Copyright © Cambridge University Press 2007.
- Contributors
- Preface
- I. Introduction: definition and classification of the human
herpesviruses
- 1. Overview of classification
- 2. Comparative analysis of the genomes
- 3. Comparative virion structures of human herpesviruses
- Introduction
- Different virus-related particles found in infected cells
- Compositions and three-dimensional structural comparisons of alpha, beta and gammaherpesvirus capsids
- Structure and packaging of viral genomic DNA
- Structure and assembly of tegument
- Structure and assembly of viral envelope
- Other constituents in the virions
- References
- 4. Comparative analysis of herpesvirus-common proteins
- II.1. Basic virology and viral gene effects on host cell functions:
alphaherpesviruses
- 5. Genetic comparison of human alphaherpesvirus genomes
- 6. Alphaherpes viral genes and their functions
- 7. Entry of alphaherpesviruses into the cell
- 8. Early events pre-initiation of alphaherpes viral gene expression
- The HSV IE regulatory domains: multiple sites for differential regulation
- The assembly of the HSV IE enhancer core complex
- Ancillary factors: Sp1 and GABP
- VZV IE gene expression: parallels and divergence
- Regulation of the IE genes: multiple levels and response potentials
- The regulation of the IE genes: reactivation of HSV from the latent state
- Questions and future directions
- References
- 9. Initiation of transcription and RNA synthesis, processing and transport in HSV and VZV infected cells
- 10. Alphaherpesvirus DNA replication
- 11. Envelopment of herpes simplex virus nucleocapsids at the inner nuclear membrane
- 12. The egress of alphaherpesviruses from the cell
- 13. The strategy of herpes simplex virus replication and takeover of the
host cell
- Introduction
- Gene content, organization, and fundamental design of the viral genome
- Mobilization of cellular proteins for enhanced replication of HSV
- The objectives and general strategy of anti-host functions
- The activation of NF-κB
- Degradation of mRNA in infected cells
- Specific degradation of cellular proteins in wild-type virus-infected cells
- Shut down of the interferon pathways to host resistance to infection
- HSV blocks pro-apoptotic cellular functions
- Conclusions
- References
- II.2. Basic virology and viral gene effects on host cell functions:
betaherpesviruses
- 14. Comparative genome and virion structure
- 15. Betaherpes viral genes and their functions
- 16. Early events in human cytomegalovirus infection
- 17. Immediate–early viral gene regulation and function
- Introduction
- Betaherpesvirus immediate early genes
- Betaherpesvirus transcriptional enhancers upstream of the MIE genes
- Function of the betaherpesvirus major immediate–early enhancers
- Silencing of the immediate-early genes
- Reactivation of the immediate–early genes
- Betaherpesvirus major immediate–early genes
- Functions of the major immediate–early viral proteins
- Factors that stimulate betaherpesvirus immediate–early gene expression
- Infection and dysregulation of the cell cycle by betaherpesviruses
- Summary
- References
- 18. Early viral gene expression and function
- Introduction
- Identification of HCMV early genes
- HCMV-mediated changes in the cellular environment prior to early gene expression
- Functions of viral early genes
- Transactivating functions of the major IE proteins
- Additional immediate early proteins have regulatory roles
- UL112–113 transcription is differentially controlled at early and late times
- Multiple cis-acting sequences regulate UL54 expression
- UL4 expression is controlled at the transcriptional and translational levels
- Human herpesviruses 6 and 7
- Conclusions
- References
- 19. DNA synthesis and late viral gene expression
- 20. Maturation and egress
- 21. Viral modulation of the host response to infection
- II.3. Basic virology and viral gene effects on host cell functions:
gammaherpesviruses
- 22. Introduction to the human γ-herpesviruses
- Introduction
- The γ-herpesvirus family
- The discovery of Epstein–Barr virus (EBV)
- Human disease associated with EBV infection
- EBV life cycle
- The discovery of Kaposi’s sarcoma-associated herpesvirus (KSHV)
- KSHV life cycle
- Human disease associated with KSHV infection
- Phylogenetic relationship between EBV, KSHV, and non-human γ-herpesvirus genomes
- Human γ-herpesviruses genomes
- Characteristics of the γ-herpesvirus virion
- Conclusions
- General historical reading
- References
- 23. Gammaherpesviruses entry and early events during infection
