Inhibition of Clathrin-dependent Endocytosis Has Multiple Effects on Human Rhinovirus Serotype 2 Cell Entry

Bayer, Nora; Schober, Daniela; Hüttinger, Manfred; Blaas, Dieter; Fuchs, Renate

doi:10.1074/jbc.m004722200

Cited by 59 publications

(68 citation statements)

References 60 publications

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“…Notably, bafilomycin A1 may interfere with the endocytic route in two different ways. Bafilomycin A1 is known to prevent endosomal acidification by blocking vacuolar proton ATPase, but it also blocks the transport from early to late endosomes (37,66). Direct support for the relevance of endocytic uptake for cell entry was provided by the inhibition of ARV infection with M␤CD and nystatin together with dynamin-2 and caveolin-1 siRNA.…”

Section: Discussionmentioning

confidence: 99%

Cell Entry of Avian Reovirus Follows a Caveolin-1-mediated and Dynamin-2-dependent Endocytic Pathway That Requires Activation of p38 Mitogen-activated Protein Kinase (MAPK) and Src Signaling Pathways as Well as Microtubules and Small GTPase Rab5 Protein

Huang

Wang

et al. 2011

Journal of Biological Chemistry

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Very little is known about the mechanism of cell entry of avian reovirus (ARV). The aim of this study was to explore the mechanism of ARV entry and subsequent infection. Cholesterol mainly affected the early steps of the ARV life cycle, because the presence of cholesterol before and during viral adsorption greatly blocked ARV infectivity. Although we have demonstrated that ARV facilitating p38 MAPK is beneficial for virus replication, its mechanism remains unknown. Here, we show that ARV-induced phosphorylation of caveolin-1 (Tyr 14 ), dynamin-2 expression, and Rac1 activation through activation of p38 MAPK and Src in the early stage of the virus life cycle is beneficial for virus entry and productive infection. The strong inhibition by dynasore, a specific inhibitor of dynamin-2, and depletion of endogenous caveolin-1 or dynamin-2 by siRNAs as well as the caveolin-1 colocalization study implicate caveolin-1-mediated and dynamin-2-dependent endocytosis as a significant avenue of ARV entry. By means of pharmacological inhibitors, dominant negative mutants, and siRNA of various cellular proteins and signaling molecules, phosphorylation of caveolin-1, dynamin-2 expression, and Rac1 activation were suppressed, suggesting that by orchestrating p38 MAPK, Src, and Rac1 signaling cascade in the target cells, ARV creates an appropriate intracellular environment facilitating virus entry and productive infection. Furthermore, disruption of microtubules, Rab5, or endosome acidification all inhibited ARV infection, suggesting that microtubules and small GTPase Rab5, which regulate transport to early endosome, are crucial for survival of ARV and that exposure of the virus to acidic pH is required for productive infection.

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Section: Discussionmentioning

confidence: 99%

Cell Entry of Avian Reovirus Follows a Caveolin-1-mediated and Dynamin-2-dependent Endocytic Pathway That Requires Activation of p38 Mitogen-activated Protein Kinase (MAPK) and Src Signaling Pathways as Well as Microtubules and Small GTPase Rab5 Protein

Huang

Wang

et al. 2011

Journal of Biological Chemistry

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“…Heparinase I and III digestions were performed at 37 uC in an isotonic buffer containing KCl (10 mM KCl, 130 mM NaCl, 20 mM HEPES, 1 mM CaCl 2 , 1 mM MgCl 2 , 1 mg glucose ml 21 and 0.5 % BSA, pH 7.4) in order to avoid disruption of clathrin-mediated endocytosis (Bayer et al, 2001;Culp et al, 2006a). Cells and ECM were rinsed with PBS and then fixed following digestion.…”

Section: Methodsmentioning

confidence: 99%

Differential binding patterns to host cells associated with particles of several human alphapapillomavirus types

Broutian

Brendle

Christensen

2009

Journal of General Virology

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The focus of this research was to compare the binding profiles of human papillomavirus (HPV) 11, 16, 18 and 45 virus-like particles (VLPs) to HaCaT cells and to the extracellular matrix (ECM) secreted by these cells. All four HPV types tested bind to a component(s) of the ECM. HPV11 VLP binding is blocked when the ECM is pretreated with an anti-laminin 5 (LN5) polyclonal antibody. A series of treatments utilizing heparins and heparinase revealed that HPV18 VLPs are dependent on heparan sulfates (HS) for binding to cells and ECM. HPV16 and HPV45 VLPs are dependent on HS for binding to HaCaT cells and dependent on both HS and LN5 for binding to ECM. These studies emphasize the need to study the binding characteristics of different HPV types before applying universal binding principles to all papillomaviruses.

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“…Clathrinmediated endocytosis was assessed by K ϩ depletion following hypotonic shock and by inhibition with chlorpromazine. K ϩ depletion following hypotonic shock was performed by cell exposure to hypotonic medium, followed by incubation in the absence of extracellular potassium (32)(33)(34). This treatment results in dissociation of clathrin coats from the plasma membrane and nonproductive assembly of clathrin cages in the cytoplasm adjacent to coated pits.…”

Section: Capture Of Ppv-vlps Requires Macropinocytosis Lipids Raftsmentioning

confidence: 99%

In Vivo, Dendritic Cells Can Cross-Present Virus-Like Particles Using an Endosome-to-Cytosol Pathway

Morón

Rueda

Sedlik

2003

The Journal of Immunology

102

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Recombinant parvovirus-like particles (PPV-VLPs) are particulate exogenous Ags that induce strong CTL response in the absence of adjuvant. In the present report to decipher the mechanisms responsible for CTL activation by such exogenous Ag, we analyzed ex vivo and in vitro the mechanisms of capture and processing of PPV-VLPs by dendritic cells (DCs). In vivo, PPV-VLPs are very efficiently captured by CD8α− and CD8α+ DCs and then localize in late endosomes of DCs. Macropinocytosis and lipid rafts participate in PPV-VLPs capture. Processing of PPV-VLPs does not depend upon recycling of MHC class I molecules, but requires vacuolar acidification as well as proteasome activity, TAP translocation, and neosynthesis of MHC class I molecules. This study therefore shows that in vivo DCs can cross-present PPV-VLPs using an endosome-to-cytosol processing pathway.

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Inhibition of Clathrin-dependent Endocytosis Has Multiple Effects on Human Rhinovirus Serotype 2 Cell Entry

Cited by 59 publications

References 60 publications

Cell Entry of Avian Reovirus Follows a Caveolin-1-mediated and Dynamin-2-dependent Endocytic Pathway That Requires Activation of p38 Mitogen-activated Protein Kinase (MAPK) and Src Signaling Pathways as Well as Microtubules and Small GTPase Rab5 Protein

Cell Entry of Avian Reovirus Follows a Caveolin-1-mediated and Dynamin-2-dependent Endocytic Pathway That Requires Activation of p38 Mitogen-activated Protein Kinase (MAPK) and Src Signaling Pathways as Well as Microtubules and Small GTPase Rab5 Protein

Differential binding patterns to host cells associated with particles of several human alphapapillomavirus types

In Vivo, Dendritic Cells Can Cross-Present Virus-Like Particles Using an Endosome-to-Cytosol Pathway

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