Regulation of Polyomavirus Transcription by Viral and Cellular Factors

Yang, June F; You, Jianxin

doi:10.3390/v12101072

Cited by 20 publications

(31 citation statements)

References 133 publications

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“…This strain displays three 68-bp tandem repeat within the NCRR (O-P-P-P-S arrangement) with respect to the archetype strain, carrying a single 68-bp motif. This strain showed less enhancer activity than the prototype strain, thus confirming the significance of the triplicated motifs on transcriptional regulation, and on viral infectious activity [83]. In fact, BKPyV strains isolated from kidney transplant recipients with rearranged NCRR showed higher viral gene expression and viral loads with more extensive pathogenicity [84].…”

Section: Virus Original Source Associated Disease Referencementioning

confidence: 60%

Genetic Diversity of the Noncoding Control Region of the Novel Human Polyomaviruses

Moens

Prezioso

Pietropaolo

2020

Viruses

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The genomes of polyomaviruses are characterized by their tripartite organization with an early region, a late region and a noncoding control region (NCCR). The early region encodes proteins involved in replication and transcription of the viral genome, while expression of the late region generates the capsid proteins. Transcription regulatory sequences for expression of the early and late genes, as well as the origin of replication are encompassed in the NCCR. Cell tropism of polyomaviruses not only depends on the appropriate receptors on the host cell, but cell-specific expression of the viral genes is also governed by the NCCR. Thus far, 15 polyomaviruses have been isolated from humans, though it remains to be established whether all of them are genuine human polyomaviruses (HPyVs). The sequences of the NCCR of these HPyVs show high genetic variability and have been best studied in the human polyomaviruses BK and JC. Rearranged NCCRs in BKPyV and JCPyV, the first HPyVs to be discovered approximately 30 years ago, have been associated with the pathogenic properties of these viruses in nephropathy and progressive multifocal leukoencephalopathy, respectively. Since 2007, thirteen novel PyVs have been isolated from humans: KIPyV, WUPyV, MCPyV, HPyV6, HPyV7, TSPyV, HPyV9, HPyV10, STLPyV, HPyV12, NJPyV, LIPyV and QPyV. This review describes all NCCR variants of the new HPyVs that have been reported in the literature and discusses the possible consequences of NCCR diversity in terms of promoter strength, putative transcription factor binding sites and possible association with diseases.

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Section: Virus Original Source Associated Disease Referencementioning

confidence: 60%

Genetic Diversity of the Noncoding Control Region of the Novel Human Polyomaviruses

Moens

Prezioso

Pietropaolo

2020

Viruses

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“…Another key mechanism is operated by two viral non-structural proteins with oncogenic potential, large T (LT) and small t (ST) antigens ( 5 ). Indeed, the expression of these viral oncoproteins modulate several cell signaling pathways, thereby leading to MCC, through a multistep process ( 6 ). Other MCPyV proteins include structural proteins named major capsid viral protein 1 (VP1) and minor capsid protein 2 (VP2) ( 6 ).…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, the expression of these viral oncoproteins modulate several cell signaling pathways, thereby leading to MCC, through a multistep process ( 6 ). Other MCPyV proteins include structural proteins named major capsid viral protein 1 (VP1) and minor capsid protein 2 (VP2) ( 6 ). Unlike other human polyomaviruses (PyVs) ( 1 ), MCPyV does not seem to express VP3 ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

Serum Antibodies Against the Oncogenic Merkel Cell Polyomavirus Detected by an Innovative Immunological Assay With Mimotopes in Healthy Subjects

Mazziotta¹,

Lanzillotti²,

Torreggiani³

et al. 2021

Front. Immunol.

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Merkel cell polyomavirus (MCPyV), a small DNA tumor virus, has been detected in Merkel cell carcinoma (MCC) and in normal tissues. Since MCPyV infection occurs in both MCC-affected patients and healthy subjects (HS), innovative immunoassays for detecting antibodies (abs) against MCPyV are required. Herein, sera from HS were analyzed with a novel indirect ELISA using two synthetic peptides mimicking MCPyV capsid protein epitopes of VP1 and VP2. Synthetic peptides were designed to recognize IgGs against MCPyV VP mimotopes using a computer-assisted approach. The assay was set up evaluating its performance in detecting IgGs anti-MCPyV on MCPyV-positive (n=65) and -negative (n=67) control sera. Then, the ELISA was extended to sera (n=548) from HS aged 18-65 yrs old. Age-specific MCPyV-seroprevalence was investigated. Performance evaluation indicated that the assay showed 80% sensitivity, 91% specificity and 83.9% accuracy, with positive and negative predictive values of 94.3% and 71%, respectively. The ratio expected/obtained data agreement was 86%, with a Cohen’s kappa of 0.72. Receiver-operating characteristic (ROC) curves analysis indicated that the areas under the curves (AUCs) for the two peptides were 0.82 and 0.74, respectively. Intra-/inter-run variations were below 9%. The overall prevalence of serum IgGs anti-MCPyV in HS was 62.9% (345/548). Age-specific MCPyV-seroprevalence was 63.1% (82/130), 56.7% (68/120), 64.5% (91/141), and 66.2% (104/157) in HS aged 18-30, 31-40, 41-50 and 51-65 yrs old, respectively (p>0.05). Performance evaluation suggests that our indirect ELISA is reliable in detecting IgGs anti-MCPyV. Our immunological data indicate that MCPyV infection occurs asymptomatically, at a relatively high prevalence, in humans.

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“…Although numerous transcription factors (TFs) have been predicted or confirmed to bind to the NCCR of various polyomaviruses to regulate viral early and late gene expression and determine the polyomavirus cell or tissue tropism, few studies have been performed to investigate how viral miRNA expression is regulated by TFs, even though the TFs that could regulate viral late gene expression probably may also control miRNA expression (Yang and You, 2020). Sp1 was among the first TFs identified to bind the NCCR of SV40 and is predicted to bind to the NCCR of all human polyomaviruses (Dynan and Tjian, 1983;Gidoni et al, 1985;Bethge et al, 2015;Ajuh et al, 2018).…”

Section: Regulation Of Polyomavirus Mirna Expressionmentioning

confidence: 99%

Biology of Polyomavirus miRNA

Zou

Imperiale

2021

Front. Microbiol.

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Polyomaviruses are a family of non-enveloped DNA viruses with wide host ranges. Human polyomaviruses typically cause asymptomatic infection and establish persistence but can be reactivated under certain conditions and cause severe diseases. Most well studied polyomaviruses encode a viral miRNA that regulates viral replication and pathogenesis by targeting both viral early genes and host genes. In this review, we summarize the current knowledge of polyomavirus miRNAs involved in virus infection. We review in detail the regulation of polyomavirus miRNA expression, as well as the role polyomavirus miRNAs play in viral pathogenesis by controlling both host and viral gene expression. An overview of the potential application of polyomavirus miRNA as a marker for the progression of polyomaviruses associated diseases and polyomaviruses reactivation is also included.

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Regulation of Polyomavirus Transcription by Viral and Cellular Factors

Cited by 20 publications

References 133 publications

Genetic Diversity of the Noncoding Control Region of the Novel Human Polyomaviruses

Genetic Diversity of the Noncoding Control Region of the Novel Human Polyomaviruses

Serum Antibodies Against the Oncogenic Merkel Cell Polyomavirus Detected by an Innovative Immunological Assay With Mimotopes in Healthy Subjects

Biology of Polyomavirus miRNA

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