- 24. Maintenance and replication during latency
- Introduction
- EBV (lymphocryptovirus)
- Properties of the episomal latent viral genome
- Chromatin organization of the latent episome
- DNA methylation of latent EBV
- Molecular biology of OriP
- Properties of EBNA 1
- Cellular proteins that interact with EBNA 1
- Cellular proteins that interact with OriP
- Mechanism of OriP- DNA replication
- Mechanism of viral chromosome replication
- Mechanisms of plasmid segregation
- KSHV (Rhadinovirus)
- The KSHV episome in latently infected cells
- Properties of the latency-associated nuclear antigen (LANA)
- Latent DNA replication and segregation
- Summary
- References
- 25. Reactivation and lytic replication of EBV
- Viral pathogenesis
- Activation of lytic EBV infection
- EBV immediate-early proteins
- Early lytic EBV gene regulation
- Early lytic EBV gene products
- Viral replication
- Late viral gene regulation
- Late viral proteins
- Viral assembly and egress
- Treatment of lytic EBV infection
- Lytic induction as a strategy for treating EBV -positive tumors
- Unresolved issues for the future
- References
- 26. Reactivation and lytic replication of KSHV
- Overview: goals of lytic replication
- Lytic reactivation of KSHV is a critical pathogenic step in development of KS and other human diseases
- The immune system tempers lytic reactivation of KSHV and KS development
- MHV-68 is a model for immune control of gamma-herpesvirus reactivation from latency
- Sites of latency and reservoirs for viral amplification in vivo
- Primary effusion lymphoma (PEL) cells: a tissue culture model for KSHV latency and reactivation
- Kinetic classification of KHSV lytic gene expression
- ORF50/Rta is the viral lytic switch protein
- Signals that control lytic reactivation of KSHV
- Lytic replication and interactions with the host cell
- Regulation of lytic DNA replication
- Late genes and KSHV virion structure
- Perspectives
- References
- 27. EBV gene expression and regulation
- Introduction
- Virus and genome structure
- EBV latency in vitro and in vivo
- Other forms of EBV latency
- EBV replication/the lytic cascade
- Functions and associated properties of lytic cycle gene products
- EBV persistence in vivo
- EBV strain variation
- Function of the EBV latent genes: from persistence to pathology
- EBNA1
- EBNA2
- EBNA3 family
- EBNA-LP
- LMP1
- LMP2
- EBERs
- BARTs
- MicroRNAs
- Conclusions
- References
- 28. KSHV gene expression and regulation
- 29. Effects on apoptosis, cell cycle and transformation, and comparative
aspects of EBV with other known DNA tumor viruses
- Viral strategy at the molecular level as a tumor risk factor
- Three types of virus–host cell interactions may carry a risk
- Early history: up and down
- Up again, and how!
- Classes of experimental tumor viruses
- What does the type of virus-cell interaction tell us about tumorigenic risk?
- EBV exploits B-cell specific regulatory mechanisms and signals
- Growth transformation associated EBV encoded proteins
- The latent membrane proteins (LMP) of EBV
- EBV and Burkitt lymphoma (BL)
- Hodgkin’s lymphoma (HL)
- EBV and nasopharyngeal carcinoma
- Viral expression in carcinoma cells, cell behavior and host relationships in NPC
- Immune surveillance and the oncogenic herpesviruses – the role of immunological “anticipation”
- Double HHV8/EBV carrying PEL cells
- References
- 30. KSHV manipulation of the cell cycle and apoptosis
- 31. Human gammaherpesvirus immune evasion strategies
- 22. Introduction to the human γ-herpesviruses
- III.1. Pathogenesis, clinical disease, host response, and epidemiology:
alphaherpes viruses
- 32. Pathogenesis and disease
- Pathogenesis
- Unique biologic properties of HSV that influence pathogenesis
- Pathology
- Pathology of central nervous system disease
- Impact of host response to infection on disease
- Orolabial infection
- Genital infection
- Keratoconjunctivitis
- Cutaneous infections
- Central nervous system infections
- Neonatal infection
- Infection in compromised hosts
- References
- 33. Molecular basis of HSV latency and reactivation
- 34. Immunobiology and host response
- Introduction
- HSV interactions with dendritic cells
- CD8 T-cell responses to HSV
- CD4 T-cell responses to HSV
- T-cell costimulation and HSV
- Antibody responses to HSV
- Innate immunity
- Immunomodulators and HSV
- Chemokines
- NK cells
- NKT cells
- TCRγδ cells
- Additional interactions between HSV and the immune system
- Summary
- References
- 35. Immunopathological aspects of HSV infection
