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Chapter 6 : Cell Biology of Enterovirus Infection

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Cell Biology of Enterovirus Infection, Page 1 of 2

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Abstract:

Poliovirus, coxsackievirus, and echoviruses are cytopathic in most cell types, and the cytopathic effect (CPE) of enteroviral infection has been frequently described. This chapter discusses alterations in chromatin structure and transcription, rearrangement of cytoskeleton, accumulation of membranous vesicles, inhibition of protein secretion, and eventual lysis of cells infected with cytopathic enteroviruses. Wherever possible, the known or suspected viral proteins involved in these processes are identified, and the evidence for their involvement is presented. The chapter first discusses nuclear effects of enteroviral infection. While many changes in the cell biology of infected cells may result directly from the inhibition of cellular translation, it is also true that several preexisting proteins in the infected cell are specifically degraded during infection by poliovirus. The cell cytoskeleton is composed of three distinct but interconnected filament systems: actin microfilaments, microtubules, and intermediate filaments. A variety of findings support the hypothesis that the synthesis of viral RNA is membrane associated. First, subcellular fractions of poliovirus-infected cells that contain virus-induced membranes are able to synthesize viral RNA. Second, a complex of proteins containing the RNA-dependent RNA polymerase was shown to be membrane associated: when such complexes were isolated from poliovirus-infected cells under conditions that disrupted the membranes, many proteins, including the RNA polymerase, associated spontaneously with liposomes in vitro. Third, membranous complexes isolated from poliovirus-infected cells contain all of the viral proteins thought to be involved in RNA replication.

Citation: Schlegel A, Kirkegaard K. 1995. Cell Biology of Enterovirus Infection, p 135-154. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch6

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Rough Endoplasmic Reticulum
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Foot-and-mouth disease virus
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Figures

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FIGURE 1

Morphologic changes in human embryonic lung cells upon poliovirus infection. Phase contrast photomicrographs are of uninfected (A) and infected (B) cells. Reprinted from reference 2 with permission.

Citation: Schlegel A, Kirkegaard K. 1995. Cell Biology of Enterovirus Infection, p 135-154. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch6
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Image of FIGURE 2
FIGURE 2

Electron micrographs of HEp-2 cells: (A) uninfected; (B) infected with poliovirus for 3 h; (C) infected with poliovirus for 4 h. NU, nucleus; Nu, nucleolus; rER, rough endoplasmic reticulum; G, Golgi apparatus; V, virus-induced vesicles. Images courtesy of K. Bienz and D. Egger, University of Basel.

Citation: Schlegel A, Kirkegaard K. 1995. Cell Biology of Enterovirus Infection, p 135-154. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch6
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Image of FIGURE 3
FIGURE 3

Model for vesicle accumulation and inhibition of vesicular transport in poliovirus (pv)-infected cells. In uninfected cells (A), secretory material is transported from the ER and the TEN to the -Golgi-network and via the Golgi apparatus further down the secretory pathway. Transport in this direction (anterograde transport) is inhibited by BFA, whereas backward (retrograde) transport remains unaffected by BFA. Infection (B and C) leads to the accumulation of poliovirus-induced vesicles (pvv). The inhibitory effect of BFA on poliovirus replication may be because the generation of poliovirus-induced vesicles is inhibited. A viral product may inhibit further transport of virus-induced vesicles and therefore cause vesicle accumulation and secretion inhibition. This virus-induced block of membrane traffic may lead to the disintegration of the Golgi apparatus, which may be consumed by upstream (B) or downstream (C) compartments as schematically depicted for a Golgi resident protein (☆). For details, see the text.

Citation: Schlegel A, Kirkegaard K. 1995. Cell Biology of Enterovirus Infection, p 135-154. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch6
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Image of FIGURE 4
FIGURE 4

Models for release of poliovirus from polarized Caco-2 cells, redrawn from reference 94. (A) Cell membrane of infected cell within an epithelial sheet lyses on its apical surface only. (B) An infected cell is expelled from an epithelial sheet before lysis. (C) A portion of the cytoplasm of an infected cell that contains a high concentration of virus, termed viroplasm, is released from the infected cell without cell lysis.

Citation: Schlegel A, Kirkegaard K. 1995. Cell Biology of Enterovirus Infection, p 135-154. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch6
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Tables

Generic image for table
TABLE 1

Known effects of individual viral proteins on host functions or proteins

Citation: Schlegel A, Kirkegaard K. 1995. Cell Biology of Enterovirus Infection, p 135-154. In Rotbart H (ed), Human Enterovirus Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818326.ch6

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