Molecular and Cellular Biology of Viruses [Mīkstie vāki]

(Colorado College, USA)
  • Formāts: Paperback / softback, 501 pages, height x width: 279x216 mm, weight: 590 g, 425 Line drawings, color; 87 Halftones, color; 6 Tables, color; 512 Illustrations, color
  • Izdošanas datums: 29-Jul-2019
  • Izdevniecība: CRC Press Inc
  • ISBN-10: 0815345232
  • ISBN-13: 9780815345237
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  • Formāts: Paperback / softback, 501 pages, height x width: 279x216 mm, weight: 590 g, 425 Line drawings, color; 87 Halftones, color; 6 Tables, color; 512 Illustrations, color
  • Izdošanas datums: 29-Jul-2019
  • Izdevniecība: CRC Press Inc
  • ISBN-10: 0815345232
  • ISBN-13: 9780815345237
Citas grāmatas par šo tēmu:
Viruses interact with host cells in ways that uniquely reveal a great deal about general aspects of molecular and cellular structure and function. Molecular and Cellular Biology of Viruses leads students on an exploration of viruses by supporting engaging and interactive learning. All the major classes of viruses are covered, with separate chapters for their replication and expression strategies, and chapters for mechanisms such as attachment that are independent of the virus genome type. Specific cases drawn from primary literature foster student engagement. End-of-chapter questions focus on analysis and interpretation with answers being given at the back of the book. Examples come from the most-studied and medically important viruses such as HIV, influenza, and poliovirus. Plant viruses and bacteriophages are also included. There are chapters on the overall effect of viral infection on the host cell. Coverage of the immune system is focused on the interplay between host defenses and viruses, with a separate chapter on medical applications such as anti-viral drugs and vaccine development. The final chapter is on virus diversity and evolution, incorporating contemporary insights from metagenomic research. Key selling feature: Readable but rigorous coverage of the molecular and cellular biology of viruses Molecular mechanisms of all major groups, including plant viruses and bacteriophages, illustrated by example Host-pathogen interactions at the cellular and molecular level emphasized throughout Medical implications and consequences included Quality illustrations available to instructors Extensive questions and answers for each chapter
Preface xvii
Acknowledgments xix
Author xxi
1 The Fundamentals Of Molecular And Cellular Virology 1(18)
1.1 Molecular and cellular virology focuses on the molecular interactions that occur when a virus infects a host cell
2(1)
1.2 The discipline of virology can be traced historically to agricultural and medical science
3(3)
1.3 Basic research in virology is critical for molecular biology, both historically and today
6(2)
1.4 Viruses, whether understood as living or not, are the most abundant evolving entities known
8(1)
1.5 Viruses can be defined unambiguously by four traits
8(2)
1.6 Virions are infectious particles minimally made up of nucleic acids and proteins
10(1)
1.7 Viruses can be classified according to the ways they synthesize and use mRNA
11(1)
1.8 Viruses are propagated in the laboratory by mixing them with host cells
12(2)
1.9 Viral sequences are ubiquitous in animal genomes, including the human genome
14(3)
Essential Concepts
17(1)
Questions
17(1)
Further Reading
18(1)
2 The Virus Replication Cycle 19(14)
2.1 Viruses reproduce through a lytic virus replication cycle
20(2)
2.2 Molecular events during each stage of the virus replication cycle
22(1)
2.3 The influenza virus is a model for replication of an animal virus
23(1)
2.4 The host surface is especially important for attachment, penetration, and uncoating
23(3)
2.5 Viral gene expression and genome replication take advantage of host transcription, translation, and replication features