- 36. Persistence in the population: epidemiology, transmission
- 32. Pathogenesis and disease
- III.2. Pathogenesis, clinical disease, host response, and epidemiology:
alphaherpes viruses VZV
- 37. VZV: pathogenesis and the disease consequences of primary infection
- Introduction
- Systems for evaluating determinants of VZV pathogenesis in human skin and T-cells
- Effects of VZV replication on cellular cyclin-dependent kinases and cyclins
- Investigation of events in the pathogenesis of primary VZV infection in the SCIDhu model
- The role of VZV glycoproteins in T-cell and skin tropism
- Glycoprotein C
- Glycoprotein E
- Glycoprotein I
- The role of regulatory proteins and viral kinases in T-cell and skin tropism
- IE62 protein
- IE63 protein
- ORF64 protein
- ORF10 protein
- ORF47 protein
- ORF66 protein
- Disease consequences of primary VZV infection in healthy and immunocompromised hosts
- Varicella in the immunocompromised host
- Varicella in pregnancy and the newborn
- Summary
- References
- 38. VZV: molecular basis of persistence (latency and reactivation)
- Site of VZV latency
- Quantification of VZV DNA load during latency
- Animal models for VZV latency
- VZV transcripts expressed during latency
- VZV proteins expressed during latency
- Function of VZV latency-associated proteins
- VZV genes required for establishment of latent infection
- In vitro models for VZV latency
- Reactivation of VZV
- Comparison of VZV latency with that of other alphaherpesviruses
- Is the large number of transcripts in VZV latency due to reactivation?
- Models for VZV latency
- VZV proteins localize to the cytoplasm, instead of the nucleus of neurons and thus are unable to carry out their activities
- VZV proteins have different activities in neurons than in permissive cells due to differences in cellular proteins
- Future directions
- References
- 39. VZV: immunobiology and host response
- 40. VSV: persistence in the population
- 37. VZV: pathogenesis and the disease consequences of primary infection
- III.3. Pathogenesis, clinical disease, host response, and epidemiology:
betaherpesviruses
- 41. Virus entry into host, establishment of infection, spread in host, mechanisms of tissue damage
- 42. Molecular basis of persistence and latency
- 43. Immunobiology and host response
- 44. Persistence in the population: epidemiology and transmisson
- Introduction
- Epidemiology of HCMV infection
- Transmission of HCMV by mothers to infants: perinatal infections
- Children-to-children transmission of HCMV
- Transmission of HCMV by children to parents
- HCMV transmission through sexual activity
- Transmission of HCMV to child-care providers
- Transmission of CMV in health-care settings
- Transfusion acquired HCMV infection
- Transplantation and HCMV infection
- HCMV transmission from artificial insemination by donor semen
- Summary
- References
- 45. HCMV persistence in the population: potential transplacental transmission
- III.4. HHV-6A, 6B, and 7
- III.5. Pathogenesis, clinical disease, host response, and epidemiology:
gammaherpesviruses
- 50. Clinical and pathological aspects of EBV and KSHV infection
- 51. EBV: immunobiology and host response
- Introduction
- Response during acute infection
- Response in healthy virus carriers
- Role of CD4+ and CD8+ CTL in control of EBV infection
- Role of CTL effector cells in resolution of acute IM
- T-cell receptor usage
- Virus-driven immune modulation
- T-cell control of EBV-associated malignancies
- Future prospects for an EBV vaccine
- References
- 52. Immunobiology and host response to KSHV infection
- 53. The epidemiology of EBV and its association with malignant disease
- 54. The epidemiology of KSHV and its association with malignant disease
- 55. EBV-induced oncogenesis
- 56. KSHV-induced oncogenesis
- IV. Non-human primate herpesviruses
- 57. Monkey B virus
- 58. Simian varicella virus
- 59. Primate betaherpesviruses
- 60. Gammaherpesviruses of New World primates
- 61. EBV and KSHV – related herpesviruses in non-human primates
- Introduction
- Nomenclature
- Evolution of New and Old World lymphocryptoviruses
- Lymphocryptoviruses of Old World monkeys
- The rhesus LCV genome
- Latency, immune-modulatory and transforming genes of rhesus LCV
- Rhesus LCV as an animal model system for EBV
- Other lymphocryptoviruses in Old World primates
- Lymphocryptoviruses of New World monkeys
- New World primates as an animal model system for EBV
- Evolution of New and Old World rhadinoviruses
- Rhadinoviruses of Old World primates
