Molecular and Cellular Biology of Viruses 1st edition by Phoebe Lostroh 0367076322 9780367076320

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ISBN 10: 0367076322

ISBN 13: 9780367076320

Author: Phoebe Lostroh

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 Virusesleads 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

Molecular and Cellular Biology of Viruses 1st Table of contents:

1. The Fundamentals of Molecular and Cellular Virology
1.1 Molecular and cellular virology focuses on the molecular interactions that occur when a virus infects a host cell
1.2 The discipline of virology can be traced historically to agricultural and medical science
1.3 Basic research in virology is critical for molecular biology, both historically and today
1.4 Viruses, whether understood as living or not, are the most abundant evolving entities known
1.5 Viruses can be defined unambiguously by four traits
1.6 Virions are infectious particles minimally made up of nucleic acids and proteins
1.7 Viruses can be classified according to the ways they synthesize and use mRNA
1.8 Viruses are propagated in the laboratory by mixing them with host cells
1.9 Viral sequences are ubiquitous in animal genomes, including the human genome
Essential concepts
Questions
Further reading
2. The Virus Replication Cycle
2.1 Viruses reproduce through a lytic virus replication cycle
2.2 Molecular events during each stage of the virus replication cycle
2.3 The influenza virus is a model for replication of an animal virus
2.4 The host surface is especially important for attachment, penetration, and uncoating
2.5 Viral gene expression and genome replication take advantage of host transcription, translation, and replication features
2.6 The host cytoskeleton and membranes are typically crucial during virus assembly
2.7 Host-cell surfaces influence the mechanism of virus release
2.8 Viruses can also cause long-term infections
2.9 Herpesvirus is a model for latent infections
2.10 Research in molecular and cellular virology often focuses on the molecular details of each stage of the replication cycle
Essential concepts
Questions
Further reading
3. Attachment, Penetration, And Uncoating
3.1 Viruses enter the human body through one of six routes
3.2 The likelihood of becoming HIV+ depends on the route of transmission and the amount of virus in the infected tissue
3.3 Viruses are selective in their host range and tissue tropism
3.4 The virion is a genome delivery device
3.5 The genomic contents of a virion are irrelevant for attachment, penetration, and uncoating
3.6 Animal viruses attach to specific cells and can spread to multiple tissues
3.7 Noncovalent intermolecular forces are responsible for attaching to host cells
3.8 Most animal virus receptors are glycoproteins
3.9 Animal virus receptors can be identified through genetic, biochemical, and immunological approaches
3.10 Animal virus receptors can be identified through molecular cloning
3.11 Animal virus receptors can be identified through affinity chromatography
3.12 Antibodies can be used to identify animal virus receptors
3.13 Rhinovirus serves as a model for attachment by animal viruses lacking spikes
3.14 Several independent lines of evidence indicate that ICAM-1 is the rhinovirus receptor
3.15 Experiments using molecular genetics support the conclusion that ICAM-1 is the rhinovirus receptor
3.16 Structural biology experiments support the conclusion that ICAM-1 is the rhinovirus receptor
3.17 Bioinformatics comparisons support the conclusion that ICAM-1 is the rhinovirus receptor
3.18 Influenza serves as a model for attachment by enveloped viruses
3.19 The influenza HA spike protein binds to sialic acids
3.20 The second stage of the virus replication cycle includes both penetration and uncoating and, if necessary, transport to the nucleus
3.21 Viruses subvert the two major eukaryotic mechanisms for internalizing particles
3.22 Many viruses subvert receptor-mediated endocytosis for penetration
3.23 Herpesvirus penetrates the cell through phagocytosis
3.24 Common methods for determining the mode of viral penetration include use of drugs and RNA interference
3.25 The virion is a metastable particle primed for uncoating once irreversible attachment and penetration have occurred
