Do viruses require the cytoskeleton?

Matthews, Jonathan; Morgan, Rachel; Sleigher, Christie; Frey, Teryl K.

doi:10.1186/1743-422x-10-121

Cited by 24 publications

(25 citation statements)

References 13 publications

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“…Furthermore, VSV transport to the cell surface is reported to be Research article MT-dependent (Das et al, 2006). However, a recent study found no effect of MT depolymerization on VSV and SINV replication (Matthews et al, 2013). Thus the role of MTs in VSV and SINV replication remains unresolved.…”

Section: Discussionmentioning

confidence: 99%

A single vertebrate DNA virus protein disarms invertebrate immunity to RNA virus infection

Gammon

Duraffour

Rozelle

et al. 2014

eLife

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Virus-host interactions drive a remarkable diversity of immune responses and countermeasures. We found that two RNA viruses with broad host ranges, vesicular stomatitis virus (VSV) and Sindbis virus (SINV), are completely restricted in their replication after entry into Lepidopteran cells. This restriction is overcome when cells are co-infected with vaccinia virus (VACV), a vertebrate DNA virus. Using RNAi screening, we show that Lepidopteran RNAi, Nuclear Factor-κB, and ubiquitin-proteasome pathways restrict RNA virus infection. Surprisingly, a highly conserved, uncharacterized VACV protein, A51R, can partially overcome this virus restriction. We show that A51R is also critical for VACV replication in vertebrate cells and for pathogenesis in mice. Interestingly, A51R colocalizes with, and stabilizes, host microtubules and also associates with ubiquitin. We show that A51R promotes viral protein stability, possibly by preventing ubiquitin-dependent targeting of viral proteins for destruction. Importantly, our studies reveal exciting new opportunities to study virus-host interactions in experimentally-tractable Lepidopteran systems.DOI: http://dx.doi.org/10.7554/eLife.02910.001

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Section: Discussionmentioning

confidence: 99%

A single vertebrate DNA virus protein disarms invertebrate immunity to RNA virus infection

Gammon

Duraffour

Rozelle

et al. 2014

eLife

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“…Reports have been inconsistent in describing the effect on virus release of drugs that disrupt the cytoskeleton (4,(23)(24)(25). One of the problems is that viral mRNAs require cytoskeletal function to be efficiently translated (13,26).…”

Section: Resultsmentioning

confidence: 99%

Migration of Nucleocapsids in Vesicular Stomatitis Virus-Infected Cells Is Dependent on both Microtubules and Actin Filaments

Yacovone

Smelser

Macosko

et al. 2016

J Virol

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The distribution of vesicular stomatitis virus (VSV) nucleocapsids in the cytoplasm of infected cells was analyzed by scanning confocal fluorescence microscopy using a newly developed quantitative approach called the border-to-border distribution method. Nucleocapsids were located near the cell nucleus at early times postinfection (2 h) but were redistributed during infection toward the edges of the cell. This redistribution was inhibited by treatment with nocodazole, colcemid, or cytochalasin D, indicating it is dependent on both microtubules and actin filaments. The role of actin filaments in nucleocapsid mobility was also confirmed by live-cell imaging of fluorescent nucleocapsids of a virus containing P protein fused to enhanced green fluorescent protein. However, in contrast to the overall redistribution in the cytoplasm, the incorporation of nucleocapsids into virions as determined in pulse-chase experiments was dependent on the activity of actin filaments with little if any effect on inhibition of microtubule function. These results indicate that the mechanisms by which nucleocapsids are transported to the farthest reaches of the cell differ from those required for incorporation into virions. This is likely due to the ability of nucleocapsids to follow shorter paths to the plasma membrane mediated by actin filaments. IMPORTANCENucleocapsids of nonsegmented negative-strand viruses like VSV are assembled in the cytoplasm during genome RNA replication and must migrate to the plasma membrane for assembly into virions. Nucleocapsids are too large to diffuse in the cytoplasm in the time required for virus assembly and must be transported by cytoskeletal elements. Previous results suggested that microtubules were responsible for migration of VSV nucleocapsids to the plasma membrane for virus assembly. Data presented here show that both microtubules and actin filaments are responsible for mobility of nucleocapsids in the cytoplasm, but that actin filaments play a larger role than microtubules in incorporation of nucleocapsids into virions. N ucleocapsids of negative-strand RNA viruses must be transported from their sites of assembly in the cytoplasm to sites of virus budding from host membranes (1). For example, the nucleocapsids of vesicular stomatitis virus (VSV) behave as random coils with a hydrodynamic radius of approximately 90 nm (2), which is too large to diffuse through the cytoplasm in the time required for virus assembly (3). Transport of nucleocapsids to the membrane after assembly in the cytoplasm has been proposed to occur primarily along microtubules (4). The goal of the experiments presented here was to further test mechanisms of nucleocapsid transport by evaluating both microtubule-dependent and actin-dependent transport using recently developed analytical tools.Actin filaments and microtubules have a general orientation in which the growing (plus) end is oriented toward the cell periphery and the minus end is oriented toward the center of the cell (5). Assembly of microtubules is usually...

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“…Cytoskeleton is important for maintenance of cell shape, cell motility and intracellular transport [21], and it is generally thought that viruses need cytoskeleton during infection [20]. Here the interaction of several cytoskeletonassociated proteins with BmNPV was determined, and they were actin, enolase (En) and phosphoglycerate kinase (PGK).…”

Section: Discussionmentioning

confidence: 99%

A hypothetical model of crossingBombyx morinucleopolyhedrovirus through its host midgut physical barrier

Xu¹

2016

2016 International Congress of Entomology

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Bombyx mori nucleopolyhedrovirus (BmNPV) is a primary pathogen of silkworm (B. mori) that causes severe economic losses each year. However, the molecular mechanisms of silkworm-BmNPV interactions, especially the silkworm proteins that can interact with the virus, are still largely unknown. In this study, the total and membrane proteins of silkworm midguts were displayed using one-and twodimensional electrophoresis. A virus overlay assay was used to detect B. mori proteins that specifically bind to BmNPV particles. Twelve proteins were located and identified using mass spectrometry, and the different expression of the corresponding genes in BmNPV susceptible and resistant silkworm strains also indicated their involvement in BmNPV infection. The 12 proteins are grouped based on their potential roles in viral infection, for example, endocytosis, intracellular transportation, and host responses. Based on these results, we hypothesize the following: I) vacuolar ATP synthase catalytic subunit A and subunit B may be implicated in the process of the membrane fusion of virus and the release of the nucleocapsid into cytoplasm; II) actin, enolase and phosphoglycerate kinase are cytoskeleton associated proteins and may play an important role in BmNPV intracellular transportation; III) mitochondrial prohibitin complex protein 2, ganglioside-induced differentiation-associated protein, calreticulin, regucalcin-like isoform X1 and 60 kDa heat shock protein are involved in cell apoptosis regulation during BmNPV infection in larvae midguts; IV) ribosomal P0 may be associated with BmNPV infection by regulating gene expression of BmNPV; V) arginine kinase has a role in the antiviral activities against BmNPV. Our work should prove

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Do viruses require the cytoskeleton?

Cited by 24 publications

References 13 publications

A single vertebrate DNA virus protein disarms invertebrate immunity to RNA virus infection

A single vertebrate DNA virus protein disarms invertebrate immunity to RNA virus infection

Migration of Nucleocapsids in Vesicular Stomatitis Virus-Infected Cells Is Dependent on both Microtubules and Actin Filaments

A hypothetical model of crossingBombyx morinucleopolyhedrovirus through its host midgut physical barrier

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