Special Issue "Viral Subversion of Stress Responses and Translational Control"

A special issue of Viruses (ISSN 1999-4915).

Deadline for manuscript submissions: closed (29 February 2016).

Special Issue Editor

Dr. Craig McCormick

Guest Editor
Department of Microbiology and Immunology, Dalhousie University, Sir Charles Tupper Medical Building, Room 7-P 5850 College Street, Halifax, Nova Scotia, Canada B3H 4R2
Interests: influenza A virus; Kaposi’s sarcoma-associated herpesvirus; viral oncogenes; mRNA turnover and translation; stress granules; p-bodies; autophagy; unfolded protein response; inflammation; host shutoff
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Special Issue Information

Dear Colleagues,

The cellular translation apparatus swiftly responds to changing environmental conditions, altering gene expression to promote survival in times of stress, and restoring homeostasis following stress resolution. Accumulating evidence indicates that the translation apparatus is a nexus for control of antiviral responses. Viruses are obligate intracellular parasites that repurpose the host translation apparatus for efficient conversion of viral mRNAs into protein products. Sentinel pattern-recognition receptors and associated kinases sense viral infection and activate antiviral defences that include near-global shutdown of cap-dependent translation, thereby limiting accumulation of viral proteins. Coincident signal transduction events lead to the production of interferon, eliciting a local antiviral state. The molecular mechanisms that coordinate these responses remain incompletely understood.

In recent years, many viral countermeasures have been identified that limit activation of innate antiviral stress responses and maintain ongoing translation of viral gene products. This Special Issue of Viruses is dedicated to understanding how successful viruses subvert these antiviral responses. We hope to assemble a collection of research papers and reviews that enhance our understanding of these fascinating host defences and viral countermeasures. Topics may include studies on the evolution and function of innate antiviral stress responses and/or viral countermeasures; viral mechanisms of host shutoff and direct control of the translation apparatus; viral control of host stress responses intimately linked with translation, including DNA damage responses, hypoxia, autophagy and the unfolded protein response; and impact of these interactions on cell fate and a variety of pathogenic outcomes of infection, including cancer.

We hope that this Special Issue will serve as a valuable resource to new and established researchers in the field, and frame important unanswered questions to focus future research efforts.

Dr. Craig McCormick
Guest Editor

Manuscript Submission Information

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Keywords

  • translation control
  • host shutoff
  • alternative viral translation mechanisms
  • stress
  • antiviral defences
  • mTOR
  • interferon
  • unfolded protein response
  • autophagy

Published Papers (15 papers)

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Research

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Open AccessArticle
Temporal Regulation of Distinct Internal Ribosome Entry Sites of the Dicistroviridae Cricket Paralysis Virus
Viruses 2016, 8(1), 25; https://doi.org/10.3390/v8010025 - 19 Jan 2016
Cited by 13
Abstract
Internal ribosome entry is a key mechanism for viral protein synthesis in a subset of RNA viruses. Cricket paralysis virus (CrPV), a member of Dicistroviridae, has a positive-sense single strand RNA genome that contains two internal ribosome entry sites (IRES), a 5′untranslated [...] Read more.
Internal ribosome entry is a key mechanism for viral protein synthesis in a subset of RNA viruses. Cricket paralysis virus (CrPV), a member of Dicistroviridae, has a positive-sense single strand RNA genome that contains two internal ribosome entry sites (IRES), a 5′untranslated region (5′UTR) and intergenic region (IGR) IRES, that direct translation of open reading frames (ORF) encoding the viral non-structural and structural proteins, respectively. The regulation of and the significance of the CrPV IRESs during infection are not fully understood. In this study, using a series of biochemical assays including radioactive-pulse labelling, reporter RNA assays and ribosome profiling, we demonstrate that while 5′UTR IRES translational activity is constant throughout infection, IGR IRES translation is delayed and then stimulated two to three hours post infection. The delay in IGR IRES translation is not affected by inhibiting global translation prematurely via treatment with Pateamine A. Using a CrPV replicon that uncouples viral translation and replication, we show that the increase in IGR IRES translation is dependent on expression of non-structural proteins and is greatly stimulated when replication is active. Temporal regulation by distinct IRESs within the CrPV genome is an effective viral strategy to ensure optimal timing and expression of viral proteins to facilitate infection. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Review

