Chapter 45 : Enteroviruses

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The original taxonomic classification of the enteroviruses (EVs) recognized 64 prototype serotypes within the family . The majority of what is known about the pathogenesis of EV infections in humans has been based on the study of the polioviruses, the prototypic members of the genus, in experimental infections using chimpanzees more than four decades ago and, most recently, from transgenic mice expressing the poliovirus receptor CD155. The study of cell-mediated immune responses to EVs has been much more limited, and the importance of the cellular response in preventing or clearing infection is still unclear. A 20-year evaluation of the epidemiology of neonatal EV infections identified case fatality rates that ranged from approximately 17 to 20% for infants <1 month of age infected with echoviruses 6, 11, 20, and 30 and coxsackievirus B4. The clinical manifestations of EV-associated upper respiratory infections (URIs), otitis media, wheezing, and pharyngotonsillitis are indistinguishable from those due to other respiratory viruses. Although it is the most sensitive method for laboratory diagnosis of some coxsackievirus A infections, isolation of EVs in suckling mice is rarely performed any longer because of the difficulties of the technique and of animal maintenance. As with other viral pathogens, there are several steps in the replication cycle of the picornaviruses that are potential targets in antiviral therapy. Cell susceptibility, viral attachment, viral uncoating, viral RNA replication, and viral protein synthesis have all been studied as targets of antipicornaviral compounds.

Citation: Romero J. 2009. Enteroviruses, p 1031-1061. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch45
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Image of FIGURE 1

(a) Schematic representation of the icosahedral viral capsid structure of the EV. The fivefold (5x) and threefold (3x) axes of symmetry are indicated, as is the position of one of the 60 repeating protomeric units, each comprised of VP1, VP2, and VP3 surface proteins. (b) Line drawing of the VP1 and VP2 proteins in their tertiary configuration. The canyon structure, into which the cellular receptor for the EVs fits, is illustrated with its sphingosine (sph) hydrocarbon-binding pocket. (Reprinted from reference with permission.)

Citation: Romero J. 2009. Enteroviruses, p 1031-1061. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch45
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Image of FIGURE 2

Genomic organization and translation products of the EVs, as represented by poliovirus. The cross-hatched circle indicates the covalently attached VPg molecule at the 5′ end of the RNA. The coding region (nt 743 to 7370 on this map) is shown as a thick line. The poly(A) tail at the 3′ end of the RNA is indicated by “A.” The polyprotein coded for by the single ORF is then posttranslationally modified by viral proteases to form the viral protein cleavage products. (Reprinted from reference with permission.)

Citation: Romero J. 2009. Enteroviruses, p 1031-1061. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch45
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Image of FIGURE 3

Cytopathic effect of poliovirus type 1 infection of tissue culture cells. (panel 1) Uninfected rhesus monkey kidney cells. (panel 2) Poliovirus-infected rhesus monkey kidney cells 24 h after infection. (panel 3) Uninfected HEp-2 cells. (panel 4) Poliovirus-infected HEp-2 cells 24 h after infection. (Reprinted from reference with permission.)

Citation: Romero J. 2009. Enteroviruses, p 1031-1061. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch45
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Image of FIGURE 4

In situ hybridization study of an adult patient with EV myocarditis. Darkly staining cells indicate the presence of EV RNA. Infection is seen within the inflammatory infiltrate (A and B) as well as in nearby myocardial muscle cells (C). (Reprinted from reference .)

Citation: Romero J. 2009. Enteroviruses, p 1031-1061. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch45
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Image of FIGURE 5

Natural history of EV aseptic meningitis. Comp. Fix., complement fixation. (Reprinted from reference with permission.)

Citation: Romero J. 2009. Enteroviruses, p 1031-1061. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch45
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Image of FIGURE 6

Clinical features of young infants with EV infections and the relationship of those features to the infecting serotype (echoviruses [ECHO] versus coxsackieviruses [COXSACKIE B], top panel) and to the presence or absence of meningitis (bottom panel). LRI, lower respiratory infection; URI, upper respiratory infection. (Reprinted from reference with permission.)

Citation: Romero J. 2009. Enteroviruses, p 1031-1061. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch45
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Image of FIGURE 7

Herpangina due to coxsackie A viruses. Small, discrete vesicles surrounded by erythema are seen on the palate and uvula and elsewhere in the posterior oropharynx.

Citation: Romero J. 2009. Enteroviruses, p 1031-1061. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch45
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Image of FIGURE 8

Characteristic lesions of EV hand-foot-and-mouth syndrome involving the dorsum of the hand and fingers.

Citation: Romero J. 2009. Enteroviruses, p 1031-1061. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch45
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