Epigenetics and the dynamics of chromatin during adenovirus infections

Lynch, Kelsey L.; Gooding, Linda R.; Garnett-Benson, Charlie; Ornelles, David A.; Avgousti, Daphne C.

doi:10.1002/1873-3468.13697

Cited by 29 publications

(23 citation statements)

References 205 publications

(391 reference statements)

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“…However, AdRCs are formed by biologically active proteins and nucleic acids—not inert aggregates—and should now be more properly regarded as virus‐induced compartments that contain proteins involved in viral genome replication, as well as transcription and splicing factors regulating viral gene expression (Table ). In addition, AdRCs also impact on cellular antiviral mechanisms, since cellular factors that would otherwise restrict viral replication are inhibited, recruited, and concentrated at AdRCs (described below, see also reviews by Lynch et al , Sohn S‐Y & Hearing P ; and Charman et al in this issue) . Taking into account that formation and regulation of AdRCs are key to viral replication and virus–host interactions, the evidence reviewed here calls for a redefinition of AdRCs as nuclear hubs for virus–host cell interaction.…”

Section: Adenovirus Replication Compartments Definedmentioning

confidence: 96%

“…The major core protein VII remains associated with the incoming viral DNA and protects the viral genome from cellular components of the DNA damage response (DDR) , participating in the initial inhibition of the cellular antiviral response , before expression of the E1A , E1B , E2, and E4 genes. These early genes encode multifunctional proteins that are at least transiently localized in AdRCs and are known to alter or to regulate many of the molecular processes that take place there (described in the following sections and see also reviews by Hidalgo et al ; Lynch et al ; Sohn S‐Y & Hearing P ; Hidalgo & Gonzalez ; Charman et al in this issue). Shortly after the viral genome has entered the cell nucleus (30 min after infection in HeLa cells), the viral core protein VII and the cellular template‐activating factor I (TAF Iβ) and acidic nuclear phosphoprotein pp32, two subunits of the histone acetyltransferase inhibitor complex, localize at discrete nuclear foci that are thought to regulate viral chromatin formation (see review by Lynch et al in this issue).…”

Section: Overview Of Adrc Biogenesismentioning

confidence: 99%

“…These early genes encode multifunctional proteins that are at least transiently localized in AdRCs and are known to alter or to regulate many of the molecular processes that take place there (described in the following sections and see also reviews by Hidalgo et al ; Lynch et al ; Sohn S‐Y & Hearing P ; Hidalgo & Gonzalez ; Charman et al in this issue). Shortly after the viral genome has entered the cell nucleus (30 min after infection in HeLa cells), the viral core protein VII and the cellular template‐activating factor I (TAF Iβ) and acidic nuclear phosphoprotein pp32, two subunits of the histone acetyltransferase inhibitor complex, localize at discrete nuclear foci that are thought to regulate viral chromatin formation (see review by Lynch et al in this issue). After a few hours (4 hpi in Hep‐2 cells), the viral DNA is found adjacent to promyelocytic leukemia protein (PML)‐NB, as visualized by in situ hybridization .…”

Section: Overview Of Adrc Biogenesismentioning

confidence: 99%

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Formation of adenovirus DNA replication compartments

Hidalgo

González

2019

FEBS Letters

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Adenoviruses induce an extensive reorganization of the host cell nucleus during replication. Such a process results in the assembly of viral and cellular macromolecules into nuclear structures called adenovirus replication compartments (AdRCs), which function as platforms for viral DNA replication and gene expression. AdRCs co-opt host proteins and cellular pathways that restrict viral replication, suggesting that the mechanisms that control AdRC formation and function are essential for viral replication and lay at the basis of virus-host interactions. Here, we review the hallmarks of AdRCs and recent progress in our understanding of the formation, composition, and function of AdRCs. Furthermore, we discuss how AdRCs facilitate the interplay between viral and cellular machineries and hijack cellular functions to promote viral genome replication and expression.

