Decay-Accelerating Factor Binding Determines the Entry Route of Echovirus 11 in Polarized Epithelial Cells

Sobo, Komla; Rubbia‐Brandt, Laura; Brown, T. D. K.; Stuart, Amanda D.; Mckee, Thomas Alexander

doi:10.1128/jvi.00016-11

Cited by 20 publications

(20 citation statements)

References 56 publications

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“…TJ components have been shown to play a crucial role in the life-cycle of many viruses. Proteins of TJ complex promote viral infection by acting as receptors/co-receptors for viral entry [52], [53]. RNA viruses such as vesicular stomatitis virus, influenza virus and rotavirus have been shown to influence the permeability barrier functions of epithelial cells with or without cytopathic effects at later stages of infection [54], [55].…”

Section: Discussionmentioning

confidence: 99%

Japanese Encephalitis Virus Disrupts Cell-Cell Junctions and Affects the Epithelial Permeability Barrier Functions

et al. 2013

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Japanese encephalitis virus (JEV) is a neurotropic flavivirus, which causes viral encephalitis leading to death in about 20–30% of severely-infected people. Although JEV is known to be a neurotropic virus its replication in non-neuronal cells in peripheral tissues is likely to play a key role in viral dissemination and pathogenesis. We have investigated the effect of JEV infection on cellular junctions in a number of non-neuronal cells. We show that JEV affects the permeability barrier functions in polarized epithelial cells at later stages of infection. The levels of some of the tight and adherens junction proteins were reduced in epithelial and endothelial cells and also in hepatocytes. Despite the induction of antiviral response, barrier disruption was not mediated by secreted factors from the infected cells. Localization of tight junction protein claudin-1 was severely perturbed in JEV-infected cells and claudin-1 partially colocalized with JEV in intracellular compartments and targeted for lysosomal degradation. Expression of JEV-capsid alone significantly affected the permeability barrier functions in these cells. Our results suggest that JEV infection modulates cellular junctions in non-neuronal cells and compromises the permeability barrier of epithelial and endothelial cells which may play a role in viral dissemination in peripheral tissues.

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Section: Discussionmentioning

confidence: 99%

Japanese Encephalitis Virus Disrupts Cell-Cell Junctions and Affects the Epithelial Permeability Barrier Functions

et al. 2013

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“…2). More importantly, the overall change in the apical F-actin organization was concomitant with the transfer of EV11-207 to tight junctions (Sobo et al, 2011) where a clear colocalization of the virus, F-actin and ZO-1 was observed (Fig. 2).…”

Section: Ev11-207 Binding Induces Actin Rearrangementmentioning

confidence: 91%

Echovirus 11 infection induces dramatic changes in the actin cytoskeleton of polarized Caco-2 cells

Sobo

Stuart

Rubbia‐Brandt

et al. 2012

Journal of General Virology

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Binding of echovirus 11 strain 207 (EV11-207) to Caco-2 monolayers results in rapid transfer of the virus to tight junctions prior to uptake. Using a confocal microscopy based-method, this study quantified the spatiotemporal distribution of actin during the time course of infection by EV11-207 in Caco-2 polarized cells. It was found that binding of EV11-207 to the apical surface resulted in rapid rearrangement of the actin cytoskeleton, concomitant with transport of the virus particles to tight junctions. By interfering with the actin network dynamics, the virus remained trapped at the cell surface, leading to abortion of infection. In addition, it was observed that at 4 h post-infection, concomitant with the detection of virus replication, actin filament was depolymerized and degraded. Finally, it was shown that the mechanisms leading to loss of actin were independent of viral genome synthesis, indicating a potential role for the viral protein synthesis seen in late infection. These data confirmed a previous study on the requirement for an intact actin cytoskeleton for EV11-207 to infect cells and reinforce the notion of actin cytoskeleton subversion by picornaviruses during infection in polarized epithelial cells

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“…The example of variant Nar3 is not unprecedented, since single or a few amino acid changes in echovirus (46), enterovirus (47)(48)(49), coxsackievirus (50)(51)(52), and foot-and-mouth disease virus (53)(54)(55) have been shown to be sufficient to alter the receptor specificity and the endocytic mode of entry of these viruses. In the case of rotaviruses, however, it seems that the cell surface molecule used to attach to cells does not by itself determine the type of endocytosis pathway employed for virus cell entry.…”

Section: Discussionmentioning

confidence: 99%

The Spike Protein VP4 Defines the Endocytic Pathway Used by Rotavirus To Enter MA104 Cells

Díaz-Salinas

Romero

Espinosa

et al. 2013

J Virol

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bRotaviruses are internalized into MA104 cells by endocytosis, with different endocytic pathways used depending on the virus strain. The bovine rotavirus UK strain enters cells through a clathrin-mediated endocytic process, while the simian rhesus rotavirus (RRV) strain uses a poorly defined endocytic pathway that is clathrin and caveolin independent. The viral surface protein VP7 and the spike protein VP4 interact with cellular receptors during cell binding and penetration. To determine the viral protein that defines the mechanism of internalization, we used a panel of UK ؋ RRV reassortant viruses having different combinations of the viral structural proteins. Characterization of the infectivities of these reassortants in MA104 cells either transfected with a small interfering RNA (siRNA) against the heavy chain of clathrin or incubated with hypertonic medium that destabilizes the clathrin coat clearly showed that VP4 determines the pathway of virus entry. Of interest, the characterization of Nar3, a sialic acid-independent variant of RRV, showed that a single amino acid change in VP4 shifts the route of entry from being clathrin dependent to clathrin independent. Furthermore, characterizations of several additional rotavirus strains that differ in their use of cellular receptors showed that all entered cells by clathrin-mediated endocytosis, suggesting that diverse VP4-cell surface interactions can lead to rotavirus cell entry through this endocytic pathway.

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Decay-Accelerating Factor Binding Determines the Entry Route of Echovirus 11 in Polarized Epithelial Cells

Cited by 20 publications

References 56 publications

Japanese Encephalitis Virus Disrupts Cell-Cell Junctions and Affects the Epithelial Permeability Barrier Functions

Japanese Encephalitis Virus Disrupts Cell-Cell Junctions and Affects the Epithelial Permeability Barrier Functions

Echovirus 11 infection induces dramatic changes in the actin cytoskeleton of polarized Caco-2 cells

The Spike Protein VP4 Defines the Endocytic Pathway Used by Rotavirus To Enter MA104 Cells

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