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Open AccessReview
KSHV-Mediated Angiogenesis in Tumor Progression
Viruses 2016, 8(7), 198; https://doi.org/10.3390/v8070198 - 20 Jul 2016
Cited by 17
Abstract
Human herpesvirus 8 (HHV-8), also known as Kaposi’s sarcoma-associated herpesvirus (KSHV), is a malignant human oncovirus belonging to the gamma herpesvirus family. HHV-8 is closely linked to the pathogenesis of Kaposi’s sarcoma (KS) and two other B-cell lymphoproliferative diseases: primary effusion lymphoma (PEL) [...] Read more.
Human herpesvirus 8 (HHV-8), also known as Kaposi’s sarcoma-associated herpesvirus (KSHV), is a malignant human oncovirus belonging to the gamma herpesvirus family. HHV-8 is closely linked to the pathogenesis of Kaposi’s sarcoma (KS) and two other B-cell lymphoproliferative diseases: primary effusion lymphoma (PEL) and a plasmablastic variant of multicentric Castleman’s disease (MCD). KS is an invasive tumor of endothelial cells most commonly found in untreated HIV-AIDS or immuno-compromised individuals. KS tumors are highly vascularized and have abnormal, excessive neo-angiogenesis, inflammation, and proliferation of infected endothelial cells. KSHV directly induces angiogenesis in an autocrine and paracrine fashion through a complex interplay of various viral and cellular pro-angiogenic and inflammatory factors. KS is believed to originate due to a combination of KSHV’s efficient strategies for evading host immune systems and several pro-angiogenic and pro-inflammatory stimuli. In addition, KSHV infection of endothelial cells produces a wide array of viral oncoproteins with transforming capabilities that regulate multiple host-signaling pathways involved in the activation of angiogenesis. It is likely that the cellular-signaling pathways of angiogenesis and lymph-angiogenesis modulate the rate of tumorigenesis induction by KSHV. This review summarizes the current knowledge on regulating KSHV-mediated angiogenesis by integrating the findings reported thus far on the roles of host and viral genes in oncogenesis, recent developments in cell-culture/animal-model systems, and various anti-angiogenic therapies for treating KSHV-related lymphoproliferative disorders. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Regulation of Stress Responses and Translational Control by Coronavirus
Viruses 2016, 8(7), 184; https://doi.org/10.3390/v8070184 - 04 Jul 2016
Cited by 14
Abstract
Similar to other viruses, coronavirus infection triggers cellular stress responses in infected host cells. The close association of coronavirus replication with the endoplasmic reticulum (ER) results in the ER stress responses, which impose a challenge to the viruses. Viruses, in turn, have come [...] Read more.
Similar to other viruses, coronavirus infection triggers cellular stress responses in infected host cells. The close association of coronavirus replication with the endoplasmic reticulum (ER) results in the ER stress responses, which impose a challenge to the viruses. Viruses, in turn, have come up with various mechanisms to block or subvert these responses. One of the ER stress responses is inhibition of the global protein synthesis to reduce the amount of unfolded proteins inside the ER lumen. Viruses have evolved the capacity to overcome the protein translation shutoff to ensure viral protein production. Here, we review the strategies exploited by coronavirus to modulate cellular stress response pathways. The involvement of coronavirus-induced stress responses and translational control in viral pathogenesis will also be briefly discussed. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Who Regulates Whom? An Overview of RNA Granules and Viral Infections
Viruses 2016, 8(7), 180; https://doi.org/10.3390/v8070180 - 28 Jun 2016
Cited by 32
Abstract
After viral infection, host cells respond by mounting an anti-viral stress response in order to create a hostile atmosphere for viral replication, leading to the shut-off of mRNA translation (protein synthesis) and the assembly of RNA granules. Two of these RNA granules have [...] Read more.
After viral infection, host cells respond by mounting an anti-viral stress response in order to create a hostile atmosphere for viral replication, leading to the shut-off of mRNA translation (protein synthesis) and the assembly of RNA granules. Two of these RNA granules have been well characterized in yeast and mammalian cells, stress granules (SGs), which are translationally silent sites of RNA triage and processing bodies (PBs), which are involved in mRNA degradation. This review discusses the role of these RNA granules in the evasion of anti-viral stress responses through virus-induced remodeling of cellular ribonucleoproteins (RNPs). Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
Open AccessReview
Stress Beyond Translation: Poxviruses and More
Viruses 2016, 8(6), 169; https://doi.org/10.3390/v8060169 - 14 Jun 2016
Cited by 10
Abstract
Poxviruses are large double-stranded DNA viruses that form viral factories in the cytoplasm of host cells. These viruses encode their own transcription machinery, but rely on host translation for protein synthesis. Thus, poxviruses have to cope with and, in most cases, reprogram host [...] Read more.