26(1)
2.6 The host cytoskeleton and membranes are typically crucial during virus assembly
27(1)
2.7 Host-cell surfaces influence the mechanism of virus release
27(1)
2.8 Viruses can also cause long-term infections
27(2)
2.9 Herpesvirus is a model for latent infections
29(1)
2.10 Research in molecular and cellular virology often focuses on the molecular details of each stage of the replication cycle
29(1)
Essential Concepts
30(1)
Questions
30(1)
Further Reading
31(2)
3 Attachment, Penetration, And Uncoating 33(44)
3.1 Viruses enter the human body through one of six routes
33(1)
3.2 The likelihood of becoming HIV+ depends on the route of transmission and the amount of virus in the infected tissue
34(1)
3.3 Viruses are selective in their host range and tissue tropism
35(1)
3.4 The virion is a genome delivery device
36(1)
3.5 The genomic contents of a virion are irrelevant for attachment, penetration, and uncoating
37(3)
3.6 Animal viruses attach to specific cells and can spread to multiple tissues
40(1)
3.7 Noncovalent intermolecular forces are responsible for attaching to host cells
41(1)
3.8 Most animal virus receptors are glycoproteins
42(1)
3.9 Animal virus receptors can be identified through genetic, biochemical, and immunological approaches
43(1)
3.10 Animal virus receptors can be identified through molecular cloning
43(1)
3.11 Animal virus receptors can be identified through affinity chromatography
44(1)
3.12 Antibodies can be used to identify animal virus receptors
45(2)
3.13 Rhinovirus serves as a model for attachment by animal viruses lacking spikes
47(3)
3.14 Several independent lines of evidence indicate that ICAM-1 is the rhinovirus receptor
50(1)
3.15 Experiments using molecular genetics support the conclusion that ICAM-1 is the rhinovirus receptor
50(1)
3.16 Structural biology experiments support the conclusion that ICAM-1 is the rhinovirus receptor
51(1)
3.17 Bioinformatics comparisons support the conclusion that ICAM-1 is the rhinovirus receptor
51(1)
3.18 Influenza serves as a model for attachment by enveloped viruses
52(1)
3.19 The influenza HA spike protein binds to sialic acids
53(2)
3.20 The second stage of the virus replication cycle includes both penetration and uncoating and, if necessary, transport to the nucleus
55(1)
3.21 Viruses subvert the two major eukaryotic mechanisms for internalizing particles
56(1)
3.22 Many viruses subvert receptor-mediated endocytosis for penetration
56(1)
3.23 Herpesvirus penetrates the cell through phagocytosis
57(1)
3.24 Common methods for determining the mode of viral penetration include use of drugs and RNA interference
58(1)
3.25 The virion is a metastable particle primed for uncoating once irreversible attachment and penetration have occurred
59(1)
3.26 Picornaviruses are naked viruses that release their genomic contents through pore formation
60(1)
3.27 Some enveloped viruses use membrane fusion with the outside surface of the cell for penetration
60(1)
3.28 Vesicle fusion in neuroscience is a model for viral membrane fusion
61(2)
3.29 HIV provides a model of membrane fusion triggered by a cascade of protein-protein interactions
63(1)
3.30 Influenza provides a model for viral envelope fusion triggered by acidification of an endocytic vesicle
64(1)
3.31 The destination for the virus genome may be the cytoplasm or the nucleus
65(1)
3.32 Subversion of the cellular cytoskeleton is critical for uncoating
65(1)
3.33 Viruses that enter an intact nucleus must manipulate gated nuclear pores
66(1)
3.34 Viruses introduce their genomes into the nucleus in a variety of ways
67(1)
3.35 Adenovirus provides a model for uncoating that delivers the viral genome into the nucleus
68(1)
3.36 The unusual uncoating stages of reoviruses and poxviruses leave the virions partially intact in the cytoplasm
69(2)
3.37 Viruses that penetrate plant cells face plant-specific barriers to infection