3.26 Picornaviruses are naked viruses that release their genomic contents through pore formation
3.27 Some enveloped viruses use membrane fusion with the outside surface of the cell for penetration
3.28 Vesicle fusion in neuroscience is a model for viral membrane fusion
3.29 HIV provides a model of membrane fusion triggered by a cascade of protein–protein interactions
3.30 Influenza provides a model for viral envelope fusion triggered by acidification of an endocytic vesicle
3.31 The destination for the virus genome may be the cytoplasm or the nucleus
3.32 Subversion of the cellular cytoskeleton is critical for uncoating
3.33 Viruses that enter an intact nucleus must manipulate gated nuclear pores
3.34 Viruses introduce their genomes into the nucleus in a variety of ways
3.35 Adenovirus provides a model for uncoating that delivers the viral genome into the nucleus
3.36 The unusual uncoating stages of reoviruses and poxviruses leave the virions partially intact in the cytoplasm
3.37 Viruses that penetrate plant cells face plant-specific barriers to infection
3.38 Plant viruses are often transmitted by biting arthropod vectors
Essential concepts
Questions
Further reading
4. Gene Expression and Genome Replication in Model Bacteriophages
4.1 Bacterial host cell transcription is catalyzed by a multisubunit machine that catalyzes initiation, elongation, and termination
4.2 Bacterial host cell and bacteriophage mRNA are typically polycistronic
4.3 Transcription and translation in bacterial host cells and bacteriophages are nearly simultaneous because of the proximity of ribosomes and chromosomes
4.4 Bacterial translation initiation, elongation, and termination are controlled by translation factors
4.5 Bacteriophages, like all viruses, encode structural and nonstructural proteins
4.6 The T7 bacteriophage has naked, complex virions and a large double-stranded DNA genome
4.7 Bacteriophage T7 encodes 55 proteins in genes that are physically grouped together by function
4.8 Bacteriophage T7 proteins are expressed in three major waves
4.9 The functions of bacteriophage proteins often correlate with the timing of their expression
4.10 Bacteriophage T7 gene expression is highly regulated at the level of transcription initiation
4.11 Bacterial host chromosome replication is regulated by the DnaA protein and occurs via a intermediate
4.12 Many bacterial proteins are needed to catalyze chromosome replication
4.13 Although many bacteriophages have linear dsDNA genomes, bacterial hosts cannot replicate the ends of linear DNA
4.14 T7 bacteriophage genome replication is catalyzed by one of the simplest known replication machines
4.15 The bacteriophage has naked, complex virions and a large double-stranded DNA genome
4.16 Bacteriophage can cause lytic or long-term infections
4.17 There are three waves of gene expression during lytic replication
4.18 The λ control region is responsible for early gene expression because of its promoters and the Cro and N proteins it encodes
4.19 The λ N antitermination protein controls the onset of delayed-early gene expression
4.20 The λ Q antitermination protein and Cro repressor protein control the switch to late gene expression
4.21 Bacteriophages T7 and λ both have three waves of gene expression but the molecular mechanisms controlling them differ
4.22 Bacteriophage λ genome replication occurs in two stages, through two different intermediates
4.23 Lambda genome replication requires phage proteins O and P and many subverted host proteins
4.24 The abundance of host DnaA protein relative to the amount of phage DNA controls the switch to rolling-circle replication
4.25 There are billions of other bacteriophages that regulate gene expression in various ways
4.26 Some bacteriophages have ssDNA, dsDNA, or (+) ssRNA genomes
4.27 The replication cycles of ssDNA bacteriophages always include formation of a double-stranded replicative form
4.28 Bacteriophage φχf.174 is of historical importance
4.29 Bacteriophage φχf.174 has extremely overlapping protein-coding sequences
4.30 Bacteriophage φχf.174 proteins are expressed in different amounts
4.31 A combination of mRNA levels and differential translation accounts for levels of bacteriophage φχf.174 protein expression
4.32 Bacteriophage M13 genome replication is catalyzed by host proteins and occurs via a replicative form