- Retroperitoneal fibromatosis herpesviruses: RFHVMm and RFHVMn
- Rhesus monkey rhadinovirus (RRV)
- RRV as an animal model system for KSHV
- Conclusions
- References
- V. Subversion of adaptive immunity
- 62. Herpesvirus evasion of T-cell immunity
- 63. Subversion of innate and adaptive immunity: immune evasion from
antibody and complement
- Role of the herpesvirus IgG Fc receptor in immune evasion
- Herpes simplex virus FcγR
- Human CMV FcγR
- Varicella zoster FcγR
- vFcγRs on non-human mammalian herpesviruses
- Summary of vFcγR studies
- Role of the herpesvirus complement receptors in immune evasion
- Strategies employed by human herpesviruses to evade complement immunity
- Strategies employed by non-human mammalian herpesviruses to evade complement immunity
- Summary of viral complement regulatory proteins
- References
- VI. Antiviral therapy
- 64. Antiviral therapy of HSV-1 and -2
- 65. Antiviral therapy of varicella-zoster virus infections
- 66. Antiviral therapy for human cytomegalovirus
- 67. New approaches to antiviral drug discovery (genomics/proteomics)
- Introduction
- Development of bioinformatics and computational tools
- Impact of genomics and related fields on herpesvirus research
- New resources for use in drug discovery
- Application of new technologies to cell-based antiviral assays
- Application of new technologies to biochemical assays
- Application of new technologies to functional assays
- Application of new technologies to characterize mechanism of action and spectrum of activity
- Conclusions
- References
- 68. Candidate anti-herpesviral drugs; mechanisms of action and
resistance
- The drug development process: an overview
- Host cell targets as an approach to virus inhibition
- Antiviral targets in early replication events
- Antiviral targets in the herpesvirus DNA replication complex
- Inhibitors of DNA processing and packaging
- Antivirals with activity against EBV, HHV-6, HHV-7, and HHV-8
- Conclusions
- References
- VII. Vaccines and immunotherapy
- 69. Herpes simplex vaccines
- 70. Varicella-zoster vaccine
- Varicella vaccines: background
- History of development of the live attenuated vaccine
- Virology of the attenuated Oka strain of VZV
- Safety of the varicella vaccine for healthy individuals
- Immunogenicity of varicella vaccine in healthy children and adolescents
- Efficacy and post-licensure effectiveness of varicella vaccine
- Considerations of vaccine use
- Persistent questions regarding varicella vaccine
- Does immunity to varicella wane with time after immunization?
- Zoster: effects and potential effects on its incidence in the vaccine era
- Vaccination to prevent zoster in the elderly
- Use of inactivated varicella vaccine in patients at high risk to develop zoster
- Recent developments
- Conclusions
- References
- 71. Human cytomegalovirus vaccines
- 72. Epstein–barr virus vaccines
- 73. DNA vaccines for human herpesviruses
- 74. Adoptive immunotherapy for herpesviruses
- Introduction
- Therapy for herpesvirus-related infections and diseases
- Cytomegalovirus
- Epstein–Barr virus
- T-cell activation
- Strategies for producing T-cells for adoptive immunotherapy
- Adoptive immunotherapy for cytomegalovirus
- Adoptive immunotherapy for EBV post-transplant lymphoproliferation disease
- Adoptive immunotherapy for EBV post-solid organ transplant
- Adoptive transfer of EBV-specific CTL for Hodgkin’s lymphoma
- Adoptive transfer of EBV-specific CTL for nasopharyngeal carcinoma
- Multivirus-specific CTL lines
- CMV and EBV immunotherapy in HIV positive individuals
- Alternative approaches for activating virus-specific CTLs
- Conclusions and future considerations
- References
- 75. Immunotherapy of HSV infections – antibody delivery
- VIII. Herpesviruses as therapeutic agents
- 76. Herpesviruses as therapeutic agents
- Introduction
- Properties of therapeutic HSV vectors
- Properties of non-replicating HSV vectors for therapeutic use
- Use of HSV vectors to modify the nervous system
- Towards optimizing HSV vectors for therapeutic use
- Non-replicating vectors: current trends
- Oncolytic HSV
- Oncolytic HSV: current directions
- References
- 76. Herpesviruses as therapeutic agents
- Plates
NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.
Arvin A, Campadelli-Fiume G, Mocarski E, et al., editors. Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge: Cambridge University Press; 2007.
Bookshelf ID: NBK47384
Part VIIIHerpesviruses as therapeutic agents
Edited by Richard Whitley and Bernard Roizman.
