Actin and Rho GTPase in herpesvirus biology

Department of Virology, Parasitology, and Immunology, Faculty of Veterinary Medicine, Ghent University, 9820 Merelbeke, Belgium.
Trends in Microbiology (Impact Factor: 9.19). 10/2007; 15(9):426-33. DOI: 10.1016/j.tim.2007.08.003
Source: PubMed


Viruses have evolved a variety of interactions with host cells to create an optimal niche for viral replication, persistence and spread. The actin cytoskeleton of the host cell and actin-regulating Rho GTPase signaling pathways can be involved in several of these interactions. This review focuses on recent findings on herpesvirus interactions with actin and Rho GTPases during viral entry, replication in the nucleus and egress. Unraveling these often fascinating interactions might also provide additional insights into sometimes poorly known aspects of actin biology (e.g. its role in the nucleus) and in the development of novel antiviral therapies.

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Available from: Lynn Enquist
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    • "We also found that inactivated cofilin is recruited to the nucleus, possibly hampering the disassembly of nuclear actin to promote viral replication during HSV-1 replication (Xiang et al., 2014). This might explain the previous observation that HSV-1 promotes the formation of nuclear actin filaments in neurons (Favoreel et al., 2007; Feierbach et al., 2006). HSV- 1 induces cofilin inactivation via the ubiquitin-proteasome dependent downregulation of SSH1 phosphatase. "
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    ABSTRACT: Actin-depolymerizing factor (ADF)/cofilin proteins are key players in controlling the temporal and spatial extent of actin dynamics, which is crucial for mediating host-pathogen interactions. Pathogenic microbes have evolved molecular mechanisms to manipulate cofilin activity to subvert the actin cytoskeletal system in host cells, promoting their internalization into the target cells, modifying the replication niche and facilitating their intracellular and intercellular dissemination. The study of how these pathogens exploit cofilin pathways is crucial for understanding infectious disease and providing potential targets for drug therapies.
    Full-text · Article · Apr 2015 · Critical Reviews in Microbiology
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    • "Above-mentioned structures seemed to contribute to the direct spread of virus particles to adjacent cells without being exposed to the external environment. Moreover, similar projections have been also found to be induced by HSV-1 in Vero and BHK-21 cells and for VZV in HFF cells [6]. For that reason, it can be assumed that this mechanism could be an example of a strategy used by herpesviruses to enhance intercellular spread of infection. "
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    ABSTRACT: Equine herpesvirus type 1 (EHV-1) causes respiratory disease, abortion and neurological disorders in horses. In the present study, we investigated reorganization of the cytoskeleton in neurons infected with two EHV-1 strains: Jan-E (wild-type strain) and Rac-H (attenuated strain). The studies were performed on primary murine neurons, which are an excellent model for studying neurotropism and neurovirulence of EHV-1. We have demonstrated for the first time that EHV-1 infection causes rearrangements in the actin network of neurons that are dependent on the virus strain and its adaptation to cell culture in vitro. Immunofluorescent labeling and confocal microscopy revealed the formation of long, thin projections in neurons infected with the Jan-E strain, which was probably associated with enhanced intracellular spread of the virus. The EHV-1 Rac-H strain caused disruption of the microfilaments system and general depolymerization of actin, but treatment of neurons with cytochalasin D or latrunculin A resulted in limitation of viral replication. It can therefore be assumed that actin filaments are required only at the early stages of infection. Our results allow us to suggest that the actin cytoskeleton participates in EHV-1 infection of primary murine neurons but is not essential, and that other components of the cytoskeleton and/or cellular mechanisms may be also involved during EHV-1 infection.
    Full-text · Article · Dec 2013 · Archives of Virology
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    • "Activation these three genes is host cell-type dependent and also dependent on the type of herpesvirus. Indeed, HSV-1 entry involves Rac1 and cdc42 activation in canine kidney cells (MDCKII) without RhoA, but have needs to RhoA activation in primary corneal fibroblasts [46]. Our analysis found that the rac1 gene is under expressed in infected animals. "
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    ABSTRACT: Massive mortalities have been observed in France since 2008 on spat and juvenile Pacific oysters, Crassostrea gigas. A herpes virus called OsHV-1, easily detectable by PCR, has been implicated in the mortalities as demonstrated by the results of numerous field studies linking mortality with OsHV-1 prevalence. Moreover, experimental infections using viral particles have documented the pathogenicity of OsHV-1 but the physiological responses of host to pathogen are not well known. The aim of this study was to understand mechanisms brought into play against the virus during infection in the field. A microarray assay has been developed for a major part of the oyster genome and used for studying the host transcriptome across mortality on field. Spat with and without detectable OsHV-1 infection presenting or not mortality respectively were compared by microarray during mortality episodes. In this study, a number of genes are regulated in the response to pathogen infection on field and seems to argue to an implication of the virus in the observed mortality. The result allowed establishment of a hypothetic scheme of the host cell's infection by, and response to, the pathogen. This response shows a "sensu stricto" innate immunity through genic regulation of the virus OsHV-1 life cycle, but also others biological processes resulting to complex interactions between host and pathogens in general.
    Full-text · Article · Aug 2013 · BMC Genomics
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