4.33 Bacteriophage MS2 is a (+) ssRNA virus that encodes four proteins
4.34 Bacteriophage MS2 protein abundance is controlled by secondary structure in the genome
4.35 Bacteriophage RdRp enzymes subvert abundant host proteins to create an efficient replicase complex
4.36 Bacteriophage proteins are common laboratory tools
Essential concepts
Questions
Further reading
5. Gene Expression and Genome Replication in The Positive-Strand RNA Viruses
5.1 Class IV virus replication cycles have common gene expression and genome replication strategies
5.2 Terminal features of eukaryotic mRNA are essential for translation
5.3 Monopartite Class IV (+) strand RNA viruses express multiple proteins from a single genome
5.4 Picornaviruses are models for the simplest (+) strand RNA viruses
5.5 Class IV viruses such as poliovirus encode one or more polyproteins
5.6 Class IV viruses such as poliovirus use proteolysis to release small proteins from viral polyproteins
5.7 Translation of Class IV virus genomes occurs despite the lack of a 5′ cap
5.8 Class IV virus genome replication occurs inside a virus replication compartment
5.9 The picornavirus 3Dpol is an RdRp and synthesizes a protein-based primer
5.10 Structural features of the viral genome are essential for replication of Class IV viral genomes
5.11 Picornavirus genome replication occurs in four phases
5.12 Flaviviruses are models for simple enveloped (+) strand RNA viruses
5.13 The linear (+) strand RNA flavivirus genomes have unusual termini
5.14 Enveloped HCV encodes 10 proteins including several with transmembrane segments
5.15 Togaviruses are small enveloped viruses with replication cycles more complex than those of the flaviviruses
5.16 Four different togavirus polyproteins are found inside infected cells
5.17 Different molecular events predominate early and late during togavirus infection
5.18 Translation of togavirus sgRNA requires use of the downstream hairpin loop
5.19 Suppression of translation termination is necessary for production of the nonstructural p1234 Sindbis virus polyprotein
5.20 Sindbis virus uses an unusual mechanism to encode the TF protein
5.21 A programmed -1 ribosome frameshift is needed to produce the togavirus TF protein
5.22 The picornaviruses, flaviviruses, and togaviruses illustrate many common properties among (+) strand RNA viruses
5.23 Coronaviruses have long (+) strand RNA genomes and novel mechanisms of gene expression and genome replication
5.24 Coronaviruses have enveloped spherical virions and encode conserved and species-specific accessory proteins
5.25 Coronaviruses express a nested set of sgRNAs with leader and TRS sequences
5.26 Coronaviruses use a discontinuous mechanism for synthesis of replicative forms
5.27 Most coronavirus sgRNA is translated into a single protein
5.28 Coronaviruses use a leaky scanning mechanism to synthesize proteins from overlapping sequences
5.29 Coronaviruses may proofread RNA during synthesis
5.30 Plants can also be infected by Class IV RNA viruses
5.31 Comparing Class IV viruses reveals common themes with variations
Essential concepts
Questions
Further reading
6. Gene Expression and Genome Replication in The Negative-Strand RNA Viruses
6.1 Study of two historically infamous Class V viruses, rabies and influenza, were instrumental in the development of molecular and cellular virology
6.2 The mononegavirus replication cycle includes primary and secondary transcription catalyzed by the viral RdRp
6.3 Rhabdoviruses have linear (-) RNA genomes and encode five proteins
6.4 Rhabdoviruses produce five mRNAs with 5′ caps and polyadenylated 3′ tails through a start–stop mechanism
6.5 Rhabdovirus genome replication occurs through the use of a complete antigenome cRNP as a template
6.6 The paramyxoviruses are mononegaviruses that use RNA editing for gene expression
6.7 Filoviruses are filamentous mononegaviruses that encode seven to nine proteins
6.8 The filovirus VP30 protein, not found in other mononegaviruses, is required for transcription
6.9 Influenza is an example of an orthomyxovirus
6.10 Of the 17 influenza A proteins, 9 are found in the virion
6.11 Orthomyxovirus nucleic acid synthesis occurs in the host cell nucleus, not in the cytoplasm
6.12 The first step of transcription by influenza virus is cap snatching
