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Special Issue "Cytoskeleton in Viral Infections"

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A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (28 February 2011)

Special Issue Editors

Guest Editor
Prof. Dr. Urs Greber (Website)

Institute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland
Interests: membranes; transport; virology; pathogens; infection
Guest Editor
Prof. Dr. Beate Sodeik (Website)

Institute of Virology, OE 5230, Hannover Medical School, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany
Phone: +49 (511) 532 2846
Fax: +49 (0)511 532 8736

Published Papers (11 papers)

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Research

Jump to: Review

Open AccessCommunication Herpesviruses and Intermediate Filaments: Close Encounters with the Third Type
Viruses 2011, 3(7), 1015-1040; doi:10.3390/v3071015
Received: 2 February 2011 / Revised: 7 June 2011 / Accepted: 24 June 2011 / Published: 4 July 2011
Cited by 6 | PDF Full-text (464 KB)
Abstract
Intermediate filaments (IF) are essential to maintain cellular and nuclear integrity and shape, to manage organelle distribution and motility, to control the trafficking and pH of intracellular vesicles, to prevent stress-induced cell death, and to support the correct distribution of specific proteins. [...] Read more.
Intermediate filaments (IF) are essential to maintain cellular and nuclear integrity and shape, to manage organelle distribution and motility, to control the trafficking and pH of intracellular vesicles, to prevent stress-induced cell death, and to support the correct distribution of specific proteins. Because of this, IF are likely to be targeted by a variety of pathogens, and may act in favor or against infection progress. As many IF functions remain to be identified, however, little is currently known about these interactions. Herpesviruses can infect a wide variety of cell types, and are thus bound to encounter the different types of IF expressed in each tissue. The analysis of these interrelationships can yield precious insights into how IF proteins work, and into how viruses have evolved to exploit these functions. These interactions, either known or potential, will be the focus of this review. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)
Open AccessArticle The Dynactin Complex Enhances the Speed of Microtubule-Dependent Motions of Adenovirus Both Towards and Away from the Nucleus
Viruses 2011, 3(3), 233-253; doi:10.3390/v3030233
Received: 10 February 2011 / Accepted: 28 February 2011 / Published: 9 March 2011
Cited by 19 | PDF Full-text (1718 KB) | Supplementary Files
Abstract
Unlike transport vesicles or organelles, human adenovirus (HAdV) directly binds to the microtubule minus end-directed motor dynein for transport to the nucleus. The dynein cofactor dynactin enhances nuclear transport of HAdV and boosts infection. To determine if dynactin has a specific role [...] Read more.
Unlike transport vesicles or organelles, human adenovirus (HAdV) directly binds to the microtubule minus end-directed motor dynein for transport to the nucleus. The dynein cofactor dynactin enhances nuclear transport of HAdV and boosts infection. To determine if dynactin has a specific role in cytoplasmic trafficking of incoming HAdV on microtubules, we used live cell spinning disc confocal microscopy at 25 Hz acquisition frequency and automated tracking of single virus particles at 20–50 nm spatial resolution. Computational dissection by machine-learning algorithms extracted specific motion patterns of viral trajectories. We found that unperturbed cells supported two kinds of microtubule-dependent motions, directed motions (DM) and fast drifts (FD). DM had speeds of 0.2 to 2 µm/s and run lengths of 0.4 up to 7 µm, while FD were slower and less extensive at 0.02 to 0.4 µm/s and 0.05 to 2.5 µm. Dynactin interference by overexpression of p50/dynamitin or a coiled-coil domain of p150/Glued reduced the speeds and amounts of both center- and periphery-directed DM but not FD, and inhibited infection. These results indicate that dynactin enhances adenovirus infection by increasing the speed and efficiency of dynein-mediated virus motion to the nucleus, and, surprisingly, also supports a hereto unknown motor activity for virus transport to the cell periphery. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)