71(1)
3.38 Plant viruses are often transmitted by biting arthropod vectors
72(1)
Essential Concepts
73(1)
Questions
74(1)
Further Reading
74(3)
4 Gene Expression And Genome Replication In Model Bacteriophages 77(48)
4.1 Bacterial host cell transcription is catalyzed by a multisubunit machine that catalyzes initiation, elongation, and termination
78(2)
4.2 Bacterial host cell and bacteriophage mRNA are typically polycistronic
80(1)
4.3 Transcription and translation in bacterial host cells and bacteriophages are nearly simultaneous because of the proximity of ribosomes and chromosomes
81(1)
4.4 Bacterial translation initiation, elongation, and termination are controlled by translation factors
81(2)
4.5 Bacteriophages, like all viruses, encode structural and nonstructural proteins
83(1)
4.6 The T7 bacteriophage has naked, complex virions and a large double- stranded DNA genome
84(1)
4.7 Bacteriophage T7 encodes 55 proteins in genes that are physically grouped together by function
85(1)
4.8 Bacteriophage T7 proteins are expressed in three major waves
85(1)
4.9 The functions of bacteriophage proteins often correlate with the timing of their expression
86(1)
4.10 Bacteriophage T7 gene expression is highly regulated at the level of transcription initiation
87(1)
4.11 Bacterial host chromosome replication is regulated by the DnaA protein and occurs via a theta intermediate
88(2)
4.12 Many bacterial proteins are needed to catalyze chromosome replication
90(2)
4.13 Although many bacteriophages have linear dsDNA genomes, bacterial hosts cannot replicate the ends of linear DNA
92(1)
4.14 T7 bacteriophage genome replication is catalyzed by one of the simplest known replication machines
93(3)
4.15 The λ bacteriophage has naked, complex virions and a large double- stranded DNA genome
96(1)
4.16 Bacteriophage λ can cause lytic or long- term infections
96(2)
4.17 There are three waves of gene expression during lytic λ replication
98(1)
4.18 The λ control region is responsible for early gene expression because of its promoters and the Cro and N proteins it encodes
99(1)
4.19 The λ N antitermination protein controls the onset of delayed-early gene expression
99(1)
4.20 The λ Q antitermination protein and Cro repressor protein control the switch to late gene expression
100(1)
4.21 Bacteriophages T7 and λ both have three waves of gene expression but the molecular mechanisms controlling them differ
100(1)
4.22 Bacteriophage λ genome replication occurs in two stages, through two different intermediates
101(1)
4.23 Lambda genome replication requires phage proteins O and P and many subverted host proteins
102(1)
4.24 The abundance of host DnaA protein relative to the amount of phage DNA controls the switch to rolling-circle replication
102(1)
4.25 There are billions of other bacteriophages that regulate gene expression in various ways
103(1)
4.26 Some bacteriophages have ssDNA, dsDNA, or (+) ssRNA genomes
104(1)
4.27 The replication cycles of ssDNA bacteriophages always include formation of a double-stranded replicative form
104(1)
4.28 Bacteriophage Φχ174 is of historical importance
105(1)
4.29 Bacteriophage Φχ174 has extremely overlapping protein-coding sequences
105(1)
4.30 Bacteriophage Φχ174 proteins are expressed in different amounts
106(1)
4.31 A combination of mRNA levels and differential translation accounts for levels of bacteriophage Φχ174 protein expression
107(1)
4.32 Bacteriophage M13 genome replication is catalyzed by host proteins and occurs via a replicative form
108(2)
4.33 Bacteriophage MS2 is a (+) ssRNA virus that encodes four proteins
110(1)
4.34 Bacteriophage MS2 protein abundance is controlled by secondary structure in the genome
111(3)
4.35 Bacteriophage RdRp enzymes subvert abundant host proteins to create an efficient replicase complex
114(1)
4.36 Bacteriophage proteins are common laboratory tools
115(6)