6.13 An influenza cRNP intermediate is used as the template for genome replication
6.14 Arenavirus RNA genomes are ambisense
6.15 Expression of the four arenavirus proteins reflects the ambisense nature of the genome
Essential concepts
Questions
Further reading
7. Gene Expression and Genome Replication in The Double-Stranded RNA Viruses
7.1 The rotavirus replication cycle includes primary transcription, genome replication, and secondary transcription inside partially intact capsids in the host cytoplasm
7.2 Rotavirus A has a naked capsid with three protein layers enclosing 11 segments of dsRNA
7.3 Rotavirus A encodes 13 proteins
7.4 Synthesis of rotavirus nucleic acids occurs in a fenestrated double-layered particle
7.5 Translation of rotavirus mRNA requires NSP3 and occurs in viroplasm formed by NSP2 and NSP5
7.6 Rotavirus genome replication precedes secondary transcription
Essential concepts
Questions
Further reading
8. Gene Expression and Genome Replication in The Double-Stranded DNA Viruses
8.1 DNA viruses can cause productive lytic infections, cellular transformation, or latent infections
8.2 Most Class I animal viruses rely on host transcription machinery for gene expression
8.3 Eukaryotic transcription is affected by the state of the chromatin
8.4 Eukaryotic capping, splicing, and polyadenylation occur co-transcriptionally
8.5 Polyomaviruses are small DNA viruses with early and late gene expression
8.6 The SV40 polyomavirus encodes seven proteins in only 5,243 bp of DNA
8.7 The synthesis of mRNA in SV40 is controlled by the noncoding control region
8.8 Late SV40 transcription is regulated by both host and viral proteins
8.9 Most Baltimore Class I viruses including polyomaviruses manipulate the eukaryotic cell cycle
8.10 Most Class I viruses prevent or delay cellular apoptosis
8.11 SV40 forces the host cell to express S phase genes and uses large T antigen and host proteins for genome replication
8.12 SV40 genome replication requires viral and host proteins to form active DNA replication forks
8.13 The papillomavirus replication cycle is tied closely to the differentiation status of its host cell
8.14 Human papillomaviruses encode about 13 proteins that are translated from polycistronic mRNA
8.15 The long control region of HPV regulates papillomavirus transcription in which pre-mRNA is subjected to alternative splicing
8.16 Leaky scanning, internal ribosome entry sites, and translation re-initiation lead to the expression of papillomavirus proteins from polycistronic mRNA
8.17 DNA replication in papillomaviruses is linked to host cell differentiation status
8.18 Papillomaviruses use early proteins to manipulate the host cell cycle and apoptosis
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
8.20 Adenoviruses are large dsDNA viruses with three waves of gene expression
8.21 Adenoviruses have large naked spherical capsids with prominent spikes and large linear dsDNA genomes
8.22 Adenoviruses encode early, delayed-early, and late proteins
8.23 The large E1A protein is important for regulating the adenovirus cascade of gene expression
8.24 Splicing of pre-mRNA was first discovered through studying adenovirus gene expression
8.25 Both host cells and adenovirus rely on alternative splicing to encode multiple proteins using the same DNA sequence
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
8.27 Adenovirus shuts off translation of host mRNA, while ensuring translation of its own late mRNAs through a ribosome-shunting mechanism
8.28 DNA replication in adenovirus requires three viral proteins even though the genome is replicated in the host cell nucleus
8.29 Herpesviruses have very large enveloped virions and large linear dsDNA genomes
8.30 Lytic herpesvirus replication involves a cascade with several waves of gene expression
8.31 Groups of herpes simplex virus 1 proteins have functions relating to the timing of their expression
8.32 Waves of gene expression in herpesviruses are controlled by transcription activation and chromatin remodeling
8.33 Herpesvirus genome replication results in concatamers
8.34 Poxviruses are extremely large dsDNA viruses that replicate in the host cytoplasm
8.35 Many vaccinia virus proteins are associated with the virion itself
8.36 Vaccinia RNA polymerase transcribes genes in three waves using different transcription activators
