Book contents
- Frontmatter
- Contents
- Preface
- Contributors
- Part I Clinical Syndromes – General
- Part II Clinical Syndromes – Head and Neck
- Part III Clinical Syndromes – Eye
- Part IV Clinical Syndromes – Skin and Lymph Nodes
- Part V Clinical Syndromes – Respiratory Tract
- Part VI Clinical Syndromes – Heart and Blood Vessels
- Part VII Clinical Syndromes – Gastrointestinal Tract, Liver, and Abdomen
- Part VIII Clinical Syndromes – Genitourinary Tract
- Part IX Clinical Syndromes – Musculoskeletal System
- Part X Clinical Syndromes – Neurologic System
- Part XI The Susceptible Host
- Part XII HIV
- Part XIII Nosocomial Infection
- Part XIV Infections Related to Surgery and Trauma
- Part XV Prevention of Infection
- Part XVI Travel and Recreation
- Part XVII Bioterrorism
- Part XVIII Specific Organisms – Bacteria
- Part XIX Specific Organisms – Spirochetes
- Part XX Specific Organisms – Mycoplasma and Chlamydia
- Part XXI Specific Organisms – Rickettsia, Ehrlichia, and Anaplasma
- Part XXII Specific Organisms – Fungi
- Part XXIII Specific Organisms – Viruses
- 180 Cytomegalovirus
- 181 Dengue and Dengue-Like Illness
- 182 Enteroviruses
- 183 Epstein–Barr Virus and Other Causes of the Mononucleosis Syndrome
- 184 Hantavirus Cardiopulmonary Syndrome in the Americas
- 185 Herpes Simplex Viruses 1 and 2
- 186 Human Herpesviruses 6, 7, and 8
- 187 Influenza
- 188 Papillomavirus
- 189 Acute and Chronic Parvovirus Infection
- 190 Rabies
- 191 Varicella-Zoster Virus
- 192 Viral Hemorrhagic Fevers
- Part XXIV Specific Organisms – Parasites
- Part XXV Antimicrobial Therapy – General Considerations
- Index
185 - Herpes Simplex Viruses 1 and 2
from Part XXIII - Specific Organisms – Viruses
Published online by Cambridge University Press: 05 March 2013
- Frontmatter
- Contents
- Preface
- Contributors
- Part I Clinical Syndromes – General
- Part II Clinical Syndromes – Head and Neck
- Part III Clinical Syndromes – Eye
- Part IV Clinical Syndromes – Skin and Lymph Nodes
- Part V Clinical Syndromes – Respiratory Tract
- Part VI Clinical Syndromes – Heart and Blood Vessels
- Part VII Clinical Syndromes – Gastrointestinal Tract, Liver, and Abdomen
- Part VIII Clinical Syndromes – Genitourinary Tract
- Part IX Clinical Syndromes – Musculoskeletal System
- Part X Clinical Syndromes – Neurologic System
- Part XI The Susceptible Host
- Part XII HIV
- Part XIII Nosocomial Infection
- Part XIV Infections Related to Surgery and Trauma
- Part XV Prevention of Infection
- Part XVI Travel and Recreation
- Part XVII Bioterrorism
- Part XVIII Specific Organisms – Bacteria
- Part XIX Specific Organisms – Spirochetes
- Part XX Specific Organisms – Mycoplasma and Chlamydia
- Part XXI Specific Organisms – Rickettsia, Ehrlichia, and Anaplasma
- Part XXII Specific Organisms – Fungi
- Part XXIII Specific Organisms – Viruses
- 180 Cytomegalovirus
- 181 Dengue and Dengue-Like Illness
- 182 Enteroviruses
- 183 Epstein–Barr Virus and Other Causes of the Mononucleosis Syndrome
- 184 Hantavirus Cardiopulmonary Syndrome in the Americas
- 185 Herpes Simplex Viruses 1 and 2
- 186 Human Herpesviruses 6, 7, and 8
- 187 Influenza
- 188 Papillomavirus
- 189 Acute and Chronic Parvovirus Infection
- 190 Rabies
- 191 Varicella-Zoster Virus
- 192 Viral Hemorrhagic Fevers
- Part XXIV Specific Organisms – Parasites
- Part XXV Antimicrobial Therapy – General Considerations
- Index
Summary
THE VIRUS
Herpesviruses are generally defined as large enveloped virions with an icosapentahedral nucleocapsid consisting invariably of 162 capsomeres arranged around a double-stranded DNA core. The two antigenically distinct types of herpes simplex virus (HSV) are HSV-1 and HSV-2. Considerable homology exists between the HSV-1 and HSV-2 genomes, with most of the polypeptides specified by one viral type being antigenically related to polypeptides of the other viral type. Although this results in considerable cross-reactivity between the HSV-1 and HSV-2 glycoproteins (g), unique antigenic determinants allow for differentiation between these two viruses (eg, gG-1 and gG-2). Surrounding the viral genome and nucleocapsid is a tightly adherent membrane known as the tegument. A lipid envelope containing the viral glycoproteins loosely surrounds the tegument.
PATHOLOGY AND PATHOGENESIS
Cutaneous HSV infection causes ballooning of infected epithelial cells, with nuclear degeneration, loss of intact cellular membranes, and the formation of multinucleated giant cells. Ultimately, cells lyse and release clear fluid containing large quantities of virus, with subsequent accumulation of cellular debris and inflammatory cells between the epidermal and dermal layers. Multinucleated giant cells are usually present at the base of the vesicle. An intense inflammatory response extends from the base of the vesicle into the dermis, producing the erythema that classically surrounds a cluster of HSV vesicles. As the lesions heal, vesicular fluid becomes purulent as more inflammatory cells are recruited to the site of infection. Scab formation then follows.
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- Clinical Infectious Disease , pp. 1275 - 1280Publisher: Cambridge University PressPrint publication year: 2008