Essential Concepts
121(1)
Questions
122(1)
Further Reading
123(2)
5 Gene Expression And Genome Replication In The Positive-Strand RNA Viruses 125(38)
5.1 Class IV virus replication cycles have common gene expression and genome replication strategies
126(1)
5.2 Terminal features of eukaryotic mRNA are essential for translation
127(1)
5.3 Monopartite Class IV (+) strand RNA viruses express multiple proteins from a single genome
128(1)
5.4 Picornaviruses are models for the simplest (+) strand RNA viruses
128(2)
5.5 Class IV viruses such as poliovirus encode one or more polyproteins
130(2)
5.6 Class IV viruses such as poliovirus use proteolysis to release small proteins from viral polyproteins
132(2)
5.7 Translation of Class IV virus genomes occurs despite the lack of a 5' cap
134(2)
5.8 Class IV virus genome replication occurs inside a virus replication compartment
136(1)
5.9 The picornavirus 3Dpol is an RdRp and synthesizes a protein-based primer
137(1)
5.10 Structural features of the viral genome are essential for replication of Class IV viral genomes
137(1)
5.11 Picornavirus genome replication occurs in four phases
138(3)
5.12 Flaviviruses are models for simple enveloped (+) strand RNA viruses
141(1)
5.13 The linear (+) strand RNA flavivirus genomes have unusual termini
141(1)
5.14 Enveloped HCV encodes 10 proteins including several with transmembrane segments
142(1)
5.15 Togaviruses are small enveloped viruses with replication cycles more complex than those of the flaviviruses
143(2)
5.16 Four different togavirus polyproteins are found inside infected cells
145(1)
5.17 Different molecular events predominate early and late during togavirus infection
146(1)
5.18 Translation of togavirus sgRNA requires use of the downstream hairpin loop
147(1)
5.19 Suppression of translation termination is necessary for production of the nonstructural p1234 Sindbis virus polyprotein
148(1)
5.20 Sindbis virus uses an unusual mechanism to encode the TF protein
149(1)
5.21 A programmed -1 ribosome frameshift is needed to produce the togavirus TF protein
150(1)
5.22 The picornaviruses, flaviviruses, and togaviruses illustrate many common properties among (+) strand RNA viruses
151(1)
5.23 Coronaviruses have long (+) strand RNA genomes and novel mechanisms of gene expression and genome replication
152(1)
5.24 Coronaviruses have enveloped spherical virions and encode conserved and species-specific accessory proteins
152(1)
5.25 Coronaviruses express a nested set of sgRNAs with leader and TRS sequences
153(2)
5.26 Coronaviruses use a discontinuous mechanism for synthesis of replicative forms
155(1)
5.27 Most coronavirus sgRNA is translated into a single protein
156(1)
5.28 Coronaviruses use a leaky scanning mechanism to synthesize proteins from overlapping sequences
156(1)
5.29 Coronaviruses may proofread RNA during synthesis
157(2)
5.30 Plants can also be infected by Class IV RNA viruses
159(1)
5.31 Comparing Class IV viruses reveals common themes with variations
160(1)
Essential Concepts
161(1)
Questions
161(1)
Further Reading
162(1)
6 Gene Expression And Genome Replication In The Negative-Strand RNA Viruses 163(22)
6.1 Study of two historically infamous Class V viruses, rabies and influenza, were instrumental in the development of molecular and cellular virology
163(1)
6.2 The mononegavirus replication cycle includes primary and secondary transcription catalyzed by the viral RdRp
164(2)
6.3 Rhabdoviruses have linear (-) RNA genomes and encode five proteins
166(1)
6.4 Rhabdoviruses produce five mRNAs with 5' caps and polyadenylated 3' tails through a start-stop mechanism
167(2)
6.5 Rhabdovirus genome replication occurs through the use of a complete antigenome cRNP as a template
169(1)
6.6 The paramyxoviruses are mononegaviruses that use RNA editing for gene expression
170(3)
6.7 Filoviruses are filamentous mononegaviruses that encode seven to nine proteins
