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
35 - HSV: immunopathological aspects of HSV infection
from Part III - Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2
Published online by Cambridge University Press: 24 December 2009
- 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
“What is food to one man is bitter poison to others”
Lucretius De Rerum Natura (50BCE)Foreign material entering multicellular organisms triggers a range of defense reactions which, when successful, subjugates and removes the invaders. Invertebrates and plants have natural defense systems, which recognize commonly shared patterns and usually react in a stereotypical manner. Long-lived animals such as vertebrates add to these natural defenses with adaptive systems that show discriminating recognition machinery, complex and varying effector mechanisms and development of persistent or “memory” responses. Under ideal circumstances, immune defense proceeds with minimal or inapparent damage to the host. In other situations, the defense system is less successful and the host tissues become damaged by the reaction. We usually consider the former situation as immunity and the latter as immunopathology. However, in both instances, mechanisms at play may be similar and deciding if the process is one or the other may require Lucretian logic.
With microorganisms, the commonest circumstance that results in immunopathology is where the microbe persists and continues to cause an innate and adaptive response. These, however, prove ineffective to remove or neutralize the agent. Thus the reaction becomes chronic and host tissues become damaged as a consequence. This situation occurs in tuberculosis as well as hepatitis B and C virus infections. Over time, many microbes with a long association with a host species find ways of persisting by evading responses that would either eliminate them or cause too much tissue damage.
- Type
- Chapter
- Information
- Human HerpesvirusesBiology, Therapy, and Immunoprophylaxis, pp. 642 - 655Publisher: Cambridge University PressPrint publication year: 2007
References
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