Review

Jump to: Research

Open AccessReview The Actin Cytoskeleton as a Barrier to Virus Infection of Polarized Epithelial Cells
Viruses 2011, 3(12), 2462-2477; doi:10.3390/v3122462
Received: 17 November 2011 / Revised: 7 December 2011 / Accepted: 15 December 2011 / Published: 21 December 2011
Cited by 24 | PDF Full-text (845 KB) | HTML Full-text | XML Full-text
Abstract
Many diverse viruses target a polarized epithelial monolayer during host invasion. The polarized epithelium is adept at restricting the movement of solutes, ions, macromolecules, and pathogens across the mucosa. This regulation can be attributed to the presence of a junctional complex between [...] Read more.
Many diverse viruses target a polarized epithelial monolayer during host invasion. The polarized epithelium is adept at restricting the movement of solutes, ions, macromolecules, and pathogens across the mucosa. This regulation can be attributed to the presence of a junctional complex between adjacent cells and to an intricate network of actin filaments that provides support to the subapical membrane and stabilizes intercellular junctions. It is therefore not surprising that many viruses have evolved highly varied strategies to dissolve or modulate the cortical actin meshwork to promote infection of polarized cells. In this review, we will discuss the cell biological properties of the actin cytoskeleton in polarized epithelial cells and review the known mechanisms utilized by viral pathogens to manipulate this system in order to facilitate their infection. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)
Open AccessReview How HIV-1 Takes Advantage of the Cytoskeleton during Replication and Cell-to-Cell Transmission
Viruses 2011, 3(9), 1757-1776; doi:10.3390/v3091757
Received: 8 July 2011 / Revised: 26 August 2011 / Accepted: 30 August 2011 / Published: 15 September 2011
Cited by 13 | PDF Full-text (2443 KB)
Abstract
Human immunodeficiency virus 1 (HIV-1) infects T cells, macrophages and dendritic cells and can manipulate their cytoskeleton structures at multiple steps during its replication cycle. Based on pharmacological and genetic targeting of cytoskeleton modulators, new imaging approaches and primary cell culture models, [...] Read more.
Human immunodeficiency virus 1 (HIV-1) infects T cells, macrophages and dendritic cells and can manipulate their cytoskeleton structures at multiple steps during its replication cycle. Based on pharmacological and genetic targeting of cytoskeleton modulators, new imaging approaches and primary cell culture models, important roles for actin and microtubules during entry and cell-to-cell transfer have been established. Virological synapses and actin-containing membrane extensions can mediate HIV-1 transfer from dendritic cells or macrophage cells to T cells and between T cells. We will review the role of the cytoskeleton in HIV-1 entry, cellular trafficking and cell-to-cell transfer between primary cells. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)
Open AccessReview Adenovirus Recruits Dynein by an Evolutionary Novel Mechanism Involving Direct Binding to pH-Primed Hexon
Viruses 2011, 3(8), 1417-1431; doi:10.3390/v3081417
Received: 19 July 2011 / Revised: 3 August 2011 / Accepted: 6 August 2011 / Published: 12 August 2011
Cited by 15 | PDF Full-text (480 KB)
Abstract
Following receptor-mediated uptake into endocytic vesicles and escape from the endosome, adenovirus is transported by cytoplasmic dynein along microtubules to the perinuclear region of the cell. How motor proteins are recruited to viruses for their own use has begun to be investigated [...] Read more.
Following receptor-mediated uptake into endocytic vesicles and escape from the endosome, adenovirus is transported by cytoplasmic dynein along microtubules to the perinuclear region of the cell. How motor proteins are recruited to viruses for their own use has begun to be investigated only recently. We review here the evidence for a role for dynein and other motor proteins in adenovirus infectivity. We also discuss the implications of recent studies on the mechanism of dynein recruitment to adenovirus for understanding the relationship between pathogenic and physiological cargo recruitment and for the evolutionary origins of dynein-mediated adenovirus transport. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)
Figures