173(2)
6.8 The filovirus VP30 protein, not found in other mononegaviruses, is required for transcription
175(1)
6.9 Influenza is an example of an orthomyxovirus
175(1)
6.10 Of the 17 influenza A proteins, 9 are found in the virion
176(1)
6.11 Orthomyxovirus nucleic acid synthesis occurs in the host cell nucleus, not in the cytoplasm
177(1)
6.12 The first step of transcription by influenza virus is cap snatching
178(1)
6.13 An influenza cRNP intermediate is used as the template for genome replication
179(2)
6.14 Arenavirus RNA genomes are ambisense
181(1)
6.15 Expression of the four arenavirus proteins reflects the ambisense nature of the genome
182(1)
Essential Concepts
183(1)
Questions
184(1)
Further Reading
184(1)
7 Gene Expression And Genome Replication In The Double-Stranded RNA Viruses 185(8)
7.1 The rotavirus replication cycle includes primary transcription, genome replication, and secondary transcription inside partially intact capsids in the host cytoplasm
186(1)
7.2 Rotavirus A has a naked capsid with three protein layers enclosing 11 segments of dsRNA
186(2)
7.3 Rotavirus A encodes 13 proteins
188(1)
7.4 Synthesis of rotavirus nucleic acids occurs in a fenestrated double-layered particle
188(1)
7.5 Translation of rotavirus mRNA requires NSP3 and occurs in viroplasm formed by NSP2 and NSP5
189(2)
7.6 Rotavirus genome replication precedes secondary transcription
191(1)
Essential Concepts
191(1)
Questions
191(1)
Further Reading
192(1)
8 Gene Expression And Genome Replication In The Double-Stranded DNA Viruses 193(48)
8.1 DNA viruses can cause productive lytic infections, cellular transformation, or latent infections
194(1)
8.2 Most Class I animal viruses rely on host transcription machinery for gene expression
194(1)
8.3 Eukaryotic transcription is affected by the state of the chromatin
195(1)
8.4 Eukaryotic capping, splicing, and polyadenylation occur co-transcriptionally
196(3)
8.5 Polyomaviruses are small DNA viruses with early and late gene expression
199(1)
8.6 The SV40 polyomavirus encodes seven proteins in only 5,243 bp of DNA
200(1)
8.7 The synthesis of mRNA in SV40 is controlled by the noncoding control region
201(1)
8.8 Late SV40 transcription is regulated by both host and viral proteins
202(2)
8.9 Most Baltimore Class I viruses including polyomaviruses manipulate the eukaryotic cell cycle
204(2)
8.10 Most Class I viruses prevent or delay cellular apoptosis
206(1)
8.11 SV40 forces the host cell to express S phase genes and uses large T antigen and host proteins for genome replication
207(1)
8.12 SV40 genome replication requires viral and host proteins to form active DNA replication forks
208(1)
8.13 The papillomavirus replication cycle is tied closely to the differentiation status of its host cell
209(2)
8.14 Human papillomaviruses encode about 13 proteins that are translated from polycistronic mRNA
211(2)
8.15 The long control region of HPV regulates papillomavirus transcription in which pre-mRNA is subjected to alternative splicing
213(1)
8.16 Leaky scanning, internal ribosome entry sites, and translation re-initiation lead to the expression of papillomavirus proteins from polycistronic mRNA
213(2)
8.17 DNA replication in papillomaviruses is linked to host cell differentiation status
215(1)
8.18 Papillomaviruses use early proteins to manipulate the host cell cycle and apoptosis
216(1)
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
216(1)
8.20 Adenoviruses are large dsDNA viruses with three waves of gene expression
217(1)
8.21 Adenoviruses have large naked spherical capsids with prominent spikes and large linear dsDNA genomes
217(1)
8.22 Adenoviruses encode early, delayed- early, and late proteins
218(2)
8.23 The large E1A protein is important for regulating the adenovirus cascade of gene expression
220(1)
8.24 Splicing of pre-mRNA was first discovered through studying adenovirus gene expression
