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184 - Enteroviruses
- from Part XXIII - Specific organisms: viruses
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- By Michael N. Oxman, University of California
- 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 1172-1182
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Summary
Enteroviruses (EVs), so named because most members infect the alimentary tract and are shed in the feces, cause a variety of diseases in humans and lower animals. They constitute one of the six major subgroups, or genera, of the family Picornaviridae [pico, “small”; rna, “ribonucleic acid”]. The other genera of Picornaviridae are the Rhinovirus, Cardiovirus, Aphthovirus, and two newly designated genera, Hepatovirus, the prototypic member of which is human hepatitis A virus; and Parechovirus, which contains two serotypes that were previously classified as echoviruses types 22 and 23, and at least 14 additional serotypes.
Physical and biochemical properties
EVs, like all members of the picornavirus family, are small, nonenveloped, spherical (icosahedral) viruses approximately 30 nm in diameter. Their capsids consist of 60 structural subunits, each composed of 4 unique polypeptides: VP1, VP2, VP3, and VP4. Their genome consists of a linear, single-stranded, unsegmented molecule of RNA (of approximately 7500 nucleotides) that has the same polarity as messenger RNA.
EVs are stable over a wide range of pH (pH 3 to 10), permitting them to retain infectivity during passage through the gastrointestinal tract. They are not inactivated by ether, alcohol, or other lipid solvents, but are readily inactivated by formaldehyde or phenol. EVs retain infectivity for days at room temperature, weeks at refrigerator temperature, and indefinitely when frozen at −20°C or lower. Molar MgCl2 further increases their thermostability, facilitating the use of oral polio vaccines in tropical areas where availability of refrigeration is limited.
Contributors
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- By Aakash Agarwala, Linda S. Aglio, Rae M. Allain, Paul D. Allen, Houman Amirfarzan, Yasodananda Kumar Areti, Amit Asopa, Edwin G. Avery, Patricia R. Bachiller, Angela M. Bader, Rana Badr, Sibinka Bajic, David J. Baker, Sheila R. Barnett, Rena Beckerly, Lorenzo Berra, Walter Bethune, Sascha S. Beutler, Tarun Bhalla, Edward A. Bittner, Jonathan D. Bloom, Alina V. Bodas, Lina M. Bolanos-Diaz, Ruma R. Bose, Jan Boublik, John P. Broadnax, Jason C. Brookman, Meredith R. Brooks, Roland Brusseau, Ethan O. Bryson, Linda A. Bulich, Kenji Butterfield, William R. Camann, Denise M. Chan, Theresa S. Chang, Jonathan E. Charnin, Mark Chrostowski, Fred Cobey, Adam B. Collins, Mercedes A. Concepcion, Christopher W. Connor, Bronwyn Cooper, Jeffrey B. Cooper, Martha Cordoba-Amorocho, Stephen B. Corn, Darin J. Correll, Gregory J. Crosby, Lisa J. Crossley, Deborah J. Culley, Tomas Cvrk, Michael N. D'Ambra, Michael Decker, Daniel F. Dedrick, Mark Dershwitz, Francis X. Dillon, Pradeep Dinakar, Alimorad G. Djalali, D. John Doyle, Lambertus Drop, Ian F. Dunn, Theodore E. Dushane, Sunil Eappen, Thomas Edrich, Jesse M. Ehrenfeld, Jason M. Erlich, Lucinda L. Everett, Elliott S. Farber, Khaldoun Faris, Eddy M. Feliz, Massimo Ferrigno, Richard S. Field, Michael G. Fitzsimons, Hugh L. Flanagan Jr., Vladimir Formanek, Amanda A. Fox, John A. Fox, Gyorgy Frendl, Tanja S. Frey, Samuel M. Galvagno Jr., Edward R. Garcia, Jonathan D. Gates, Cosmin Gauran, Brian J. Gelfand, Simon Gelman, Alexander