- Contributors
- Preface
- I. Introduction: definition and classification of the human
herpesviruses
- 1. Overview of classification
- 2. Comparative analysis of the genomes
- 3. Comparative virion structures of human herpesviruses
- Introduction
- Different virus-related particles found in infected cells
- Compositions and three-dimensional structural comparisons of alpha, beta and gammaherpesvirus capsids
- Structure and packaging of viral genomic DNA
- Structure and assembly of tegument
- Structure and assembly of viral envelope
- Other constituents in the virions
- References
- 4. Comparative analysis of herpesvirus-common proteins
- II.1. Basic virology and viral gene effects on host cell functions:
alphaherpesviruses
- 5. Genetic comparison of human alphaherpesvirus genomes
- 6. Alphaherpes viral genes and their functions
- 7. Entry of alphaherpesviruses into the cell
- 8. Early events pre-initiation of alphaherpes viral gene expression
- The HSV IE regulatory domains: multiple sites for differential regulation
- The assembly of the HSV IE enhancer core complex
- Ancillary factors: Sp1 and GABP
- VZV IE gene expression: parallels and divergence
- Regulation of the IE genes: multiple levels and response potentials
- The regulation of the IE genes: reactivation of HSV from the latent state
- Questions and future directions
- References
- 9. Initiation of transcription and RNA synthesis, processing and transport in HSV and VZV infected cells
- 10. Alphaherpesvirus DNA replication
- 11. Envelopment of herpes simplex virus nucleocapsids at the inner nuclear membrane
- 12. The egress of alphaherpesviruses from the cell
- 13. The strategy of herpes simplex virus replication and takeover of the
host cell
- Introduction
- Gene content, organization, and fundamental design of the viral genome
- Mobilization of cellular proteins for enhanced replication of HSV
- The objectives and general strategy of anti-host functions
- The activation of NF-κB
- Degradation of mRNA in infected cells
- Specific degradation of cellular proteins in wild-type virus-infected cells
- Shut down of the interferon pathways to host resistance to infection
- HSV blocks pro-apoptotic cellular functions
- Conclusions
- References
- II.2. Basic virology and viral gene effects on host cell functions:
betaherpesviruses
- 14. Comparative genome and virion structure
- 15. Betaherpes viral genes and their functions
- 16. Early events in human cytomegalovirus infection
- 17. Immediate–early viral gene regulation and function
- Introduction
- Betaherpesvirus immediate early genes
- Betaherpesvirus transcriptional enhancers upstream of the MIE genes
- Function of the betaherpesvirus major immediate–early enhancers
- Silencing of the immediate-early genes
- Reactivation of the immediate–early genes
- Betaherpesvirus major immediate–early genes
- Functions of the major immediate–early viral proteins
- Factors that stimulate betaherpesvirus immediate–early gene expression
- Infection and dysregulation of the cell cycle by betaherpesviruses
- Summary
- References
- 18. Early viral gene expression and function
- Introduction
- Identification of HCMV early genes
- HCMV-mediated changes in the cellular environment prior to early gene expression
- Functions of viral early genes
- Transactivating functions of the major IE proteins
- Additional immediate early proteins have regulatory roles
- UL112–113 transcription is differentially controlled at early and late times
- Multiple cis-acting sequences regulate UL54 expression
- UL4 expression is controlled at the transcriptional and translational levels
- Human herpesviruses 6 and 7
- Conclusions
- References
- 19. DNA synthesis and late viral gene expression
- 20. Maturation and egress
- 21. Viral modulation of the host response to infection
- II.3. Basic virology and viral gene effects on host cell functions:
gammaherpesviruses
- 22. Introduction to the human γ-herpesviruses
- Introduction
- The γ-herpesvirus family
- The discovery of Epstein–Barr virus (EBV)
- Human disease associated with EBV infection
- EBV life cycle
- The discovery of Kaposi’s sarcoma-associated herpesvirus (KSHV)
- KSHV life cycle
- Human disease associated with KSHV infection
- Phylogenetic relationship between EBV, KSHV, and non-human γ-herpesvirus genomes
- Human γ-herpesviruses genomes
- Characteristics of the γ-herpesvirus virion
- Conclusions
- General historical reading
- References
- 23. Gammaherpesviruses entry and early events during infection
- 24. Maintenance and replication during latency