Poxviruses are large double-stranded DNA viruses that form viral factories in the cytoplasm of host cells. These viruses encode their own transcription machinery, but rely on host translation for protein synthesis. Thus, poxviruses have to cope with and, in most cases, reprogram host translation regulation. Granule structures, called antiviral granules (AVGs), have been observed surrounding poxvirus viral factories. AVG formation is associated with abortive poxvirus infection, and AVGs contain proteins that are typically found in stress granules (SGs). With certain mutant poxviruses lack of immunoregulatory factor(s), we can specifically examine the mechanisms that drive the formation of these structures. In fact, cytoplasmic macromolecular complexes form during many viral infections and contain sensing molecules that can help reprogram transcription. More importantly, the similarity between AVGs and cytoplasmic structures formed during RNA and DNA sensing events prompts us to reconsider the cause and consequence of these AVGs. In this review, we first summarize recent findings regarding how poxvirus manipulates host translation. Next, we compare and contrast SGs and AVGs. Finally, we review recent findings regarding RNA- and especially DNA-sensing bodies observed during viral infection. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Alphavirus Infection: Host Cell Shut-Off and Inhibition of Antiviral Responses
Viruses 2016, 8(6), 166; https://doi.org/10.3390/v8060166 - 11 Jun 2016
Cited by 36
Abstract
Alphaviruses cause debilitating disease in humans and animals and are transmitted by blood-feeding arthropods, typically mosquitoes. With a traditional focus on two models, Sindbis virus and Semliki Forest virus, alphavirus research has significantly intensified in the last decade partly due to the re-emergence [...] Read more.
Alphaviruses cause debilitating disease in humans and animals and are transmitted by blood-feeding arthropods, typically mosquitoes. With a traditional focus on two models, Sindbis virus and Semliki Forest virus, alphavirus research has significantly intensified in the last decade partly due to the re-emergence and dramatic expansion of chikungunya virus in Asia, Europe, and the Americas. As a consequence, alphavirus–host interactions are now understood in much more molecular detail, and important novel mechanisms have been elucidated. It has become clear that alphaviruses not only cause a general host shut-off in infected vertebrate cells, but also specifically suppress different host antiviral pathways using their viral nonstructural proteins, nsP2 and nsP3. Here we review the current state of the art of alphavirus host cell shut-off of viral transcription and translation, and describe recent insights in viral subversion of interferon induction and signaling, the unfolded protein response, and stress granule assembly. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Stress Response and Translation Control in Rotavirus Infection
Viruses 2016, 8(6), 162; https://doi.org/10.3390/v8060162 - 07 Jun 2016
Cited by 6
Abstract
The general stress and innate immune responses are closely linked and overlap at many levels. The outcomes of these responses serve to reprogram host expression patterns to prevent viral invasions. In turn, viruses counter attack these cell responses to ensure their replication. The [...] Read more.
The general stress and innate immune responses are closely linked and overlap at many levels. The outcomes of these responses serve to reprogram host expression patterns to prevent viral invasions. In turn, viruses counter attack these cell responses to ensure their replication. The mechanisms by which viruses attempt to control host cell responses are as varied as the number of different virus families. One of the most recurrent strategies used by viruses to control the antiviral response of the cell is to hijack the translation machinery of the host, such that viral proteins are preferentially synthesized, while the expression of the stress and antiviral responses of the cell are blocked at the translation level. Here, we will review how rotaviruses, an important agent of acute severe gastroenteritis in children, overcome the stress responses of the cell to establish a productive infectious cycle. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Adapting the Stress Response: Viral Subversion of the mTOR Signaling Pathway
Viruses 2016, 8(6), 152; https://doi.org/10.3390/v8060152 - 24 May 2016
Cited by 22
Abstract
The mammalian target of rapamycin (mTOR) is a central regulator of gene expression, translation and various metabolic processes. Multiple extracellular (growth factors) and intracellular (energy status) molecular signals as well as a variety of stressors are integrated into the mTOR pathway. Viral infection [...] Read more.
The mammalian target of rapamycin (mTOR) is a central regulator of gene expression, translation and various metabolic processes. Multiple extracellular (growth factors) and intracellular (energy status) molecular signals as well as a variety of stressors are integrated into the mTOR pathway. Viral infection is a significant stress that can activate, reduce or even suppress the mTOR signaling pathway. Consequently, viruses have evolved a plethora of different mechanisms to attack and co-opt the mTOR pathway in order to make the host cell a hospitable environment for replication. A more comprehensive knowledge of different viral interactions may provide fruitful targets for new antiviral drugs. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Hepatitis C Virus Infection Induces Autophagy as a Prosurvival Mechanism to Alleviate Hepatic ER-Stress Response