C. Gerhart, Peter Gerner, Omid Ghalambor, Christopher J. Gilligan, Christian D. Gonzalez, Noah E. Gordon, William B. Gormley, Thomas J. Graetz, Wendy L. Gross, Amit Gupta, James P. Hardy, Seetharaman Hariharan, Miriam Harnett, Philip M. Hartigan, Joaquim M. Havens, Bishr Haydar, Stephen O. Heard, James L. Helstrom, David L. Hepner, McCallum R. Hoyt, Robert N. Jamison, Karinne Jervis, Stephanie B. Jones, Swaminathan Karthik, Richard M. Kaufman, Shubjeet Kaur, Lee A. Kearse Jr., John C. Keel, Scott D. Kelley, Albert H. Kim, Amy L. Kim, Grace Y. Kim, Robert J. Klickovich, Robert M. Knapp, Bhavani S. Kodali, Rahul Koka, Alina Lazar, Laura H. Leduc, Stanley Leeson, Lisa R. Leffert, Scott A. LeGrand, Patricio Leyton, J. Lance Lichtor, John Lin, Alvaro A. Macias, Karan Madan, Sohail K. Mahboobi, Devi Mahendran, Christine Mai, Sayeed Malek, S. Rao Mallampati, Thomas J. Mancuso, Ramon Martin, Matthew C. Martinez, J. A. Jeevendra Martyn, Kai Matthes, Tommaso Mauri, Mary Ellen McCann, Shannon S. McKenna, Dennis J. McNicholl, Abdel-Kader Mehio, Thor C. Milland, Tonya L. K. Miller, John D. Mitchell, K. Annette Mizuguchi, Naila Moghul, David R. Moss, Ross J. Musumeci, Naveen Nathan, Ju-Mei Ng, Liem C. Nguyen, Ervant Nishanian, Martina Nowak, Ala Nozari, Michael Nurok, Arti Ori, Rafael A. Ortega, Amy J. Ortman, David Oxman, Arvind Palanisamy, Carlo Pancaro, Lisbeth Lopez Pappas, Benjamin Parish, Samuel Park, Deborah S. Pederson, Beverly K. Philip, James H. Philip, Silvia Pivi, Stephen D. Pratt, Douglas E. Raines, Stephen L. Ratcliff, James P. Rathmell, J. Taylor Reed, Elizabeth M. Rickerson, Selwyn O. Rogers Jr., Thomas M. Romanelli, William H. Rosenblatt, Carl E. Rosow, Edgar L. Ross, J. Victor Ryckman, Mônica M. Sá Rêgo, Nicholas Sadovnikoff, Warren S. Sandberg, Annette Y. Schure, B. Scott Segal, Navil F. Sethna, Swapneel K. Shah, Shaheen F. Shaikh, Fred E. Shapiro, Torin D. Shear, Prem S. Shekar, Stanton K. Shernan, Naomi Shimizu, Douglas C. Shook, Kamal K. Sikka, Pankaj K. Sikka, David A. Silver, Jeffrey H. Silverstein, Emily A. Singer, Ken Solt, Spiro G. Spanakis, Wolfgang Steudel, Matthias Stopfkuchen-Evans, Michael P. Storey, Gary R. Strichartz, Balachundhar Subramaniam, Wariya Sukhupragarn, John Summers, Shine Sun, Eswar Sundar, Sugantha Sundar, Neelakantan Sunder, Faraz Syed, Usha B. Tedrow, Nelson L. Thaemert, George P. Topulos, Lawrence C. Tsen, Richard D. Urman, Charles A. Vacanti, Francis X. Vacanti, Joshua C. Vacanti, Assia Valovska, Ivan T. Valovski, Mary Ann Vann, Susan Vassallo, Anasuya Vasudevan, Kamen V. Vlassakov, Gian Paolo Volpato, Essi M. Vulli, J. Matthias Walz, Jingping Wang, James F. Watkins, Maxwell Weinmann, Sharon L. Wetherall, Mallory Williams, Sarah H. Wiser, Zhiling Xiong, Warren M. Zapol, Jie Zhou
- Edited by Charles Vacanti, Scott Segal, Pankaj Sikka, Richard Urman
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- Book:
- Essential Clinical Anesthesia
- Published online:
- 05 January 2012
- Print publication:
- 11 July 2011, pp xv-xxviii
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182 - Enteroviruses
- from Part XXIII - Specific Organisms – Viruses
-
- By Michael N. Oxman, University of California
- Edited by David Schlossberg
-
- Book:
- Clinical Infectious Disease
- Published online:
- 05 March 2013
- Print publication:
- 12 May 2008, pp 1251-1262
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- Chapter
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Summary
