Nuclear domain 10 of the viral aspect

Rivera-Molina, Yisel; Martínez, Francisco Puerta; Tang, Qiyi

doi:10.5501/wjv.v2.i3.110

Cited by 20 publications

(16 citation statements)

References 97 publications

(146 reference statements)

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“…Disappearance or abolition of PML‐NBs was observed in a variety of human cancers of different histological origins . Many viruses, including herpes simplex virus‐1, cytomegalovirus, Epstein‐Barr virus, papillomaviruses and polyomaviruses, target PML‐NBs and disrupt their structures . In neurological diseases such as spinocerebellar ataxias and Huntington disease, neuronal intranuclear inclusions involving PML‐NBs are formed …”

Section: New Neuropathological Findings: Dot‐shaped Inclusionsmentioning

confidence: 99%

“…31 Many viruses, including herpes simplex virus-1, cytomegalovirus, Epstein-Barr virus, papillomaviruses and polyomaviruses, target PML-NBs and disrupt their structures. 32 In neurological diseases such as spinocerebellar ataxias and Huntington disease, neuronal intranuclear inclusions involving PML-NBs are formed. 28 The intranuclear target of JC virus infection was identified with help of a eukaryotic expression system established in 1997.…”

Section: New Neuropathological Findings: Dot-shaped Inclusionsmentioning

confidence: 99%

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Progressive multifocal leukoencephalopathy: Dot‐shaped inclusions and virus‐host interactions

Shishido‐Hara

2015

Neuropathology

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Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease caused by reactivation of the asymptomatic persistent pathogen human polyomavirus JC (JC virus). The pathology of affected brain tissues demonstrates oligodendroglia-like cells with viral inclusions in their enlarged nuclei, a diagnostic hallmark of this disease. Today, the pathological features of this disease are expanding, partly due to an unsteady balance between viral virulence and host immunity. Intranuclear viral inclusions were initially thought to be amphophilic materials comprising the entire enlarged nucleus, based on HE staining (full inclusions). Howevewr, recent immunohistochemical analyses detected the presence of intranuclear viral inclusions in dots (dot-shaped inclusions). The dot-shaped inclusions reflect clustered progeny virions at punctuated subnuclear domains called promyelocytic leukemia nuclear bodies, and are indicative of early-stage viral infection or suppressed viral proliferation. Second, the JC virus is usually reactivated in patients with impaired immunity, and therefore the inflammatory reactions are poor. However, the causes of immunosuppression are divergent, as seen with the frequent use of immunosuppressive drugs, including natalizumab. Therefore, the degree of host immunity is variable; some patients show marked anti-viral inflammatory reactions and a good prognosis, indicating that a strong resistance against viral infection remains. Recovery of the immune system may also induce paradoxical clinical worsening, known as immune reconstitution inflammatory syndrome, the mechanism of which has not been clarified. The virus-host interactions have increased in complexity, and the pathology of PML is diverging. In this review, the pathology of PML will be described, with a focus on the intranuclear target of JC virus infection and host inflammatory reactions.

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Section: New Neuropathological Findings: Dot‐shaped Inclusionsmentioning

confidence: 99%

Section: New Neuropathological Findings: Dot-shaped Inclusionsmentioning

confidence: 99%

Progressive multifocal leukoencephalopathy: Dot‐shaped inclusions and virus‐host interactions

Shishido‐Hara

2015

Neuropathology

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“…The genomes of several families of DNA viruses are initially associated with Pml bodies, prior to the disruption of these foci by viral gene products (72)(73)(74)(75). In adenovirus-infected cells, the E4 Orf3 protein is necessary and sufficient to induce dismantling of Pml bodies and relocalization of their components, including the Pml protein, to nuclear track-like structures formed by the viral protein (76)(77)(78).…”

Section: The Tumor Suppressor P53 a Master Regulator Of Cellular Resmentioning

confidence: 99%

Impact of the Adenoviral E4 Orf3 Protein on the Activity and Posttranslational Modification of p53

