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187 - Herpes simplex viruses 1 and 2
- from Part XXIII - Specific organisms: viruses
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- By Richard J. Whitley, University of Alabama
- Edited by David Schlossberg, Temple University, Philadelphia
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- Book:
- Clinical Infectious Disease
- Published online:
- 05 April 2015
- Print publication:
- 23 April 2015, pp 1193-1198
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- Chapter
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Summary
The virus
Herpesviruses are generally defined as large enveloped virions with an icosapentahedral nucleocapsid consisting 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 (gG) are unique antigenic determinants that allow for differentiation between these two viruses (e.g., 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. Scarring is uncommon.
Moving toward Elimination of Healthcare-Associated Infections: A Call to Action
- Denise Cardo, Penelope H. Dennehy, Paul Halverson, Neil Fishman, Mel Kohn, Cathryn L. Murphy, Richard J. Whitley, HAI Elimination White Paper Writing Group
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- Journal:
- Infection Control & Hospital Epidemiology / Volume 31 / Issue 11 / November 2010
- Published online by Cambridge University Press:
- 02 January 2015, pp. 1101-1105
- Print publication:
- November 2010
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- Article
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Jointly, the Association for Professionals in Infection Control and Epidemiology (APIC), the Society for Healthcare Epidemiology of America (SHEA), the Infectious Diseases Society of America (IDSA), the Association of State and Territorial Health Officials (ASTHO), the Council of State and Territorial Epidemiologists (CSTE), Pediatric Infectious Diseases Society (PIDS), and the Centers for Disease Control and Prevention (CDC) propose a call to action to move toward the elimination of healthcare-associated infections (HAIs) by adapting the concept and plans used for the elimination of other diseases, including infections. Elimination, as defined for other infectious diseases, is the maximal reduction of “the incidence of infection caused by a specific agent in a defined geographical area as a result of deliberate efforts; continued measures to prevent reestablishment of transmission are required.” (p24) This definition has been useful for elimination efforts directed toward polio, tuberculosis, and syphilis and can be readily adapted to HAIs. Sustained elimination of HAIs can be based on this public health model of constant action and vigilance. Elimination will require the implementation of evidence-based practices, the alignment of financial incentives, the closing of knowledge gaps, and the acquisition of information to assess progress and to enable response to emerging threats. These efforts must be under-pinned by substantial research investments, the development of novel prevention tools, improved organizational and personal accountabilities, strong collaboration among a broad coalition of public and private stakeholders, and a clear national will to succeed in this arena.
185 - Herpes Simplex Viruses 1 and 2
- from Part XXIII - Specific Organisms – Viruses
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- By David W. Kimberlin, University of Alabama at Birmingham School of Medicine, Richard J. Whitley, University of Alabama at Birmingham
- Edited by David Schlossberg
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- Book:
- Clinical Infectious Disease
- Published online:
- 05 March 2013
- Print publication:
- 12 May 2008, pp 1275-1280
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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.
64 - Antiviral therapy of HSV-1 and -2
- from Part VI - Antiviral therapy
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- By David W. Kimberlin, Department of Pediatrics, University of Alabama at Birmingham, AL, USA, Richard J. Whitley, Department of Pediatrics, University of Alabama at Birmingham, AL, USA
- Edited by Ann Arvin, Stanford University, California, Gabriella Campadelli-Fiume, Università degli Studi, Bologna, Italy, Edward Mocarski, Emory University, Atlanta, Patrick S. Moore, University of Pittsburgh, Bernard Roizman, University of Chicago, Richard Whitley, University of Alabama, Birmingham, Koichi Yamanishi, University of Osaka, Japan
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- Book:
- Human Herpesviruses
- Published online:
- 24 December 2009
- Print publication:
- 16 August 2007, pp 1153-1174
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Summary
Introduction
The discovery of effective antiviral agents has been facilitated by advances in the fields of molecular biology and virology. In the pre-antiviral era, the widely held belief was that any therapeutically meaningful interference with viral replication would destroy the host cell upon which viral replication was dependent. A growing understanding of host cell–virus interactions and viral replication, however, has led to the development of safe and effective antivirals. These agents act by impeding entry of viruses into host cells; interfering with viral assembly, release, or de-aggregation; inhibiting transcription or replication of the viral genome; or interrupting viral protein synthesis.
Antiviral agents can be used to treat disease (a therapeutic strategy), to prevent infection (a prophylactic strategy), or to prevent disease (a preemptive strategy). Prophylaxis refers to the administration of an agent to patients at risk of contracting infection (e.g., acyclovir given to HSV-seropositive renal transplant recipients). Pre-emptive treatment refers to the administration of a drug after there is evidence of infection, but before there is evidence of disease (e.g., ganciclovir given to bone marrow transplant recipients with positive CMV culture, but no symptoms of infection).
The effectiveness of antiviral therapy sometimes is limited by the development of antiviral resistance. Antiviral drug resistance has increased in parallel with the expanded use of, and indications for, antiviral therapy. Resistance most commonly occurs in patients with chronic and/or progressive infections who have been exposed to prolonged or repeated courses of therapy.
18 - Treatment of varicella
- from Part V - Treatment and Prevention
- Edited by Ann M. Arvin, Stanford University School of Medicine, California, Anne A. Gershon, Columbia University, New York
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- Book:
- Varicella-Zoster Virus
- Published online:
- 02 March 2010
- Print publication:
- 23 November 2000, pp 385-395
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Summary
This chapter emphasizes the controlled clinical trials that support the use of antiviral interventions for the treatment of varicella. Since varicella represents a primary infection, with varicella-zoster virus (VZV), the viral load is high and there is a documented viremic phase. While varicella is usually a mild and self-limiting infection in the normal host, life-threatening disease can occur in the immunocompromised host.
Therapeutic agents
Antiviral therapy was first shown to be efficacious for the management of varicella in the late 1970s and early 1980s using the nonspecific inhibitors of viral replication, vidarabine and interferon. Acyclovir, which is a second generation, specific inhibitor of VZV replication was then proven useful and has become the drug of choice. The prodrugs of acyclovir (valaciclovir) and penciclovir (famciclovir) have been licensed for the treatment of herpes zoster; but data are not yet available to prove the efficacy of these drugs in the management of varicella. Additionally, foscarnet, a pyrophosphate analog, is available for intravenous therapy of varicella infections in high-risk immunocompromised hosts who are presumed to have an infection caused by an acyclovir or penciclovir resistant virus.
Acyclovir and valaciclovir
Acyclovir has become the most widely prescribed and clinically effective antiviral drug available to date for the management of herpesvirus infection. Valaciclovir, the l-valine ester oral prodrug of acyclovir (Valtrex®), was developed to improve the oral bioavailability of acyclovir.
Chemistry, mechanism of action and antiviral activity
Acyclovir (9-{2-hydroxyethoxymethyl}guanine) is a synthetic acyclic purine nucleoside analog that is a selective inhibitor of herpes simplex virus (HSV types 1 and 2) and VZV replication (Elion et al., 1977; Schaeffer et al., 1978).