Mediation of Epstein–Barr virus EBNA-LP transcriptional coactivation by Sp100

Ling, Paul D.; Peng, Rong; Nakajima, Ayako; Jiang, Yu; Tan, Jie; Moses, Stephanie M; Yang, Wei; Kieff, Elliott; Bloch, Kenneth D.; Bloch, Donald B.

doi:10.1038/sj.emboj.7600820

Cited by 83 publications

(88 citation statements)

References 65 publications

(102 reference statements)

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“…Sp100, yet another major PML NBs component, has been implicated in repression of HSV-1 gene expression (Negorev et al, 2006) and in the regulation of Epstein-Barr virus transcription (Ling et al, 2005). It is confirmed that Sp100 is also involved in HSV-1 genome repression in the absence of ICP0 in human fibroblasts by the observation that depletion of Sp100 results in a similar increase in ICP0-null mutant gene expression (Everett et al, 2008a).…”

Section: Pml/sp100-related Repression Mechanism In the Absence Of Icp0supporting

confidence: 66%

The potential link between PML NBs and ICP0 in regulating lytic and latent infection of HSV-1

2012

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Herpes simplex virus type 1 (HSV-1) is a common human pathogen causing cold sores and even more serious diseases. It can establish a latent stage in sensory ganglia after primary epithelial infections, and reactivate in response to stress or sunlight. Previous studies have demonstrated that viral immediate-early protein ICP0 plays a key role in regulating the balance between lytic and latent infection. Recently, It has been determined that promyelocytic leukemia (PML) nuclear bodies (NBs), small nuclear sub-structures, contribute to the repression of HSV-1 infection in the absence of functional ICP0. In this review, we discuss the fundamentals of the interaction between ICP0 and PML NBs, suggesting a potential link between PML NBs and ICP0 in regulating lytic and latent infection of HSV-1.

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Section: Pml/sp100-related Repression Mechanism In the Absence Of Icp0supporting

confidence: 66%

The potential link between PML NBs and ICP0 in regulating lytic and latent infection of HSV-1

2012

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“…Genetic variation in SP140 could influence risk through differing response to antigenic challenge as its coactivation may be important for establishment of latent viral infections and B-cell immortalization. 20 Genome-wide association studies have shown that the 128-to 130-Mb interval at 8q24.21 harbors multiple independent loci with different tumor specificities, even though it is bereft of genes. The colorectal-prostate cancer association affects TCF4 binding to an enhancer for MYC, providing a mechanistic basis for this 8q24.21 association.…”

Section: Resultsmentioning

confidence: 99%

Inherited genetic susceptibility to monoclonal B-cell lymphocytosis

Crowther-Swanepoel

Corre²,

Lloyd

et al. 2010

Blood

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Monoclonal B-cell lymphocytosis (MBL)is detectable in > 3% of the general population. Recent data are compatible, at least in a proportion of cases, with MBL being a progenitor lesion for chronic lymphocytic leukemia (CLL) and a surrogate for inherited predisposition. IntroductionThe strong familial risk of chronic lymphocytic leukemia (CLL) provides evidence for inherited susceptibility to the disease. 1 Diagnosis of CLL is based on a B-cell count of more than or equal to 5 ϫ 10 9 /L and the presence of CD19, CD5, and CD23, weak expression of CD20, CD79b, and immunoglobulin receptor on B-cells. 2 Persons with peripheral CLL-phenotype monoclonal B cells less than 5 ϫ 10 9 /L but no clinical features of CLL are classified as having monoclonal B-cell lymphocytosis (MBL). 3 Approximately 10% to 15% of persons with a lymphocytosis have MBL, and 1% to 5% per year require treatment for progressive disease. 4,5 Very low levels of CLL-phenotype cells (Ͻ 0.01 ϫ 10 9 /L) are detected in more than 5% of adults. 6 A genome-wide association study 7,8 has identified single nucleotide polymorphisms (SNPs) mapping to 2q13(rs17483466), 2q37.1(rs13397985, SP140), 2q37.3(rs757978, FARP2), 6p25.3(rs872071, IRF4), 8q24.21(rs2456449), 11q24.1(rs735665), 15q21.3(rs7169431), 15q23(rs7176508), 16q24.1(rs305061), and 19q13.32(rs11083846, PRKD2), conferring a modest but significant increase in CLL risk. 7 Recent studies are compatible with MBL being a surrogate marker for inherited genetic susceptibility to CLL. 9 To explore whether the 10 SNPs influence CLL risk through predisposition to MBL, we analyzed 3 independent case-control series totaling 419 MBL cases and 1753 controls. MethodsThe first 2 series were ascertained through laboratory investigations for an asymptomatic lymphocytosis. The series ascertained by the Hematological Malignancy Diagnostic Service (HMDS) was composed of 264 MBL cases (139 male; mean age, 71 years; SD, 11 years; mean lymphocyte count, 5.9 ϫ 10 9 /L; SD, 2 ϫ 10 9 /L; mean B-cell count, 3.0 ϫ 10 9 /L; SD, 1 ϫ 10 9 /L), who were all United Kingdom residents. Blood samples from 891 healthy persons (340 male; mean age, 59 years; SD, 11 years) collected through the National Study of Colorectal Cancer Genetics 10 and Genetic Lung Cancer Predisposition Study 11 studies served as controls. These persons were all United Kingdom residents and had self-reported European ancestry. Collection of samples and clinical information was undertaken with informed consent in accordance with the Declaration of Helsinki and with ethical review board approval from the Institute of Cancer Research. The second series were ascertained through the Amedeo Avogadro University of Eastern Piedmont (AAUEP) and consisted of 78 Italian MBL cases from Novara (42 male; mean age, 68 years; SD, 10 years; mean lymphocyte count, 4.7 ϫ 10 9 /L; SD, 2 ϫ 10 9 /L; mean B-cell count, 2.7 ϫ 10 9 /L; SD, 1.1 ϫ 10 9 /L). 4 Blood samples from 170 healthy persons (95 male; mean age, 68 years; SD, 10 years) from the same geographic area with normal hematology...

