Viral Manipulation of Host Cytoskeletal Networks

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

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 14637

Special Issue Editor

Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
Interests: DNA virus; RNA virus; innate immunity; viral pathogenesis; immune evasion
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The aim of this Special Issue is to highlight new examples of the diverse mechanisms by which viral pathogens manipulate the host cytoskeleton during infection.

The cytoskeleton comprises several proteinaceous filaments: actin microfilaments, intermediate filaments, microtubules, and septins, which function in various aspects of cellular biology including the maintenance of cell morphology, regulation of cell motility and division, endocytosis, and intracellular transport of organelles, vesicles, and protein cargo. Moreover, growing evidence suggests that the cytoskeleton also plays critical roles in the immunological response to pathogen infection.

Given the wide variety of cellular functions that could be manipulated by viral interaction with the host cytoskeleton, it is perhaps not surprising that examples of viral manipulation of the host cytoskeleton can be found at virtually all stages of the viral life cycle. From usurping actin-dependent endocytic routes for viral entry to the hijacking of microtubule motor proteins for viral trafficking to and from replication sites, it has become clear that disparate viruses have acquired both unique and common mechanisms to manipulate the host cytoskeleton to facilitate their replication. Understanding the key roles played by the cytoskeleton in the viral life cycle may reveal new therapeutic strategies to prevent or treat viral disease. At the same time, viruses could also reveal basic cellular mechanisms and pathways controlling cytoskeleton-dependent processes within the cell.

All researchers working in the field are encouraged to contribute original research papers to this Special Issue of Viruses that feature new examples of viruses usurping, manipulating, or regulating components of the cytoskeleton to facilitate viral replication and/or immune evasion.

Dr. Don Gammon
Guest Editor

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Keywords

  • virus
  • virus-host interactions
  • cytoskeleton
  • microtubules
  • intermediate filaments
  • septins
  • viral trafficking
  • microtubule-associated proteins
  • nucleation
  • motor proteins

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Published Papers (5 papers)

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Editorial

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2 pages, 161 KiB  
Editorial
Manipulation of the Host Cytoskeleton by Viruses: Insights and Mechanisms
by Dahee Seo and Don B. Gammon
Viruses 2022, 14(7), 1586; https://doi.org/10.3390/v14071586 - 21 Jul 2022
Cited by 6 | Viewed by 1512
Abstract
The eukaryotic cytoskeleton comprises a network of actin, microtubules, and intermediate filaments that not only provide mechanical support to maintain cell morphology but also serve many other critical roles in cell motility, division, and intracellular transport of cargo such as vesicles and organelles [...] Read more.
The eukaryotic cytoskeleton comprises a network of actin, microtubules, and intermediate filaments that not only provide mechanical support to maintain cell morphology but also serve many other critical roles in cell motility, division, and intracellular transport of cargo such as vesicles and organelles [...] Full article
(This article belongs to the Special Issue Viral Manipulation of Host Cytoskeletal Networks)

Research

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13 pages, 2027 KiB  
Article
Host Cytoskeleton Gene Expression Is Correlated with the Formation of Ascovirus Reproductive Viral Vesicles
by Heba A. H. Zaghloul, Peter Arensburger and Brian A. Federici
Viruses 2022, 14(7), 1444; https://doi.org/10.3390/v14071444 - 30 Jun 2022
Cited by 1 | Viewed by 1817
Abstract
Ascoviruses are large DNA viruses that primarily infect lepidopteran larvae. They differ markedly from other plant or animal viruses by initiating replication in the nucleus, then inducing nuclear lysis followed by extensive cellular hypertrophy and subsequent cleavage of the entire enlarged cell into [...] Read more.
Ascoviruses are large DNA viruses that primarily infect lepidopteran larvae. They differ markedly from other plant or animal viruses by initiating replication in the nucleus, then inducing nuclear lysis followed by extensive cellular hypertrophy and subsequent cleavage of the entire enlarged cell into numerous viral vesicles. Most progeny virions are assembled in these vesicles as they circulate in the hemolymph. Here, we report transcriptome studies of host cytoskeletal genes in larvae infected with ascoviruses from 6 h to 21 days post-infection (dpi). We focused on the cabbage looper, Trichoplusia ni, infected with the Trichoplusia ni ascovirus (TnAV), along with supporting studies on the fall armyworm, Spodoptera frugiperda, infected with the Spodoptera frugiperda ascovirus (SfAV). In T. ni, many cytoskeleton genes were upregulated at 48 hours post-infection (hpi), including 29 tubulins, 21 actins, 21 dyneins, and 13 kinesins. Mitochondrial genes were upregulated as much as two-fold at 48 hpi and were expressed at levels comparable to controls in both T. ni and S. frugiperda, even after 21 dpi, when several cytoskeleton genes remained upregulated. Our studies suggest a temporal correlation between increases in the expression of certain host cytoskeletal genes and viral vesicle formation. However, these results need confirmation through functional genetic studies of proteins encoded by these genes. Full article
(This article belongs to the Special Issue Viral Manipulation of Host Cytoskeletal Networks)
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18 pages, 2954 KiB  
Article
Altered Moesin and Actin Cytoskeleton Protein Rearrangements Affect Transendothelial Permeability in Human Endothelial Cells upon Dengue Virus Infection and TNF-α Treatment
by Aroonroong Suttitheptumrong, Thanaporn Mahutchariyakul, Nantapon Rawarak, Onrapak Reamtong, Kobporn Boonnak and Sa-nga Pattanakitsakul
Viruses 2021, 13(10), 2042; https://doi.org/10.3390/v13102042 - 11 Oct 2021
Cited by 4 | Viewed by 2652
Abstract
It has been hypothesized that the host, viral factors, and secreted cytokines (especially TNF-α) play roles in the pathogenesis of secondary dengue infections. Mass spectrometry-based proteomic screening of cytoskeleton fractions isolated from human endothelial (EA.hy926) cells upon dengue virus (DENV) infection and TNF-α [...] Read more.
It has been hypothesized that the host, viral factors, and secreted cytokines (especially TNF-α) play roles in the pathogenesis of secondary dengue infections. Mass spectrometry-based proteomic screening of cytoskeleton fractions isolated from human endothelial (EA.hy926) cells upon dengue virus (DENV) infection and TNF-α treatment identified 450 differentially altered proteins. Among them, decreased levels of moesin, actin stress fiber rearrangements, and dot-like formations of vinculin were observed with western blot analyses and/or immunofluorescence staining (IFA). In vitro vascular permeability assays using EA.hy926 cells, seeded on collagen-coated transwell inserts, showed low levels of transendothelial electrical resistance in treated cells. The synergistic effects of DENV infection and TNF-α treatment caused cellular permeability changes in EA.hy926 cells, which coincided with decreasing moesin levels and the production of abnormal organizations of actin stress fibers and vinculin. Functional studies demonstrated moesin overexpression restored transendothelial permeability in DENV/TNF-α-treated EA.hy926 cells. The present study improves the understanding of the disruption mechanisms of cytoskeleton proteins in enhancing vascular permeability during DENV infection and TNF-α treatment. The study also suggests that these disruption mechanisms are major factors contributing to vascular leakage in severe dengue patients. Full article
(This article belongs to the Special Issue Viral Manipulation of Host Cytoskeletal Networks)
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Review