220(1)
8.25 Both host cells and adenovirus rely on alternative splicing to encode multiple proteins using the same DNA sequence
221(1)
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
222(2)
8.27 Adenovirus shuts off translation of host mRNA, while ensuring translation of its own late mRNAs through a ribosome- shunting mechanism
224(1)
8.28 DNA replication in adenovirus requires three viral proteins even though the genome is replicated in the host cell nucleus
225(3)
8.29 Herpesviruses have very large enveloped virions and large linear dsDNA genomes
228(1)
8.30 Lytic herpesvirus replication involves a cascade with several waves of gene expression
228(1)
8.31 Groups of herpes simplex virus 1 proteins have functions relating to the timing of their expression
229(1)
8.32 Waves of gene expression in herpesviruses are controlled by transcription activation and chromatin remodeling
230(1)
8.33 Herpesvirus genome replication results in concatamers
231(1)
8.34 Poxviruses are extremely large dsDNA viruses that replicate in the host cytoplasm
231(2)
8.35 Many vaccinia virus proteins are associated with the virion itself
233(1)
8.36 Vaccinia RNA polymerase transcribes genes in three waves using different transcription activators
233(3)
8.37 Vaccinia genome replication requires the unusual ends of the genome sequence
236(2)
8.38 The synthetic demands on the host cell make vaccinia a possible anticancer treatment
238(1)
Essential Concepts
238(1)
Questions
239(1)
Further Reading
240(1)
9 Gene Expression And Genome Replication In The Single-Stranded DNA Viruses 241(10)
9.1 The ssDNA viruses express their genes and replicate their genomes in the nucleus
242(1)
9.2 Circoviruses are tiny ssDNA viruses with circular genomes
242(1)
9.3 Although their genomes are shorter than an average human gene, circoviruses encode at least four proteins
243(1)
9.4 Both host and viral proteins are needed for circovirus genome replication
244(1)
9.5 Parvoviruses are tiny ssDNA viruses with linear genomes having hairpins at both ends
245(1)
9.6 The model parvovirus MVM encodes six proteins using alternative splicing
245(1)
9.7 The model parvovirus MVM uses a rolling-hairpin mechanism for genome replication
246(2)
Essential Concepts
248(1)
Questions
248(1)
Further Reading
249(2)
10 Gene Expression And Genome Replication In The Retroviruses And Hepadnaviruses 251(26)
10.1 Viral reverse transcriptases have polymerase and RNase H activity
254(1)
10.2 Retroviruses are enveloped and have RNA genomes yet express their proteins from dsDNA
254(1)
10.3 Reverse transcription occurs during transport of the retroviral nucleic acid to the nucleus, through a discontinuous mechanism
255(1)
10.4 Retroviral integrase inserts the viral cDNA into a chromosome, forming proviral DNA that can be transcribed by host Pol II
256(3)
10.5 All retroviruses express eight essential proteins, whereas some such as HIV encode species-specific accessory proteins
259(1)
10.6 The retroviral LTR sequences interact with host proteins to regulate transcription
259(1)
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
260(4)
10.8 The HIV-1 accessory protein TAT is essential for viral gene expression
264(1)
10.9 The HIV-1 accessory protein Rev is essential for exporting some viral mRNA from the nucleus
265(1)
10.10 Retrovirus genome replication is accomplished by host Pol II
265(1)
10.11 HIV-1 is a candidate gene therapy vector for diseases that involve the immune cells normally targeted by HIV
266(1)
10.12 Hepadnaviruses are enveloped and have genomes containing both DNA and RNA in an unusual arrangement
267(1)
10.13 Hepadnaviruses use reverse transcription to amplify their genomes
268(1)
10.14 The cccDNA of HBV is not perfectly identical to the DNA in the infecting virion
269(1)
10.15 The tiny HBV genome encodes eight proteins through alternative splicing, overlapping coding sequences, and alternative start codons
