Viral transport and the cytoskeleton

Ploubidou, Aspasia; Way, Michael

doi:10.1016/s0955-0674(00)00180-0

Cited by 134 publications

(110 citation statements)

References 83 publications

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“…Several bacteria and viruses have been shown to subvert the cytoskeleton for their intracellular trafficking (Dramsi and Cossart, 1998;Frischknecht and Way, 2001;Ploubidou and Way, 2001;Sodeik, 2000). However, despite a growing body of knowledge accumulating in this field, how retroviruses reach the nucleus of the newly infected cell is still poorly understood.…”

Section: Discussionmentioning

confidence: 99%

Targeting of incoming retroviral Gag to the centrosome involves a direct interaction with the dynein light chain 8

Petit

Giron

Tobaly-Tapiero

et al. 2003

Journal of Cell Science

108

124

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The role of cellular proteins in the replication of retroviruses,especially during virus assembly, has been partly unraveled by recent studies. Paradoxically, little is known about the route taken by retroviruses to reach the nucleus at the early stages of infection. To get insight into this stage of virus replication, we have studied the trafficking of foamy retroviruses and have previously shown that incoming viral proteins reach the microtubule organizing center (MTOC) prior to nuclear translocation of the viral genome. Here, we show that incoming viruses concentrate around the MTOC as free and structured capsids. Interestingly, the Gag protein, the scaffold component of viral capsids, targets the pericentrosomal region in transfected cells in the absence of any other viral components but in a microtubule- and dynein/dynactin-dependent manner. Trafficking of Gag towards the centrosome requires a minimal 30 amino acid coiled-coil motif in the N-terminus of the molecule. Finally, we describe a direct interaction between Gag and dynein light chain 8 that probably accounts for the specific routing of the incoming capsids to the centrosome prior to nuclear import of the viral genome.

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Section: Discussionmentioning

confidence: 99%

Targeting of incoming retroviral Gag to the centrosome involves a direct interaction with the dynein light chain 8

Petit

Giron

Tobaly-Tapiero

et al. 2003

Journal of Cell Science

108

124

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“…Several reports have documented that some enveloped viruses induce the formation of diverse actin structures to facilitate their internalization into host cells (Cudmore et al, 1997;Higley & Way, 1997;Ploubidou & Way, 2001;Chu et al, 2003Chu et al, , 2006Eash & Atwood, 2005). Viral particles of murine leukemia virus induce actin reorganization to form filopodia to which viruses have been reported to associate before cell infection (Lehmann et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Cross-talk between Rac1 and Cdc42 GTPases regulates formation of filopodia required for dengue virus type-2 entry into HMEC-1 cells

Zamudio-Meza

Castillo

González-Bonilla

et al. 2009

Journal of General Virology

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Infection with dengue virus type-2 (DENV-2) begins with virus adherence to cell surface receptors. In endothelial cells (HMEC-1), a cell model for DENV-2 infection, a5b3 integrin has been identified as a putative receptor for the virus. Previous work had suggested that the actin cytoskeleton of HMEC-1 cells plays an important role in virus entry and infection. In the present work, fixed and living HMEC-1 cells expressing enhanced green fluorescent protein-actin were monitored for actin reorganization after virus inoculation, utilizing fluorescence and time lapse microscopy. Cell infection and production of infective viruses were quantified using an anti-E protein antibody and by measuring the p.f.u. ml . Specific drugs that antagonize actin organization and regulate actin-signalling pathways were tested in viral adhesion and infection assays, as were the expression of dominant-negative Rac1 and Cdc42 proteins. Disorganization of actin precluded infection, while microtubule depolymerization had no effect. Activation of Rac1 and Cdc42 signalling, which occurs upon virus binding, induced reorganization of actin to form filopodia in the cellular periphery. Formation of filopodia was a requirement for virus entry and further cell infection. Expression of the dominant-negative proteins Rac1 and Cdc42 confirmed the role of these GTPases in the actin reorganization that is required to form filopodia. In addition, inhibition of the ATPase activity of myosin II greatly decreased infection, suggesting its participation in filopodial stability. We show here, for the first time, that internalization of DENV-2 into endothelial cells requires viral induction of dynamic filopodia regulated by Rac1 and Cdc42 cross-talk and myosin II motor activities.

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“…Importantly, once viruses enter cells they require cytoplasmic transport to reach specific subcellular sites for replication and egress. Numerous studies have revealed that retrograde and anterograde transport of animal viruses is supported by MTs and their associated proteins (14,15,73,74), and an increasing number of viral proteins that interact with MTs or MAPs have begun to be identified (Table 1). Virus-MAP interactions, be they functional or physical, can promote virus trafficking in an infected cell, by directly facilitating latching on of virus particles to cytoskeletal tracks, or modifying MT dynamics to optimize movement along the tracks.…”

Section: Promotion Of Viral Trafficking By Mapsmentioning

confidence: 99%

Role of non-motile microtubule-associated proteins in virus trafficking

Portilho

Persson²,

Arhel

2016

Biomolecular Concepts

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Viruses are entirely dependent on their ability to infect a host cell in order to replicate. To reach their site of replication as rapidly and efficiently as possible following cell entry, many have evolved elaborate mechanisms to hijack the cellular transport machinery to propel themselves across the cytoplasm. Long-range movements have been shown to involve motor proteins along microtubules (MTs) and direct interactions between viral proteins and dynein and/or kinesin motors have been well described. Although less well-characterized, it is also becoming increasingly clear that non-motile microtubule-associated proteins (MAPs), including structural MAPs of the MAP1 and MAP2 families, and microtubule plus-end tracking proteins (+ TIPs), can also promote viral trafficking in infected cells, by mediating interaction of viruses with filaments and/or motor proteins, and modulating filament stability. Here we review our current knowledge on nonmotile MAPs, their role in the regulation of cytoskeletal dynamics and in viral trafficking during the early steps of infection.

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Viral transport and the cytoskeleton

Cited by 134 publications

References 83 publications

Targeting of incoming retroviral Gag to the centrosome involves a direct interaction with the dynein light chain 8

Targeting of incoming retroviral Gag to the centrosome involves a direct interaction with the dynein light chain 8

Cross-talk between Rac1 and Cdc42 GTPases regulates formation of filopodia required for dengue virus type-2 entry into HMEC-1 cells

Role of non-motile microtubule-associated proteins in virus trafficking

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