- Introduction
- EBV (lymphocryptovirus)
- Properties of the episomal latent viral genome
- Chromatin organization of the latent episome
- DNA methylation of latent EBV
- Molecular biology of OriP
- Properties of EBNA 1
- Cellular proteins that interact with EBNA 1
- Cellular proteins that interact with OriP
- Mechanism of OriP- DNA replication
- Mechanism of viral chromosome replication
- Mechanisms of plasmid segregation
- KSHV (Rhadinovirus)
- The KSHV episome in latently infected cells
- Properties of the latency-associated nuclear antigen (LANA)
- Latent DNA replication and segregation
- Summary
- References
- 25. Reactivation and lytic replication of EBV
- Viral pathogenesis
- Activation of lytic EBV infection
- EBV immediate-early proteins
- Early lytic EBV gene regulation
- Early lytic EBV gene products
- Viral replication
- Late viral gene regulation
- Late viral proteins
- Viral assembly and egress
- Treatment of lytic EBV infection
- Lytic induction as a strategy for treating EBV -positive tumors
- Unresolved issues for the future
- References
- 26. Reactivation and lytic replication of KSHV
- Overview: goals of lytic replication
- Lytic reactivation of KSHV is a critical pathogenic step in development of KS and other human diseases
- The immune system tempers lytic reactivation of KSHV and KS development
- MHV-68 is a model for immune control of gamma-herpesvirus reactivation from latency
- Sites of latency and reservoirs for viral amplification in vivo
- Primary effusion lymphoma (PEL) cells: a tissue culture model for KSHV latency and reactivation
- Kinetic classification of KHSV lytic gene expression
- ORF50/Rta is the viral lytic switch protein
- Signals that control lytic reactivation of KSHV
- Lytic replication and interactions with the host cell
- Regulation of lytic DNA replication
- Late genes and KSHV virion structure
- Perspectives
- References
- 27. EBV gene expression and regulation
- Introduction
- Virus and genome structure
- EBV latency in vitro and in vivo
- Other forms of EBV latency
- EBV replication/the lytic cascade
- Functions and associated properties of lytic cycle gene products
- EBV persistence in vivo
- EBV strain variation
- Function of the EBV latent genes: from persistence to pathology
- EBNA1
- EBNA2
- EBNA3 family
- EBNA-LP
- LMP1
- LMP2
- EBERs
- BARTs
- MicroRNAs
- Conclusions
- References
- 28. KSHV gene expression and regulation
- 29. Effects on apoptosis, cell cycle and transformation, and comparative
aspects of EBV with other known DNA tumor viruses
- Viral strategy at the molecular level as a tumor risk factor
- Three types of virus–host cell interactions may carry a risk
- Early history: up and down
- Up again, and how!
- Classes of experimental tumor viruses
- What does the type of virus-cell interaction tell us about tumorigenic risk?
- EBV exploits B-cell specific regulatory mechanisms and signals
- Growth transformation associated EBV encoded proteins
- The latent membrane proteins (LMP) of EBV
- EBV and Burkitt lymphoma (BL)
- Hodgkin’s lymphoma (HL)
- EBV and nasopharyngeal carcinoma
- Viral expression in carcinoma cells, cell behavior and host relationships in NPC
- Immune surveillance and the oncogenic herpesviruses – the role of immunological “anticipation”
- Double HHV8/EBV carrying PEL cells
- References
- 30. KSHV manipulation of the cell cycle and apoptosis
- 31. Human gammaherpesvirus immune evasion strategies
- 22. Introduction to the human γ-herpesviruses
- III.1. Pathogenesis, clinical disease, host response, and epidemiology:
alphaherpes viruses
- 32. Pathogenesis and disease
- Pathogenesis
- Unique biologic properties of HSV that influence pathogenesis
- Pathology
- Pathology of central nervous system disease
- Impact of host response to infection on disease
- Orolabial infection
- Genital infection
- Keratoconjunctivitis
- Cutaneous infections
- Central nervous system infections
- Neonatal infection
- Infection in compromised hosts
- References
- 33. Molecular basis of HSV latency and reactivation
- 34. Immunobiology and host response
- Introduction
- HSV interactions with dendritic cells
- CD8 T-cell responses to HSV
- CD4 T-cell responses to HSV
- T-cell costimulation and HSV
- Antibody responses to HSV
- Innate immunity
- Immunomodulators and HSV
- Chemokines
- NK cells
- NKT cells
- TCRγδ cells
- Additional interactions between HSV and the immune system
- Summary
- References
- 35. Immunopathological aspects of HSV infection
- 36. Persistence in the population: epidemiology, transmission