Viruses 2016, 8(5), 150; https://doi.org/10.3390/v8050150 - 23 May 2016
Cited by 35
Abstract
Hepatitis C virus (HCV) infection frequently leads to chronic liver disease, liver cirrhosis and hepatocellular carcinoma (HCC). The molecular mechanisms by which HCV infection leads to chronic liver disease and HCC are not well understood. The infection cycle of HCV is initiated by [...] Read more.
Hepatitis C virus (HCV) infection frequently leads to chronic liver disease, liver cirrhosis and hepatocellular carcinoma (HCC). The molecular mechanisms by which HCV infection leads to chronic liver disease and HCC are not well understood. The infection cycle of HCV is initiated by the attachment and entry of virus particles into a hepatocyte. Replication of the HCV genome inside hepatocytes leads to accumulation of large amounts of viral proteins and RNA replication intermediates in the endoplasmic reticulum (ER), resulting in production of thousands of new virus particles. HCV-infected hepatocytes mount a substantial stress response. How the infected hepatocyte integrates the viral-induced stress response with chronic infection is unknown. The unfolded protein response (UPR), an ER-associated cellular transcriptional response, is activated in HCV infected hepatocytes. Over the past several years, research performed by a number of laboratories, including ours, has shown that HCV induced UPR robustly activates autophagy to sustain viral replication in the infected hepatocyte. Induction of the cellular autophagy response is required to improve survival of infected cells by inhibition of cellular apoptosis. The autophagy response also inhibits the cellular innate antiviral program that usually inhibits HCV replication. In this review, we discuss the physiological implications of the HCV-induced chronic ER-stress response in the liver disease progression. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Respiratory Syncytial Virus and Cellular Stress Responses: Impact on Replication and Physiopathology
Viruses 2016, 8(5), 124; https://doi.org/10.3390/v8050124 - 12 May 2016
Cited by 16
Abstract
Human respiratory syncytial virus (RSV), a member of the Paramyxoviridae family, is a major cause of severe acute lower respiratory tract infection in infants, elderly and immunocompromised adults. Despite decades of research, a complete integrated picture of RSV-host interaction is still missing. Several [...] Read more.
Human respiratory syncytial virus (RSV), a member of the Paramyxoviridae family, is a major cause of severe acute lower respiratory tract infection in infants, elderly and immunocompromised adults. Despite decades of research, a complete integrated picture of RSV-host interaction is still missing. Several cellular responses to stress are involved in the host-response to many virus infections. The endoplasmic reticulum stress induced by altered endoplasmic reticulum (ER) function leads to activation of the unfolded-protein response (UPR) to restore homeostasis. Formation of cytoplasmic stress granules containing translationally stalled mRNAs is a means to control protein translation. Production of reactive oxygen species is balanced by an antioxidant response to prevent oxidative stress and the resulting damages. In recent years, ongoing research has started to unveil specific regulatory interactions of RSV with these host cellular stress responses. Here, we discuss the latest findings regarding the mechanisms evolved by RSV to induce, subvert or manipulate the ER stress, the stress granule and oxidative stress responses. We summarize the evidence linking these stress responses with the regulation of RSV replication and the associated pathogenesis. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Translational Control during Calicivirus Infection
Viruses 2016, 8(4), 104; https://doi.org/10.3390/v8040104 - 20 Apr 2016
Cited by 9
Abstract
In this review, we provide an overview of the strategies developed by caliciviruses to subvert or regulate the host protein synthesis machinery to their advantage. As intracellular obligate parasites, viruses strictly depend on the host cell resources to produce viral proteins. Thus, many [...] Read more.
In this review, we provide an overview of the strategies developed by caliciviruses to subvert or regulate the host protein synthesis machinery to their advantage. As intracellular obligate parasites, viruses strictly depend on the host cell resources to produce viral proteins. Thus, many viruses have developed strategies that regulate the function of the host protein synthesis machinery, often leading to preferential translation of viral mRNAs. Caliciviruses lack a 5′ cap structure but instead have a virus-encoded VPg protein covalently linked to the 5′ end of their mRNAs. Furthermore, they encode 2–4 open reading frames within their genomic and subgenomic RNAs. Therefore, they use alternative mechanisms for translation whereby VPg interacts with eukaryotic initiation factors (eIFs) to act as a proteinaceous cap-substitute, and some structural proteins are produced by reinitiation of translation events. This review discusses our understanding of these key mechanisms during caliciviruses infection as well as recent insights into the global regulation of eIF4E activity. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Shutoff of Host Gene Expression in Influenza A Virus and Herpesviruses: Similar Mechanisms and Common Themes
Viruses 2016, 8(4), 102; https://doi.org/10.3390/v8040102 - 16 Apr 2016
