|
17.6 Viral hallmark proteins can be used to trace evolutionary history |
|
|
425 | (2) |
|
17.7 Metagenomics will revolutionize evolutionary understanding of viruses |
|
|
427 | (2) |
|
17.8 Viral genetic diversity arises through mutation and recombination |
|
|
429 | (1) |
|
17.9 Genetic diversity among influenza A viruses arises through mutation and recombination |
|
|
430 | (1) |
|
17.10 Influenza A spike proteins are particularly diverse |
|
|
431 | (1) |
|
17.11 Variations among influenza A viruses reflects genetic drift and natural selection |
|
|
432 | (1) |
|
17.12 Pandemic influenza A strains have arisen through recombination |
|
|
433 | (2) |
|
17.13 New pandemic influenza A strains may be able to arise through mutation |
|
|
435 | (1) |
|
17.14 Selective pressures and constraints influence viral evolution |
|
|
436 | (2) |
|
17.15 Some viruses and hosts coevolve |
|
|
438 | (2) |
|
17.16 Medically dangerous emerging viruses are zoonotic |
|
|
440 | (2) |
|
17.17 HIV exhibits high levels of genetic diversity and transferred from apes to humans on four occasions |
|
|
442 | (1) |
|
17.18 HIV-1 has molecular features that reflect adaptation to humans |
|
|
443 | (1) |
|
17.19 Viruses and subviral entities are common in the human genome |
|
|
444 | (1) |
|
17.20 Viruses and subviral entities have strongly affected the evolution of organisms including humans |
|
|
445 | (1) |
|
17.21 Virology unites the biosphere |
|
|
446 | (1) |
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|
446 | (1) |
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|
|
447 | (1) |
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|
|
447 | (2) |
| Glossary |
|
449 | (24) |
| Answers |
|
473 | (14) |
| Index |
|
487 | |