8.37 Vaccinia genome replication requires the unusual ends of the genome sequence
8.38 The synthetic demands on the host cell make vaccinia a possible anticancer treatment
Essential concepts
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Further reading
9. Gene Expression and Genome Replication in The Single-Stranded DNA Viruses
9.1 The ssDNA viruses express their genes and replicate their genomes in the nucleus
9.2 Circoviruses are tiny ssDNA viruses with circular genomes
9.3 Although their genomes are shorter than an average human gene, circoviruses encode at least four proteins
9.4 Both host and viral proteins are needed for circovirus genome replication
9.5 Parvoviruses are tiny ssDNA viruses with linear genomes having hairpins at both ends
9.6 The model parvovirus MVM encodes six proteins using alternative splicing
9.7 The model parvovirus MVM uses a rolling-hairpin mechanism for genome replication
Essential concepts
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Further reading
10. Gene Expression and Genome Replication in The Retroviruses and Hepadnaviruses
10.1 Viral reverse transcriptases have polymerase and RNase H activity
10.2 Retroviruses are enveloped and have RNA genomes yet express their proteins from dsDNA
10.3 Reverse transcription occurs during transport of the retroviral nucleic acid to the nucleus, through a discontinuous mechanism
10.4 Retroviral integrase inserts the viral cDNA into a chromosome, forming proviral DNA that can be transcribed by host Pol II
10.5 All retroviruses express eight essential proteins, whereas some such as HIV encode species-specific accessory proteins
10.6 The retroviral LTR sequences interact with host proteins to regulate transcription
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
10.8 The HIV-1 accessory protein TAT is essential for viral gene expression
10.9 The HIV-1 accessory protein Rev is essential for exporting some viral mRNA from the nucleus
10.10 Retrovirus genome replication is accomplished by host Pol II
10.11 HIV-1 is a candidate gene therapy vector for diseases that involve the immune cells normally targeted by HIV
10.12 Hepadnaviruses are enveloped and have genomes containing both DNA and RNA in an unusual arrangement
10.13 Hepadnaviruses use reverse transcription to amplify their genomes
10.14 The cccDNA of HBV is not perfectly identical to the DNA in the infecting virion
10.15 The tiny HBV genome encodes eight proteins through alternative splicing, overlapping coding sequences, and alternative start codons
10.16 HBV genome replication relies upon an elaborate reverse transcriptase mechanism
Essential concepts
Questions
Further reading
11. Assembly, Release, and Maturation
11.1 The last stages of the virus replication cycle are assembly, release, and maturation
11.2 Unlike cells, viruses assemble from their constituent parts
11.3 Virions more structurally complex than TMV also reproduce by assembly, not by division
11.4 Typical sites of assembly in eukaryotic viruses include the cytoplasm, plasma membrane, and nucleus
11.5 Eukaryotic virus assembly must take cellular protein localization into account
11.6 Capsids and nucleocapsids associate with genomes using one of two general strategies
11.7 Assembly of some viruses depends on DNA replication to provide the energy to fill the icosahedral heads
11.8 Assembly of some viruses depends on a packaging motor to fill the icosahedral heads
11.9 Negative RNA viruses provide a model for concerted nucleocapsid assembly
11.10 To assemble, some viruses require assistance from proteins not found in the virion
11.11 Viruses acquire envelopes through one of two pathways
11.12 The helical vRNPs of influenza virus assemble first, followed by envelope acquisition at the plasma membrane
11.13 Some viruses require maturation reactions during release in order to form infectious virions
11.14 Assembly of HIV occurs at the plasma membrane
11.15 Inhibition of HIV-1 maturation provides a classic example of structure–function research in medicine
11.16 Release from bacterial cells usually occurs by lysis
11.17 Release from animal cells can occur by lysis
11.18 Release from animal cells can occur by budding
11.19 Release from plant cells often occurs through biting arthropods
Essential concepts
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Further reading