Open AccessReview Alphaherpesviruses and the Cytoskeleton in Neuronal Infections
Viruses 2011, 3(7), 941-981; doi:10.3390/v3070941
Received: 11 May 2011 / Revised: 3 June 2011 / Accepted: 17 June 2011 / Published: 27 June 2011
Cited by 16 | PDF Full-text (644 KB)
Abstract
Following infection of exposed peripheral tissues, neurotropic alphaherpesviruses invade nerve endings and deposit their DNA genomes into the nuclei of neurons resident in ganglia of the peripheral nervous system. The end result of these events is the establishment of a life-long latent [...] Read more.
Following infection of exposed peripheral tissues, neurotropic alphaherpesviruses invade nerve endings and deposit their DNA genomes into the nuclei of neurons resident in ganglia of the peripheral nervous system. The end result of these events is the establishment of a life-long latent infection. Neuroinvasion typically requires efficient viral transmission through a polarized epithelium followed by long-distance transport through the viscous axoplasm. These events are mediated by the recruitment of the cellular microtubule motor proteins to the intracellular viral particle and by alterations to the cytoskeletal architecture. The focus of this review is the interplay between neurotropic herpesviruses and the cytoskeleton. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)
Open AccessReview Actin in Herpesvirus Infection
Viruses 2011, 3(4), 336-346; doi:10.3390/v3040336
Received: 9 February 2011 / Revised: 24 March 2011 / Accepted: 28 March 2011 / Published: 12 April 2011
Cited by 21 | PDF Full-text (242 KB)
Abstract
Actin is important for a variety of cellular processes, including uptake of extracellular material and intracellular transport. Several emerging lines of evidence indicate that herpesviruses exploit actin and actin-associated myosin motors for viral entry, intranuclear transport of capsids, and virion egress. The goal [...] Read more.
Actin is important for a variety of cellular processes, including uptake of extracellular material and intracellular transport. Several emerging lines of evidence indicate that herpesviruses exploit actin and actin-associated myosin motors for viral entry, intranuclear transport of capsids, and virion egress. The goal of this review is to explore these processes and to highlight potential future directions for this area of research. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)
Figures