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Section: Adenovirus Replication Compartments Definedmentioning

confidence: 96%

Section: Overview Of Adrc Biogenesismentioning

confidence: 99%

Section: Overview Of Adrc Biogenesismentioning

confidence: 99%

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Formation of adenovirus DNA replication compartments

Hidalgo

González

2019

FEBS Letters

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“…This raises the possibility that cellular chromatin must be manipulated to make space for VRC growth. Many DNA viruses hijack cellular chromatin modifiers to regulate their own viral chromatin, as well as cellular chromatin [70][71][72]. Furthermore, many DNA viruses activate the DDR, leading to the phosphorylation of histone γH2AX, which is a key mediator of cellular chromatin remodeling and condensation during DNA repair [8][9][10].…”

Section: What Dictates the Number Of Replication Compartments That Fomentioning

confidence: 99%

“…Furthermore, many DNA viruses activate the DDR, leading to the phosphorylation of histone γH2AX, which is a key mediator of cellular chromatin remodeling and condensation during DNA repair [8][9][10]. In addition, some DNA viruses such as HPV and HAdV encode viral proteins that can manipulate cellular chromatin [70,[73][74][75]. For example, expression of the HAdV core protein VII alone is sufficient to manipulate cellular chromatin [74].…”

Section: What Dictates the Number Of Replication Compartments That Fomentioning

confidence: 99%

Replication Compartments of DNA Viruses in the Nucleus: Location, Location, Location

Charman

Weitzman

2020

Viruses

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DNA viruses that replicate in the nucleus encompass a range of ubiquitous and clinically important viruses, from acute pathogens to persistent tumor viruses. These viruses must co-opt nuclear processes for the benefit of the virus, whilst evading host processes that would otherwise attenuate viral replication. Accordingly, DNA viruses induce the formation of membraneless assemblies termed viral replication compartments (VRCs). These compartments facilitate the spatial organization of viral processes and regulate virus-host interactions. Here, we review advances in our understanding of VRCs. We cover their initiation and formation, their function as the sites of viral processes, and aspects of their composition and organization. In doing so, we highlight ongoing and emerging areas of research highly pertinent to our understanding of nuclear-replicating DNA viruses.Viruses 2020, 12, 151 2 of 20 The Initiation and Formation of Replication CompartmentsDNA viruses that replicate in the nucleus exhibit a diverse array of strategies to complete their replication cycle and ultimately produce progeny virions. Despite their many differences, the strategies employed by DNA viruses to initiate productive infection and establish VRCs share many features in common. Indeed, it is likely that all DNA viruses that replicate in the nucleus form VRCs. Following penetration of the host cell and the transport of viral capsids/cores, viral DNA genomes enter the nucleus, where they begin a program of temporally regulated gene expression that initiates productive infection [1,2]. Early gene products include viral proteins required to manipulate the host-cell environment and replicate the viral genome. Viral replication proteins interact with the viral genome and initiate genome replication leading to VRC formation, which is often in concert with certain co-opted host proteins. However, these viruses must overcome several challenges to form VRCs successfully. Firstly, incoming genomes must avoid cellular intrinsic antiviral defenses and homeostatic regulatory pathways such as elements of the DNA damage response (DDR) that respond to the presence of foreign DNA and act to suppress viral gene expression [3][4][5][6][7][8][9][10]. Secondly, VRCs typically form at specific sites within the nucleus, suggesting that viral genomes need to be targeted to these sites in order to initiate VRC formation [6,11,12]. Furthermore, it has been hypothesized that the formation and growth of VRCs may require manipulation of the nuclear environment and the re-organization of host chromatin to overcome the spatial restraints of the nucleus [11][12][13][14][15]. In this section, we review key features of VRC initiation and highlight some major challenges to VRC formation. Interplay between Viral Replication Compartment Formation and Promyelocytic Leukemia Protein Nuclear BodiesA common theme amongst many nuclear-replicating DNA viruses is initiation of VRCs at sites in close proximity to promyelocytic leukemia protein (PML) nuclear bodies (NBs). Since the dis...

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