12. Virus–Host Interactions During Lytic Growth
12.1 All viruses subvert translation
12.2 Bacteriophages subvert translation indirectly
12.3 Animal viruses have many strategies to block translation of host mRNA
12.4 Animal viruses cause structural changes in host cells referred to as cytopathic effects
12.5 Viruses affect host cell apoptosis
12.6 Some viruses delay apoptosis in order to complete their replication cycles before the host cell dies
12.7 Some viruses subvert apoptosis in order to complete their replication cycles
12.8 Viruses use the ubiquitin system to their advantage
12.9 Viruses can block or subvert the cellular autophagy system
12.10 Viruses subvert or co-opt the misfolded protein response triggered in the endoplasmic reticulum
12.11 Viruses modify internal membranes in order to create virus replication compartments
Essential concepts
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Further reading
13. Persistent Viral Infections
13.1 Some bacteriophages are temperate and can persist as genomes integrated into their hosts’ chromosomes
13.2 Bacteriophage serves as a model for latency
13.3 The amount of stable CII protein in the cell determines whether the phage genome becomes a prophage
13.4 Activation of PRE, PI, and PantiQ by CII results in lysogeny
13.5 Stress triggers an exit from lysogeny
13.6 Some lysogens provide their bacterial hosts with virulence genes
13.7 Prophages affect the survival of their bacterial hosts
13.8 Persistent infections in humans include those with ongoing lytic replication and latent infections
13.9 Human immunodeficiency virus causes persistent infections
13.10 Human herpesvirus 1 is a model for latent infections
13.11 Oncogenic viruses cause cancer through persistent infections
13.12 DNA viruses transform cells with oncoproteins that affect the cell cycle and apoptosis
13.13 HPV oncoproteins E6 and E7 cause transformation
13.14 HPV E6 and E7 overexpression occurs when the virus genome recombines with a host chromosome
13.15 Merkel cell polyomavirus is also associated with human cancers
13.16 Epstein–Barr virus is an oncogenic herpesvirus
13.17 Latency-associated viral proteins are responsible for Epstein–Barr virus-induced oncogenesis
13.18 The Kaposi’s sarcoma herpesvirus also causes persistent oncogenic infections
13.19 Hepatocellular carcinoma is caused by persistent lytic viral infections
13.20 Retroviruses have two mechanisms by which they can cause cancer
13.21 Viral oncoproteins can be used to immortalize primary cell cultures
13.22 The human virome is largely uncharacterized but likely has effects on human physiology
Essential concepts
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Further reading
14. Viral Evasion of Innate Host Defenses
14.1 Restriction enzymes are a component of innate immunity to bacteriophages
14.2 Bacteriophages have counterdefenses against restriction-modification systems
14.3 Human innate immune defenses operate on many levels
14.4 The human innate immune system is triggered by pattern recognition
14.5 Innate immune responses include cytokine secretion
14.6 Interferon causes the antiviral state
14.7 Some viruses can evade the interferon response
14.8 Neutrophils are active during an innate immune response against viruses
14.9 Viruses manipulate immune system communication to evade the net response
14.10 Inflammation is the hallmark of an innate immune response
14.11 In order to be recognized as healthy, all cells present endogenous antigens in MHC-I molecules
14.12 Cells infected by viruses produce and display viral antigens in MHC-I
14.13 Viruses have strategies to evade MHC-I presentation of viral antigens
14.14 Natural killer cells attack cells with reduced MHC-I display
14.15 The complement system targets enveloped viruses and cells infected by them
14.16 Some viruses can evade the complement system
14.17 Viral evasion strategies depend on the coding capacity of the virus
14.18 In vertebrates, if an innate immune reaction does not clear an infection, adaptive immunity comes into play
Essential concepts
Questions
Further reading
15. Viral Evasion of Adaptive Host Defenses
15.1 CRISPR-Cas is an adaptive immune response found in bacteria
15.2 Some bacteriophages can evade or subvert the CRISPR-Cas system