DeHart

Perlman

Flint

2015

J Virol

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Our previous studies have established that the p53 populations that accumulate in normal human cells exposed to etoposide or infected by an E1B 55-kDa protein-null mutant of human adenovirus type 5 carry a large number of posttranslational modifications at numerous residues (C. J. DeHart, J. S. Chahal, S. J. Flint, and D. H. Perlman, Mol Cell Proteomics 13:1-17, 2014, http: //dx.doi.org/10.1074/mcp.M113.030254). In the absence of this E1B protein, the p53 transcriptional program is not induced, and it has been reported that the viral E4 Orf3 protein inactivates p53 (C. Soria, F. E. Estermann, K. C. Espantman, and C. C. O'Shea, Nature 466:1076 -1081, 2010, http://dx.doi.org/10.1038/nature09307). As the latter protein disrupts nuclear Pml bodies, sites at which p53 is modified, we used mass spectrometry to catalogue the posttranscriptional modifications of the p53 population that accumulates when neither the E1B 55-kDa nor the E4 Orf3 protein is made in infected cells. Eighty-five residues carrying 163 modifications were identified. The overall patterns of posttranslational modification of this population and p53 present in cells infected by an E1B 55-kDa-null mutant were similar. The efficiencies with which the two forms of p53 bound to a consensus DNA recognition sequence could not be distinguished and were lower than that of transcriptionally active p53. The absence of the E4 Orf3 protein increased expression of several p53-responsive genes when the E1B protein was also absent from infected cells. However, expression of these genes did not attain the levels observed when p53 was activated in response to etoposide treatment and remained lower than those measured in mock-infected cells. T he cellular p53 protein was discovered by virtue of its interaction with the major product of the simian virus 40 oncogene, large T antigen (1, 2). The p53 tumor suppressor is a master regulator of cellular responses to internal and external stresses, when it can induce inhibition of cell cycle progression, apoptosis, or other responses, such as changes in metabolism. Under normal conditions, the human p53 protein is maintained at low concentrations, for example, as a result of its targeting for proteasomal degradation by the E3 ubiquitin ligase Hdm2 (3-5). Once stabilized and activated in response to genotoxic and other forms of stress, p53 binds to specific promoter sequences to activate or repress the transcription of numerous target genes (6-10) and can also operate in the cytoplasm to induce apoptosis by transcription-independent mechanisms (reviewed in references 11 to 14).One of the first interactions between human adenovirus type 5 (Ad5) and cellular proteins to be identified was the association of the viral E1B 55-kDa protein with p53 (15). In view of its crucial roles in regulating cell survival and other aspects of cellular physiology, considerable effort has since been devoted to elucidation of the impacts of adenoviral gene products on the activities and properties of p53. The viral immediate-early E1A prote...

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“…Many ND10 (nuclear domain 10) components have been demonstrated to have a repressive effect on CMV gene expression and viral replication [reviewed by Saffert and Kalejta (Saffert R T, et al, 2008) and Rivera-Molina et al (Rivera-Molina Y A, et al, 2013)]. The first ND10 protein to be investigated for its role in HCMV gene expression and viral replication was Daxx.…”

Section: Cellular Intrinsic Defensive Response To the Enhancer Effectmentioning

confidence: 99%

Immediate-Early (IE) gene regulation of cytomegalovirus: IE1- and pp71-mediated viral strategies against cellular defenses

Torres

Tang

2014

Virol. Sin.

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Three crucial hurdles hinder studies on human cytomegalovirus (HCMV): strict species specificity, differences between in vivo and in vitro infection, and the complexity of gene regulation. Ever since the sequencing of the whole genome was first accomplished, functional studies on individual genes have been the mainstream in the CMV field. Gene regulation has therefore been elucidated in a more detailed fashion. However, viral gene regulation is largely controlled by both cellular and viral components. In other words, viral gene expression is determined by the virus–host interaction. Generally, cells respond to viral infection in a defensive pattern; at the same time, viruses try to counteract the cellular defense or else hide in the host (latency). Viruses evolve effective strategies against cellular defense in order to achieve replicative success. Whether or not they are successful, cellular defenses remain in the whole viral replication cycle: entry, immediate–early (IE) gene expression, early gene expression, DNA replication, late gene expression, and viral egress. Many viral strategies against cellular defense, and which occur in the immediate–early time of viral infection, have been documented. In this review, we will summarize the documented biological functions of IE1 and pp71 proteins, especially with regard to how they counteract cellular intrinsic defenses.

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Nuclear domain 10 of the viral aspect

Cited by 20 publications

References 97 publications

Progressive multifocal leukoencephalopathy: Dot‐shaped inclusions and virus‐host interactions

Progressive multifocal leukoencephalopathy: Dot‐shaped inclusions and virus‐host interactions

Impact of the Adenoviral E4 Orf3 Protein on the Activity and Posttranslational Modification of p53

Immediate-Early (IE) gene regulation of cytomegalovirus: IE1- and pp71-mediated viral strategies against cellular defenses

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