Enteroviruses (EV), so named because most members infect the alimentary tract and are shed in the feces, cause a variety of diseases in humans and lower animals. They constitute 1 of the 6 major subgroups, or genera, of the family Picornaviridae [pico, “small”; rna, “ribonucleic acid”]. The other genera of Picornaviridae are the Rhinoviruses, Cardioviruses, Aphthoviruses, and 2 newly designated genera, Hepatovirus, the prototypic member of which is human hepatitis A virus; and Parechovirus, which contains 2 serotypes that were previously classified as echoviruses types 22 and 23. Three additional genera have been proposed: Erbovirus, Kobuvirus, and Teschovirus.
PHYSICAL AND BIOCHEMICAL PROPERTIES
Enteroviruses, like all members of the Picornavirus family, are small, spherical, nonenveloped viruses approximately 30 nm in diameter. Their genome consists of a linear, single- stranded, unsegmented molecule of RNA (approximately 7500 nucleotides) that has the same polarity as messenger RNA.
Enteroviruses are stable over a wide range of pH (pH 3 to 10) and retain infectivity for days at room temperature, weeks at refrigerator temperature, and indefinitely when frozen at −20°C or lower.
CLASSIFICATION OF ENTEROVIRUSES
Historically, human EV have been subclassified into polioviruses, group A and group B coxsackieviruses, and echoviruses on the basis of antigenic relationships, differences in host range, and types of disease produced (Table 182.1). By 1969, 67 species (serotypes) of human EV had been identified and classified according to these criteria, although reclassification and redundancy have reduced this number from 67 to 61.
13 - Clinical manifestations of herpes zoster
- from Part III - Epidemiology and Clinical Manifestations
- 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 246-275
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Summary
Herpes zoster (shingles) is a localized disease characterized by unilateral radicular pain and a vesicular eruption that is generally limited to the dermatome innervated by a single spinal or cranial sensory ganglion. In contrast to varicella, which follows primary exogenous varicella-zoster virus (VZV) infection, herpes zoster is the result of reactivation of endogenous VZV that had persisted in latent form within sensory ganglia following an earlier attack of varicella.
Herpes zoster (HZ) occurs most often in dermatomes in which the rash of varicella achieves the highest density – those innervated by the first (ophthalmic) division of the trigeminal ganglion and by spinal sensory ganglia from T1 to L2 (Head & Campbell, 1900; Stern, 1937; Denny-Brown et al., 1944; Hope-Simpson, 1965; Ragozzino et al., 1982; Donahue et al., 1995). Presumably, areas of skin with a denser rash during varicella transmit larger amounts of virus to the corresponding sensory ganglia, thereby endowing these ganglia with a higher concentration of latent VZV. If subsequent reactivation occurs at random, HZ would be expected to occur most frequently in dermatomes innervated by ganglia with the highest concentrations of latent VZV. The occurrence of HZ at sites of prior vaccination with live attenuated varicella vaccine is consistent with this model of VZV latency.
Although the latent virus in the ganglia retains its potential for full infectivity, reactivation is sporadic and infrequent, and infectious virus does not appear to be present during latency. The mechanisms involved in the reactivation of VZV are unclear (see Chapter 6), but a number of conditions have been associated with the occurrence and localization of HZ.