15.3 The human adaptive immune response includes cell-mediated and humoral immunity
15.4 The human adaptive immune response has specificity because it responds to epitopes
15.5 Professional antigen-presenting cells degrade exogenous antigens and display epitopes in MHC-II molecules
15.6 Some viruses evade MHC-II presentation
15.7 Lymphocytes that control viral infections have many properties in common
15.8 CD4+ helper T lymphocytes interact with viral epitopes displayed in MHC-II molecules
15.9 Antibodies are soluble B-cell receptors that bind to extracellular antigens such as virions
15.10 During an antiviral response, B cells differentiate to produce higher-affinity antibodies
15.11 Viruses have strategies to evade or subvert the antibody response
15.12 CD8+ cytotoxic T lymphocytes are crucial for controlling viral infections
15.13 Some viruses can evade the CTL response
15.14 Viruses that cause persistent infections evade immune clearance for a long period of time
15.15 The immune response to influenza serves is a comprehensive model for antiviral immune responses in general
15.16 Influenza provides a model for how a lytic virus evades both innate and adaptive immunity long enough to replicate
Essential concepts
Questions
Further reading
16. Medical Applications of Molecular and Cellular Virology
16.1 Vaccines are critical components of an effective public health system
16.2 Attenuated vaccines are highly immunogenic because they can still replicate
16.3 Inactivated vaccines are composed of nonreplicating virions
16.4 Subunit vaccines are composed of selected antigenic proteins
16.5 Although seasonal influenza vaccines are useful, a universal flu vaccine is highly sought after
16.6 Preventative HIV vaccines are in development
16.7 Extreme antigenic variation is a problem for developing an HIV vaccine
16.8 An effective HIV vaccine may require stimulating a strong CTL response
16.9 Antiviral drugs target proteins unique to viruses and essential for their replication cycle
16.10 Many antiviral drugs are nucleoside or nucleotide structural analogs that target the active site of viral polymerases
16.11 Drugs to treat influenza target the uncoating and release stages of viral replication
16.12 Drugs to treat hepatitis C virus target the viral polymerase
16.13 Drugs to treat HIV target many stages of the virus replication cycle
16.14 Viral evolution occurs in response to selective pressure from antiviral drugs
16.15 It might be possible to develop bacteriophage therapy to treat people with antibiotic-resistant bacterial infections
16.16 Engineered viruses could in principle be used for gene therapy to treat cancer and other conditions
16.17 Gene therapy and oncolytic virus treatments currently in use
16.18 Therapeutic applications of CRISPR-Cas technology
Essential concepts
Questions
Further reading
17. Viral Diversity, Origins, And Evolution
17.1 The viral world is extremely diverse
17.2 Satellite viruses and nucleic acids require co-infection with a virus to spread
17.3 Viroids are infectious RNA molecules found in plants
17.4 Transposons and introns are subviral entities
17.5 Viruses have ancient origins
17.6 Viral hallmark proteins can be used to trace evolutionary history
17.7 Metagenomics will revolutionize evolutionary understanding of viruses
17.8 Viral genetic diversity arises through mutation and recombination
17.9 Genetic diversity among influenza A viruses arises through mutation and recombination
17.10 Influenza A spike proteins are particularly diverse
17.11 Variations among influenza A viruses reflects genetic drift and natural selection
17.12 Pandemic influenza A strains have arisen through recombination
17.13 New pandemic influenza A strains may be able to arise through mutation
17.14 Selective pressures and constraints influence viral evolution
17.15 Some viruses and hosts coevolve
17.16 Medically dangerous emerging viruses are zoonotic
17.17 HIV exhibits high levels of genetic diversity and transferred from apes to humans on four occasions
17.18 HIV-1 has molecular features that reflect adaptation to humans
17.19 Viruses and subviral entities are common in the human genome
17.20 Viruses and subviral entities have strongly affected the evolution of organisms including humans
17.21 Virology unites the biosphere

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