Open AccessReview How HIV Takes Advantage of the Cytoskeleton in Entry and Replication
Viruses 2011, 3(4), 293-311; doi:10.3390/v3040293
Received: 2 February 2011 / Revised: 11 March 2011 / Accepted: 19 March 2011 / Published: 28 March 2011
Cited by 26 | PDF Full-text (474 KB)
Abstract
The host cell cytoskeleton plays a key role in the life cycle of viral pathogens whose propagation depends on mandatory intracellular steps. Accordingly, also the human immunodeficiency virus type 1 (HIV-1) has evolved strategies to exploit and modulate in particular the actin [...] Read more.
The host cell cytoskeleton plays a key role in the life cycle of viral pathogens whose propagation depends on mandatory intracellular steps. Accordingly, also the human immunodeficiency virus type 1 (HIV-1) has evolved strategies to exploit and modulate in particular the actin cytoskeleton for its purposes. This review will recapitulate recent findings on how HIV-1 hijacks the cytoskeleton to facilitate entry into, transport within and egress from host cells as well as to commandeer communication of infected with uninfected bystander cells. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)
Open AccessReview Actin’ up: Herpesvirus Interactions with Rho GTPase Signaling
Viruses 2011, 3(4), 278-292; doi:10.3390/v3040278
Received: 31 January 2011 / Revised: 15 March 2011 / Accepted: 16 March 2011 / Published: 24 March 2011
Cited by 7 | PDF Full-text (321 KB)
Abstract
Herpesviruses constitute a very large and diverse family of DNA viruses, which can generally be subdivided in alpha-, beta- and gammaherpesvirus subfamilies. Increasing evidence indicates that many herpesviruses interact with cytoskeleton-regulating Rho GTPase signaling pathways during different phases of their replication cycle. [...] Read more.
Herpesviruses constitute a very large and diverse family of DNA viruses, which can generally be subdivided in alpha-, beta- and gammaherpesvirus subfamilies. Increasing evidence indicates that many herpesviruses interact with cytoskeleton-regulating Rho GTPase signaling pathways during different phases of their replication cycle. Because of the large differences between herpesvirus subfamilies, the molecular mechanisms and specific consequences of individual herpesvirus interactions with Rho GTPase signaling may differ. However, some evolutionary distinct but similar general effects on Rho GTPase signaling and the cytoskeleton have also been reported. Examples of these include Rho GTPase-mediated nuclear translocation of virus during entry in a host cell and Rho GTPase-mediated viral cell-to-cell spread during later stages of infection. The current review gives an overview of both general and individual interactions of herpesviruses with Rho GTPase signaling. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)
Open AccessReview The Cytoskeleton in Papillomavirus Infection
Viruses 2011, 3(3), 260-271; doi:10.3390/v3030260
Received: 10 February 2011 / Revised: 1 March 2011 / Accepted: 2 March 2011 / Published: 10 March 2011
Cited by 6 | PDF Full-text (139 KB)
Abstract
Cytoskeleton defines the shape and structural organization of the cell. Its elements participate in cell motility, intracellular transport and chromosome movement during mitosis. Papillomaviruses (PV) are strictly epitheliotropic and induce self-limiting benign tumors of skin and mucosa, which may progress to malignancy. [...] Read more.
Cytoskeleton defines the shape and structural organization of the cell. Its elements participate in cell motility, intracellular transport and chromosome movement during mitosis. Papillomaviruses (PV) are strictly epitheliotropic and induce self-limiting benign tumors of skin and mucosa, which may progress to malignancy. Like many other viruses, PV use the host cytoskeletal components for several steps during their life cycle. Prior to internalization, PV particles are transported along filopodia to the cell body. Following internalization, retrograde transport along microtubules via the dynein motor protein complex is observed. In addition, viral minichromosomes depend on the host cell machinery for partitioning of viral genomes during mitosis, which may be affected by oncoproteins E6 and E7 of high-risk human PV types. This mini-review summarizes recent advances in our understanding of papillomavirus’ interactions with the host cell cytoskeletal elements. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)
Open AccessReview Cytoskeletal Dynamics: Concepts in Measles Virus Replication and Immunomodulation
Viruses 2011, 3(2), 102-117; doi:10.3390/v3020102
Received: 6 December 2010 / Revised: 20 January 2011 / Accepted: 20 January 2011 / Published: 26 January 2011
Cited by 6 | PDF Full-text (293 KB)
Abstract
In common with most viruses, measles virus (MV) relies on the integrity of the cytoskeleton of its host cells both with regard to efficient replication in these cells, but also retention of their motility which favors viral dissemination. It is, however, the [...] Read more.
In common with most viruses, measles virus (MV) relies on the integrity of the cytoskeleton of its host cells both with regard to efficient replication in these cells, but also retention of their motility which favors viral dissemination. It is, however, the surface interaction of the viral glycoprotein (gp) complex with receptors present on lymphocytes and dendritic cells (DCs), that signals effective initiation of host cell cytoskeletal dynamics. For DCs, these may act to regulate processes as diverse as viral uptake and sorting, but also the ability of these cells to successfully establish and maintain functional immune synapses (IS) with T cells. In T cells, MV signaling causes actin cytoskeletal paralysis associated with a loss of polarization, adhesion and motility, which has been linked to activation of sphingomyelinases and subsequent accumulation of membrane ceramides. MV modulation of both DC and T cell cytoskeletal dynamics may be important for the understanding of MV immunosuppression at the cellular level. Full article
(This article belongs to the Special Issue Cytoskeleton in Viral Infections)

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