Cited by 39
Abstract
The ability to shut off host gene expression is a shared feature of many viral infections, and it is thought to promote viral replication by freeing host cell machinery and blocking immune responses. Despite the molecular differences between viruses, an emerging theme in [...] Read more.
The ability to shut off host gene expression is a shared feature of many viral infections, and it is thought to promote viral replication by freeing host cell machinery and blocking immune responses. Despite the molecular differences between viruses, an emerging theme in the study of host shutoff is that divergent viruses use similar mechanisms to enact host shutoff. Moreover, even viruses that encode few proteins often have multiple mechanisms to affect host gene expression, and we are only starting to understand how these mechanisms are integrated. In this review we discuss the multiplicity of host shutoff mechanisms used by the orthomyxovirus influenza A virus and members of the alpha- and gamma-herpesvirus subfamilies. We highlight the surprising similarities in their mechanisms of host shutoff and discuss how the different mechanisms they use may play a coordinated role in gene regulation. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Human Cytomegalovirus Strategies to Maintain and Promote mRNA Translation
Viruses 2016, 8(4), 97; https://doi.org/10.3390/v8040097 - 13 Apr 2016
Cited by 12
Abstract
mRNA translation requires the ordered assembly of translation initiation factors and ribosomal subunits on a transcript. Host signaling pathways regulate each step in this process to match levels of protein synthesis to environmental cues. In response to infection, cells activate multiple defenses that [...] Read more.
mRNA translation requires the ordered assembly of translation initiation factors and ribosomal subunits on a transcript. Host signaling pathways regulate each step in this process to match levels of protein synthesis to environmental cues. In response to infection, cells activate multiple defenses that limit viral protein synthesis, which viruses must counteract to successfully replicate. Human cytomegalovirus (HCMV) inhibits host defenses that limit viral protein expression and manipulates host signaling pathways to promote the expression of both host and viral proteins necessary for virus replication. Here we review key regulatory steps in mRNA translation, and the strategies used by HCMV to maintain protein synthesis in infected cells. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Enterovirus Control of Translation and RNA Granule Stress Responses
Viruses 2016, 8(4), 93; https://doi.org/10.3390/v8040093 - 30 Mar 2016
Cited by 16
Abstract
Enteroviruses such as poliovirus (PV) and coxsackievirus B3 (CVB3) have evolved several parallel strategies to regulate cellular gene expression and stress responses to ensure efficient expression of the viral genome. Enteroviruses utilize their encoded proteinases to take over the cellular translation apparatus and [...] Read more.
Enteroviruses such as poliovirus (PV) and coxsackievirus B3 (CVB3) have evolved several parallel strategies to regulate cellular gene expression and stress responses to ensure efficient expression of the viral genome. Enteroviruses utilize their encoded proteinases to take over the cellular translation apparatus and direct ribosomes to viral mRNAs. In addition, viral proteinases are used to control and repress the two main types of cytoplasmic RNA granules, stress granules (SGs) and processing bodies (P-bodies, PBs), which are stress-responsive dynamic structures involved in repression of gene expression. This review discusses these processes and the current understanding of the underlying mechanisms with respect to enterovirus infections. In addition, the review discusses accumulating data suggesting linkage exists between RNA granule formation and innate immune sensing and activation. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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Open AccessReview
Alphaherpesvirus Subversion of Stress-Induced Translational Arrest
Viruses 2016, 8(3), 81; https://doi.org/10.3390/v8030081 - 15 Mar 2016
Cited by 1
Abstract
In this article, we provide an overview of translational arrest in eukaryotic cells in response to stress and the tactics used specifically by alphaherpesviruses to overcome translational arrest. One consequence of translational arrest is the formation of cytoplasmic compartments called stress granules (SGs). [...] Read more.
In this article, we provide an overview of translational arrest in eukaryotic cells in response to stress and the tactics used specifically by alphaherpesviruses to overcome translational arrest. One consequence of translational arrest is the formation of cytoplasmic compartments called stress granules (SGs). Many viruses target SGs for disruption and/or modification, including the alphaherpesvirus herpes simplex virus type 2 (HSV-2). Recently, it was discovered that HSV-2 disrupts SG formation early after infection via virion host shutoff protein (vhs), an endoribonuclease that is packaged within the HSV-2 virion. We review this discovery and discuss the insights it has provided into SG biology as well as its potential significance in HSV-2 infection. A model for vhs-mediated disruption of SG formation is presented. Full article
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
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