269(1)
10.16 HBV genome replication relies upon an elaborate reverse transcriptase mechanism
270(4)
Essential Concepts
274(1)
Questions
275(1)
Further Reading
275(2)
11 Assembly, Release, And Maturation 277(24)
11.1 The last stages of the virus replication cycle are assembly, release, and maturation
278(1)
11.2 Unlike cells, viruses assemble from their constituent parts
278(2)
11.3 Virions more structurally complex than TMV also reproduce by assembly, not by division
280(1)
11.4 Typical sites of assembly in eukaryotic viruses include the cytoplasm, plasma membrane, and nucleus
281(1)
11.5 Eukaryotic virus assembly must take cellular protein localization into account
282(1)
11.6 Capsids and nucleocapsids associate with genomes using one of two general strategies
283(1)
11.7 Assembly of some viruses depends on DNA replication to provide the energy to fill the icosahedral heads
283(1)
11.8 Assembly of some viruses depends on a packaging motor to fill the icosahedral heads
284(2)
11.9 Negative RNA viruses provide a model for concerted nucleocapsid assembly
286(1)
11.10 To assemble, some viruses require assistance from proteins not found in the virion
287(1)
11.11 Viruses acquire envelopes through one of two pathways
287(1)
11.12 The helical vRNPs of influenza virus assemble first, followed by envelope acquisition at the plasma membrane
288(2)
11.13 Some viruses require maturation reactions during release in order to form infectious virions
290(1)
11.14 Assembly of HIV occurs at the plasma membrane
290(1)
11.15 Inhibition of HIV-1 maturation provides a classic example of structure-function research in medicine
291(2)
11.16 Release from bacterial cells usually occurs by lysis
293(2)
11.17 Release from animal cells can occur by lysis
295(1)
11.18 Release from animal cells can occur by budding
296(2)
11.19 Release from plant cells often occurs through biting arthropods
298(1)
Essential Concepts
298(1)
Questions
299(1)
Further Reading
299(2)
12 Virus-Host Interactions During Lytic Growth 301(16)
12.1 All viruses subvert translation
302(1)
12.2 Bacteriophages subvert translation indirectly
302(2)
12.3 Animal viruses have many strategies to block translation of host mRNA
304(2)
12.4 Animal viruses cause structural changes in host cells referred to as cytopathic effects
306(1)
12.5 Viruses affect host cell apoptosis
306(2)
12.6 Some viruses delay apoptosis in order to complete their replication cycles before the host cell dies
308(1)
12.7 Some viruses subvert apoptosis in order to complete their replication cycles
309(1)
12.8 Viruses use the ubiquitin system to their advantage
309(2)
12.9 Viruses can block or subvert the cellular autophagy system
311(1)
12.10 Viruses subvert or co-opt the misfolded protein response triggered in the endoplasmic reticulum
312(1)
12.11 Viruses modify internal membranes in order to create virus replication compartments
312(3)
Essential Concepts
315(1)
Questions
315(1)
Further Reading
316(1)
13 Persistent Viral Infections 317(28)
13.1 Some bacteriophages are temperate and can persist as genomes integrated into their hosts' chromosomes
318(1)
13.2 Bacteriophage λ serves as a model for latency
318(2)
13.3 The amount of stable CII protein in the cell determines whether the phage genome becomes a prophage
320(1)
13.4 Activation of PRE', PI', and PantiQ by CII results in lysogeny
320(2)
13.5 Stress triggers an exit from lysogeny
322(1)
13.6 Some lysogens provide their bacterial hosts with virulence genes
323(1)
13.7 Prophages affect the survival of their bacterial hosts
324(2)
13.8 Persistent infections in humans include those with ongoing lytic replication and latent infections
326(1)
13.9 Human immunodeficiency virus causes persistent infections
326(1)
13.10 Human herpesvirus 1 is a model for latent infections
327(2)
13.11 Oncogenic viruses cause cancer through persistent infections