- 32. Pathogenesis and disease
- III.2. Pathogenesis, clinical disease, host response, and epidemiology:
alphaherpes viruses VZV
- 37. VZV: pathogenesis and the disease consequences of primary infection
- Introduction
- Systems for evaluating determinants of VZV pathogenesis in human skin and T-cells
- Effects of VZV replication on cellular cyclin-dependent kinases and cyclins
- Investigation of events in the pathogenesis of primary VZV infection in the SCIDhu model
- The role of VZV glycoproteins in T-cell and skin tropism
- Glycoprotein C
- Glycoprotein E
- Glycoprotein I
- The role of regulatory proteins and viral kinases in T-cell and skin tropism
- IE62 protein
- IE63 protein
- ORF64 protein
- ORF10 protein
- ORF47 protein
- ORF66 protein
- Disease consequences of primary VZV infection in healthy and immunocompromised hosts
- Varicella in the immunocompromised host
- Varicella in pregnancy and the newborn
- Summary
- References
- 38. VZV: molecular basis of persistence (latency and reactivation)
- Site of VZV latency
- Quantification of VZV DNA load during latency
- Animal models for VZV latency
- VZV transcripts expressed during latency
- VZV proteins expressed during latency
- Function of VZV latency-associated proteins
- VZV genes required for establishment of latent infection
- In vitro models for VZV latency
- Reactivation of VZV
- Comparison of VZV latency with that of other alphaherpesviruses
- Is the large number of transcripts in VZV latency due to reactivation?
- Models for VZV latency
- VZV proteins localize to the cytoplasm, instead of the nucleus of neurons and thus are unable to carry out their activities
- VZV proteins have different activities in neurons than in permissive cells due to differences in cellular proteins
- Future directions
- References
- 39. VZV: immunobiology and host response
- 40. VSV: persistence in the population
- 37. VZV: pathogenesis and the disease consequences of primary infection
- III.3. Pathogenesis, clinical disease, host response, and epidemiology:
betaherpesviruses
- 41. Virus entry into host, establishment of infection, spread in host, mechanisms of tissue damage
- 42. Molecular basis of persistence and latency
- 43. Immunobiology and host response
- 44. Persistence in the population: epidemiology and transmisson
- Introduction
- Epidemiology of HCMV infection
- Transmission of HCMV by mothers to infants: perinatal infections
- Children-to-children transmission of HCMV
- Transmission of HCMV by children to parents
- HCMV transmission through sexual activity
- Transmission of HCMV to child-care providers
- Transmission of CMV in health-care settings
- Transfusion acquired HCMV infection
- Transplantation and HCMV infection
- HCMV transmission from artificial insemination by donor semen
- Summary
- References
- 45. HCMV persistence in the population: potential transplacental transmission
- III.4. HHV-6A, 6B, and 7
- III.5. Pathogenesis, clinical disease, host response, and epidemiology:
gammaherpesviruses
- 50. Clinical and pathological aspects of EBV and KSHV infection
- 51. EBV: immunobiology and host response
- Introduction
- Response during acute infection
- Response in healthy virus carriers
- Role of CD4+ and CD8+ CTL in control of EBV infection
- Role of CTL effector cells in resolution of acute IM
- T-cell receptor usage
- Virus-driven immune modulation
- T-cell control of EBV-associated malignancies
- Future prospects for an EBV vaccine
- References
- 52. Immunobiology and host response to KSHV infection
- 53. The epidemiology of EBV and its association with malignant disease
- 54. The epidemiology of KSHV and its association with malignant disease
- 55. EBV-induced oncogenesis
- 56. KSHV-induced oncogenesis
- IV. Non-human primate herpesviruses
- 57. Monkey B virus
- 58. Simian varicella virus
- 59. Primate betaherpesviruses
- 60. Gammaherpesviruses of New World primates
- 61. EBV and KSHV – related herpesviruses in non-human primates
- Introduction
- Nomenclature
- Evolution of New and Old World lymphocryptoviruses
- Lymphocryptoviruses of Old World monkeys
- The rhesus LCV genome
- Latency, immune-modulatory and transforming genes of rhesus LCV
- Rhesus LCV as an animal model system for EBV
- Other lymphocryptoviruses in Old World primates
- Lymphocryptoviruses of New World monkeys
- New World primates as an animal model system for EBV
- Evolution of New and Old World rhadinoviruses
- Rhadinoviruses of Old World primates
- Retroperitoneal fibromatosis herpesviruses: RFHVMm and RFHVMn
- Rhesus monkey rhadinovirus (RRV)
