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Contributors
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- By Ted Abel, Antoine Adamantidis, Karla V. Allebrandt, Simon N. Archer, Amelie Baud, Michel Billiard, Carlos Blanco-Centurion, Diane B. Boivin, Ethan Buhr, Matthew E. Carter, Nicolas Cermakian, Jennifer H.K. Choi, S.Y. Christin Chong, Chiara Cirelli, Marc Cuesta, Thomas Curie, Yves Dauvilliers, Luis de Lecea, Derk-Jan Dijk, Stephane Dissel, Annette C. Fedson, Jonathan Flint, Marcos G. Frank, Paul Franken, Ying-Hui Fu, Thorarinn Gislason, David Gozal, Devon A. Grant, Hakon Hakonarson, Makoto Honda, Hyun Hor, Christer Hublin, Peng Jiang, Takashi Kanbayashi, Jaakko Kaprio, Andrew Kasarskis, Leila Kheirandish-Gozal, RodaRani Konadhode, Michael Lazarus, Meng Liu, Michael March, Mark F. Mehler, Keivan Kaveh Moghadam, Valérie Mongrain, Charles M. Morin, Benjamin M. Neale, Seiji Nishino, Allan I. Pack, Dheeraj Pelluru, Rosa Peraita-Adrados, Giuseppe Plazzi, David A. Prober, Louis J. Ptáček, Irfan A. Qureshi, David M. Raizen, John J. Renger, Till Roenneberg, Elizabeth J. Rossin, Takeshi Sakurai, Paul Salin, Karen D. Schilli, Eva C. Schulte, Laurent Seugnet, Paul J. Shaw, Priyattam J. Shiromani, Patrick Sleiman, Mehdi Tafti, Joseph S. Takahashi, Matthew S. Thimgan, Katsushi Tokunaga, Giulio Tononi, Fred W. Turek, Yoshihiro Urade, Hans P.A. Van Dongen, Juliane Winkelmann, Christopher J. Winrow
- Edited by Paul Shaw, Mehdi Tafti, Michael J. Thorpy
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- Book:
- The Genetic Basis of Sleep and Sleep Disorders
- Published online:
- 05 November 2013
- Print publication:
- 24 October 2013, pp xi-xiv
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32 - HSV-1 AND 2: Pathogenesis and disease
- from Part III - Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2
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- By Richard Whitley, Department of Pediatrics, Microbiology, Medicine and Neurosurgery, University of Alabama at Birmingham, Birmingham, AL, USA, David W. Kimberlin, Department of Pediatrics University of Alabama at Birmingham, Birmingham, AL, USA, Charles G. Prober, Department of Pediatrics, Stanford University School of Medicine, Scientific Director, Glaser Pediatric Research Network, Stanford University Medical Center, Stanford, CA, 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 589-601
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Summary
Pathogenesis
The transmission of herpes simplex virus (HSV) infection is dependent upon intimate, personal contact of a susceptible seronegative individual with someone excreting HSV. Virus must come in contact with mucosal surfaces or abraded skin for infection to be initiated. With viral replication at the site of primary infection, either an intact virion or, more simply, the capsid is transported retrograde by neurons to the dorsal root ganglia where, after another round of viral replication, latency is established (Fig. 32.1(a), left panel). The more severe the primary infection, as reflected by the size, number, and extent of lesions, the more likely it is that recurrences will ensue. Although replication sometimes leads to disease and, infrequently, results in life-threatening infection (e.g., encephalitis), the host-virus interaction leading to latency predominates. After latency is established, a proper stimulus causes reactivation; virus becomes evident at mucocutaneous sites, appearing as skin vesicles or mucosal ulcers (Fig. 32.1(b), right panel).
Infection with HSV-1 generally occurs in the oropharyngeal mucosa. The trigeminal ganglion becomes colonized and harbors latent virus. However, it has been increasingly common to detect evidence of HSV-1 in the genital tract, usually the consequence of oral-genital sex. When such occurs, recurrences of HSV-1 in the genital tract are uncommon. Acquisition of HSV-2 infection is usually the consequence of transmission by genital contact. Virus replicates in the genital, perigenital or anal skin sites with seeding of the sacral ganglia (Fig. 32.2).
17 - Neurological sequelae of congenital perinatal infection
- from Part II - Pregnancy, Labor, and Delivery Complications Causing Brain Injury
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- By Andrea M. Enright, Stanford University School of Medicine, Department of Pediatrics, Division of Infectious Diseases, Stanford, CA, USA, Charles G. Prober, Stanford University School of Medicine, Department of Pediatrics, Division of Infectious Diseases, Stanford, CA, USA
- Edited by David K. Stevenson, Stanford University School of Medicine, California, William E. Benitz, Stanford University School of Medicine, California, Philip Sunshine, Stanford University School of Medicine, California
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- Book:
- Fetal and Neonatal Brain Injury
- Published online:
- 10 November 2010
- Print publication:
- 06 February 2003, pp 355-376
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Summary
Introduction
Maternal infections, contracted during pregnancy, may be without fetal consequence or they may have serious adverse effects on the fetus. These adverse effects may include fetal death, stillbirth, intrauterine growth retardation, or congenital infection. Congenitally infected neonates may be symptomatic or asymptomatic at birth. Those who are symptomatic at birth generally have significant long-term sequelae. Those who are asymptomatic at birth may never manifest evidence of damage or they may develop clinically evident sequelae later in life. The overwhelming morbidity attributable to congenital infections is borne by this latter group.
The following chapter will discuss the neurologic consequences of congenital infections. The specific infectious agents that will be discussed are often referred to as the TORCH agents; T represents the parasite Toxoplasma gondii; O represents other agents such as varicella-zoster virus (VZV), human immunodeficiency virus (HIV), and Treponema pallidum (syphilis); R represents rubella virus; C represents cytomegalovirus (CMV); and H represents herpes simplex virus (HSV). With the exception of HSV, the major clinical impact of these agents results from exposure in utero. Morbidity and mortality attributable to neonatal HSV infection usually result from infection contracted at delivery.
Toxoplasmosis
The etiologic agent of toxoplasmosis, Toxoplasma gondii, was first demonstrated in the brain of a newborn infant with encephalomyelitis in 1939. The incidence of congenital toxoplasmosis in the USA is estimated to range from 1:1000 to 1:10,000 live births. Among immunocompetent women, transmission to the fetus is limited almost solely to those who contract primary infection during gestation.
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