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13 pages, 1085 KiB  
Review
Manipulation of Host Microtubule Networks by Viral Microtubule-Associated Proteins
by Dahee Seo and Don B. Gammon
Viruses 2022, 14(5), 979; https://doi.org/10.3390/v14050979 - 6 May 2022
Cited by 11 | Viewed by 3091
Abstract
Diverse DNA and RNA viruses utilize cytoskeletal networks to efficiently enter, replicate, and exit the host cell, while evading host immune responses. It is well established that the microtubule (MT) network is commonly hijacked by viruses to traffic to sites of replication after [...] Read more.
Diverse DNA and RNA viruses utilize cytoskeletal networks to efficiently enter, replicate, and exit the host cell, while evading host immune responses. It is well established that the microtubule (MT) network is commonly hijacked by viruses to traffic to sites of replication after entry and to promote egress from the cell. However, mounting evidence suggests that the MT network is also a key regulator of host immune responses to infection. At the same time, viruses have acquired mechanisms to manipulate and/or usurp MT networks to evade these immune responses. Central to most interactions of viruses with the MT network are virally encoded microtubule-associated proteins (MAPs) that bind to MTs directly or indirectly. These MAPs associate with MTs and other viral or cellular MAPs to regulate various aspects of the MT network, including MT dynamics, MT-dependent transport via motor proteins such as kinesins and dyneins, and MT-dependent regulation of innate immune responses. In this review, we examine how viral MAP interactions with the MT network facilitate viral replication and immune evasion. Full article
(This article belongs to the Special Issue Viral Manipulation of Host Cytoskeletal Networks)
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15 pages, 1426 KiB  
Review
Cross Talk between Viruses and Insect Cells Cytoskeleton
by Ayda Khorramnejad, Hugo D. Perdomo, Umberto Palatini, Mariangela Bonizzoni and Laila Gasmi
Viruses 2021, 13(8), 1658; https://doi.org/10.3390/v13081658 - 20 Aug 2021
Cited by 12 | Viewed by 4407
Abstract
Viruses are excellent manipulators of host cellular machinery, behavior, and life cycle, with the host cell cytoskeleton being a primordial viral target. Viruses infecting insects generally enter host cells through clathrin-mediated endocytosis or membrane fusion mechanisms followed by transport of the viral particles [...] Read more.
Viruses are excellent manipulators of host cellular machinery, behavior, and life cycle, with the host cell cytoskeleton being a primordial viral target. Viruses infecting insects generally enter host cells through clathrin-mediated endocytosis or membrane fusion mechanisms followed by transport of the viral particles to the corresponding replication sites. After viral replication, the viral progeny egresses toward adjacent cells and reaches the different target tissues. Throughout all these steps, actin and tubulin re-arrangements are driven by viruses. The mechanisms used by viruses to manipulate the insect host cytoskeleton are well documented in the case of alphabaculoviruses infecting Lepidoptera hosts and plant viruses infecting Hemiptera vectors, but they are not well studied in case of other insect–virus systems such as arboviruses–mosquito vectors. Here, we summarize the available knowledge on how viruses manipulate the insect host cell cytoskeleton, and we emphasize the primordial role of cytoskeleton components in insect virus motility and the need to expand the study of this interaction. Full article
(This article belongs to the Special Issue Viral Manipulation of Host Cytoskeletal Networks)
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