Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Introduction: definition and classification of the human herpesviruses
- Part II Basic virology and viral gene effects on host cell functions: alphaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: betaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: gammaherpesviruses
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2
- 32 HSV-1 AND 2: Pathogenesis and disease
- 33 HSV-1 and 2: molecular basis of HSV latency and reactivation
- 34 HSV-1 and 2: immunobiology and host response
- 35 HSV: immunopathological aspects of HSV infection
- 36 HSV: persistence in the population: epidemiology, transmission
- Part III Pathogenesis, clinical disease, host response, and epidemiology: VZU
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HCMV
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HHV- 6A, 6B, and 7
- Part III Pathogenesis, clinical disease, host response, and epidemiology: gammaherpesviruses
- Part IV Non-human primate herpesviruses
- Part V Subversion of adaptive immunity
- Part VI Antiviral therapy
- Part VII Vaccines and immunothgerapy
- Part VIII Herpes as therapeutic agents
- Index
- Plate section
- References
33 - HSV-1 and 2: molecular basis of HSV latency and reactivation
from Part III - Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2
Published online by Cambridge University Press: 24 December 2009
Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Introduction: definition and classification of the human herpesviruses
- Part II Basic virology and viral gene effects on host cell functions: alphaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: betaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: gammaherpesviruses
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2
- 32 HSV-1 AND 2: Pathogenesis and disease
- 33 HSV-1 and 2: molecular basis of HSV latency and reactivation
- 34 HSV-1 and 2: immunobiology and host response
- 35 HSV: immunopathological aspects of HSV infection
- 36 HSV: persistence in the population: epidemiology, transmission
- Part III Pathogenesis, clinical disease, host response, and epidemiology: VZU
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HCMV
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HHV- 6A, 6B, and 7
- Part III Pathogenesis, clinical disease, host response, and epidemiology: gammaherpesviruses
- Part IV Non-human primate herpesviruses
- Part V Subversion of adaptive immunity
- Part VI Antiviral therapy
- Part VII Vaccines and immunothgerapy
- Part VIII Herpes as therapeutic agents
- Index
- Plate section
- References
Summary
Introduction
Primary infection with HSV-1 or HSV-2 results in productive replication of the virus at the site of infection, following the pattern of gene expression described elsewhere in this volume. During this initial phase, virus enters sensory neurons via their termini and retrograde transport takes the genome to the neuronal nuclei in the sensory ganglia that innervate the infected dermatome. At early times after infection, virus replication occurs in ganglionic neurons but within a few days no virus can be detected. The genome, however, persists in neurons in a latent state from which it reactivates periodically to resume replication and produce infectious virus. This reactivation event may be “spontaneous” but is generally thought to be provoked by stress stimuli that act on the neuron, or at a peripheral site innervated by the infected ganglion, or systemically. Three phases of latency are recognized. Establishment occurs during the period following primary infection, and although virus replication can be detected in a proportion of neurons during this phase, the initiation and normal progression of productive infection and cell death is arrested in those neurons destined to become latently infected. Unravelling the way in which the seemingly inexorable progression of the gene expression program is blocked constitutes a major challenge for the molecular virologist. The maintenance phase of latency is characterized by the lifelong retention of the HSV genome in a silent state, characterized by repression of all viral lytic genes. One region, encoding the latency-associated transcripts (LATs), remains active during latency.
- Type
- Chapter
- Information
- Human HerpesvirusesBiology, Therapy, and Immunoprophylaxis, pp. 602 - 615Publisher: Cambridge University PressPrint publication year: 2007
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