- RRV as an animal model system for KSHV
- Conclusions
- References
- V. Subversion of adaptive immunity
- 62. Herpesvirus evasion of T-cell immunity
- 63. Subversion of innate and adaptive immunity: immune evasion from
antibody and complement
- Role of the herpesvirus IgG Fc receptor in immune evasion
- Herpes simplex virus FcγR
- Human CMV FcγR
- Varicella zoster FcγR
- vFcγRs on non-human mammalian herpesviruses
- Summary of vFcγR studies
- Role of the herpesvirus complement receptors in immune evasion
- Strategies employed by human herpesviruses to evade complement immunity
- Strategies employed by non-human mammalian herpesviruses to evade complement immunity
- Summary of viral complement regulatory proteins
- References
- VI. Antiviral therapy
- 64. Antiviral therapy of HSV-1 and -2
- 65. Antiviral therapy of varicella-zoster virus infections
- 66. Antiviral therapy for human cytomegalovirus
- 67. New approaches to antiviral drug discovery (genomics/proteomics)
- Introduction
- Development of bioinformatics and computational tools
- Impact of genomics and related fields on herpesvirus research
- New resources for use in drug discovery
- Application of new technologies to cell-based antiviral assays
- Application of new technologies to biochemical assays
- Application of new technologies to functional assays
- Application of new technologies to characterize mechanism of action and spectrum of activity
- Conclusions
- References
- 68. Candidate anti-herpesviral drugs; mechanisms of action and
resistance
- The drug development process: an overview
- Host cell targets as an approach to virus inhibition
- Antiviral targets in early replication events
- Antiviral targets in the herpesvirus DNA replication complex
- Inhibitors of DNA processing and packaging
- Antivirals with activity against EBV, HHV-6, HHV-7, and HHV-8
- Conclusions
- References
- VII. Vaccines and immunotherapy
- 69. Herpes simplex vaccines
- 70. Varicella-zoster vaccine
- Varicella vaccines: background
- History of development of the live attenuated vaccine
- Virology of the attenuated Oka strain of VZV
- Safety of the varicella vaccine for healthy individuals
- Immunogenicity of varicella vaccine in healthy children and adolescents
- Efficacy and post-licensure effectiveness of varicella vaccine
- Considerations of vaccine use
- Persistent questions regarding varicella vaccine
- Does immunity to varicella wane with time after immunization?
- Zoster: effects and potential effects on its incidence in the vaccine era
- Vaccination to prevent zoster in the elderly
- Use of inactivated varicella vaccine in patients at high risk to develop zoster
- Recent developments
- Conclusions
- References
- 71. Human cytomegalovirus vaccines
- 72. Epstein–barr virus vaccines
- 73. DNA vaccines for human herpesviruses
- 74. Adoptive immunotherapy for herpesviruses
- Introduction
- Therapy for herpesvirus-related infections and diseases
- Cytomegalovirus
- Epstein–Barr virus
- T-cell activation
- Strategies for producing T-cells for adoptive immunotherapy
- Adoptive immunotherapy for cytomegalovirus
- Adoptive immunotherapy for EBV post-transplant lymphoproliferation disease
- Adoptive immunotherapy for EBV post-solid organ transplant
- Adoptive transfer of EBV-specific CTL for Hodgkin’s lymphoma
- Adoptive transfer of EBV-specific CTL for nasopharyngeal carcinoma
- Multivirus-specific CTL lines
- CMV and EBV immunotherapy in HIV positive individuals
- Alternative approaches for activating virus-specific CTLs
- Conclusions and future considerations
- References
- 75. Immunotherapy of HSV infections – antibody delivery
- VIII. Herpesviruses as therapeutic agents
- 76. Herpesviruses as therapeutic agents
- Introduction
- Properties of therapeutic HSV vectors
- Properties of non-replicating HSV vectors for therapeutic use
- Use of HSV vectors to modify the nervous system
- Towards optimizing HSV vectors for therapeutic use
- Non-replicating vectors: current trends
- Oncolytic HSV
- Oncolytic HSV: current directions
- References
- 76. Herpesviruses as therapeutic agents
- Plates
Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis.
Arvin A, Campadelli-Fiume G, Mocarski E, et al., editors.
Cambridge: Cambridge University Press; 2007.
Whitley R, Roizman B, editors. Herpesviruses as therapeutic agents. In: Arvin A, Campadelli-Fiume G, Mocarski E, et al., editors. Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge: Cambridge University Press; 2007.
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