329(1)
13.12 DNA viruses transform cells with oncoproteins that affect the cell cycle and apoptosis
330(1)
13.13 HPV oncoproteins E6 and E7 cause transformation
331(1)
13.14 HPV E6 and E7 overexpression occurs when the virus genome recombines with a host chromosome
332(1)
13.15 Merkel cell polyomavirus is also associated with human cancers
332(1)
13.16 Epstein-Barr virus is an oncogenic herpesvirus
332(2)
13.17 Latency-associated viral proteins are responsible for Epstein-Barr virus- induced oncogenesis
334(1)
13.18 The Kaposi's sarcoma herpesvirus also causes persistent oncogenic infections
335(1)
13.19 Hepatocellular carcinoma is caused by persistent lytic viral infections
336(1)
13.20 Retroviruses have two mechanisms by which they can cause cancer
337(2)
13.21 Viral oncoproteins can be used to immortalize primary cell cultures
339(1)
13.22 The human virome is largely uncharacterized but likely has effects on human physiology
340(1)
Essential Concepts
341(1)
Questions
341(1)
Further Reading
342(3)
14 Viral Evasion Of Innate Host Defenses 345(20)
14.1 Restriction enzymes are a component of innate immunity to bacteriophages
346(3)
14.2 Bacteriophages have counterdefenses against restriction-modification systems
349(1)
14.3 Human innate immune defenses operate on many levels
349(1)
14.4 The human innate immune system is triggered by pattern recognition
349(2)
14.5 Innate immune responses include cytokine secretion
351(1)
14.6 Interferon causes the antiviral state
351(2)
14.7 Some viruses can evade the interferon response
353(4)
14.8 Neutrophils are active during an innate immune response against viruses
357(1)
14.9 Viruses manipulate immune system communication to evade the net response
357(1)
14.10 Inflammation is the hallmark of an innate immune response
358(1)
14.11 In order to be recognized as healthy, all cells present endogenous antigens in MHC-I molecules
358(1)
14.12 Cells infected by viruses produce and display viral antigens in MHC-I
359(1)
14.13 Viruses have strategies to evade MHC-I presentation of viral antigens
360(1)
14.14 Natural killer cells attack cells with reduced MHC-I display
360(1)
14.15 The complement system targets enveloped viruses and cells infected by them
361(1)
14.16 Some viruses can evade the complement system
362(1)
14.17 Viral evasion strategies depend on the coding capacity of the virus
362(1)
14.18 In vertebrates, if an innate immune reaction does not clear an infection, adaptive immunity comes into play
362(1)
Essential Concepts
363(1)
Questions
364(1)
Further Reading
364(1)
15 Viral Evasion Of Adaptive Host Defenses 365(24)
15.1 CRISPR-Cas is an adaptive immune response found in bacteria
366(4)
15.2 Some bacteriophages can evade or subvert the CRISPR-Cas system
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
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)
Essential Concepts
387(1)
Questions
388(1)
Further Reading
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
415(1)
Essential Concepts
416(1)
Questions
417(1)
Further Reading
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)
Essential Concepts
446(1)
Questions
447(1)
Further Reading
447(2)
Glossary 449(24)
Answers 473(14)
Index 487
Professor Phoebe Lostroh is a molecular microbiologist whose research has focused on bacterial "sex." She has recruited a diverse team of undergraduate researchers at Colorado College where she has won multiple awards, such as the Theodore Roosevelt Collins Outstanding Faculty award for teaching, mentoring, and advising students of color and first-generation students. Her research has been supported by the NSF (2009-2018), NIH (1994-2003), and the Keck foundation (2001-2003). She's a volunteer comedienne with Science Riot, which brings science to the public through stand-up routines, and is the lead singer on Rejoice! an album of songs for activists.