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“…Nevertheless, it is clear that many adenoviruses and herpesviruses encode regulatory proteins that localize to, and disrupt the functions of, PML nuclear bodies (reviewed by Everett & Chelbi-Alix, 2007). For example, to aid replication, the AdV E4orf3 protein reorganizes PML nuclear bodies into thread-like structures (Doucas et al, 1996;Stracker et al, 2005;Hoppe et al, 2006;Ullman et al, 2007); the ICP0 protein of HSV-1 has E3 ligase activity that induces the degradation of PML and SUMO-modified forms of Sp100 (reviewed by Hagglund & Roizman, 2004); EBV nuclear antigen 5 (EBNA5) interacts with Sp100A, but this may be to release PML-associated factors from PML nuclear bodies to aid viral gene expression (Ling et al, 2005); HCMV IE72 induces the loss of SUMO-modified forms of PML to disrupt PML nuclear bodies (Ahn & Hayward, 2000;Kang et al, 2006), and pp71 localizes to PML nuclear bodies to induce the degradation of hDaxx, which inhibits HCMV IE gene expression (Cantrell & Bresnahan, 2006;Preston & Nicholl, 2006;Saffert & Kalejta, 2006). Even certain RNA viruses that replicate in the cytoplasm may block PML function.…”

Section: General Considerations Of How Viruses Evade the Ifn Responsementioning

confidence: 99%

Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures

Randall

Goodbourn

2008

Journal of General Virology

1,387

1,420

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The interferon (IFN) system is an extremely powerful antiviral response that is capable of controlling most, if not all, virus infections in the absence of adaptive immunity. However, viruses can still replicate and cause disease in vivo, because they have some strategy for at least partially circumventing the IFN response. We reviewed this topic in 2000 [Goodbourn, S., Didcock, L. & Randall, R. E. (2000). J Gen Virol 81, 2341-2364] but, since then, a great deal has been discovered about the molecular mechanisms of the IFN response and how different viruses circumvent it. This information is of fundamental interest, but may also have practical application in the design and manufacture of attenuated virus vaccines and the development of novel antiviral drugs. In the first part of this review, we describe how viruses activate the IFN system, how IFNs induce transcription of their target genes and the mechanism of action of IFN-induced proteins with antiviral action. In the second part, we describe how viruses circumvent the IFN response. Here, we reflect upon possible consequences for both the virus and host of the different strategies that viruses have evolved and discuss whether certain viruses have exploited the IFN response to modulate their life cycle (e.g. to establish and maintain persistent/latent infections), whether perturbation of the IFN response by persistent infections can lead to chronic disease, and the importance of the IFN system as a species barrier to virus infections. Lastly, we briefly describe applied aspects that arise from an increase in our knowledge in this area, including vaccine design and manufacture, the development of novel antiviral drugs and the use of IFN-sensitive oncolytic viruses in the treatment of cancer. Biology of the interferon systemThe interferons (IFNs) are a group of secreted cytokines that elicit distinct antiviral effects. They are grouped into three classes called type I, II and III IFNs, according to their amino acid sequence. Type I IFNs (discovered in 1957;Isaacs & Lindenmann, 1957) comprise a large group of molecules; mammals have multiple distinct IFN-a genes (13 in man), one to three IFN-b genes (one in man) and other genes, such as IFN-v, -e, -t, -d and -k. The IFN-a and -b genes are induced directly in response to viral infection, whereas IFN-v, -e, -d and -k play less well-defined roles, such as regulators of maternal recognition in pregnancy. Thus, rather than use the term 'type I IFN', we will use IFN-a/b when referring to the virally induced cytokines. Although the multigenic nature of IFN-a has been known for over 20 years, the significance of this is still debatedi.e. whether these genes are expressed differentially in distinct cell types, whether they are inducible by different types of viruses or whether they are functionally specialized (Brideau-Andersen et al., 2007). For the rest of this review, we will not distinguish between IFN-a subtypes. Type III IFNs have been described more recently and comprise IFNl1, -l2 and -l3, also referred to as IL-2...

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Mediation of Epstein–Barr virus EBNA-LP transcriptional coactivation by Sp100

Cited by 83 publications

References 65 publications

The potential link between PML NBs and ICP0 in regulating lytic and latent infection of HSV-1

The potential link between PML NBs and ICP0 in regulating lytic and latent infection of HSV-1

Inherited genetic susceptibility to monoclonal B-cell lymphocytosis

Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures

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