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BKPyV complete sequences

ABSTRACT: Deep sequencing of urine specimens detects two BK polyomavirus genotypes post-hematopoietic stem cell transplantation

PROVIDER: PRJEB29464 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3503321.fastq.gz	Fastqsanger.gz
	ERR3503321_1.fastq.gz	Fastqsanger.gz
	ERR3503321_2.fastq.gz	Fastqsanger.gz
	ERR3503322.fastq.gz	Fastqsanger.gz
	ERR3503322_1.fastq.gz	Fastqsanger.gz

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Array-CGH data of aneuploid tumor populations of different urothelial cancer sites in one patient

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Expression data from blood and biopsies of BKV viremia and nephropathy transplant patients

Project description:We study the global gene expression profiles of BKV viremia and nephropathy patients using microarrays in order to better understand the immunologic response to polyomavirus BK (BKV). BKV has become increasingly prevalent since the introduction of more potent immunosuppressive agents. It has been shown that as many as 30% of renal transplant recipients develop asymptomatic viral shedding in the urine shortly after transplant, 10-20% have viremia, and as many as 1-10% can go on to develop overt nephropathy (BKVN) that might lead to graft loss. To date, the genomics of BKV viremia and BKVN have not been investigated thoroughly by microarray. Patients who were enrolled in the IRB-approved Immune Monitoring Study had blood PAXGene samples taken at post-transplant visits and had clinically indicated biopsy samples were used for analysis. A total of 17 biopsy samples were used for gene expression profiling microarrays, three with histopathologic diagnosis of BKVN, 3 patients with evidence of BK viral replication in peripheral blood, but normal biopsy and 11 patients with normal biopsies or mild IFTA, and stable graft function. Blood PAXGene samples from 40 patients were used for gene expression profiling by microarrays, 14 patients with stable graft function and without BK viremia, 19 patients' blood samples at the time of BKV viremia, and 7 patients blood samples taken 1-2 months prior to development of BK viremia.

2013-05-23 | E-GEOD-47199 | biostudies-arrayexpress

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Expression data from blood and biopsies of BKV viremia and nephropathy transplant patients

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JC polyomavirus whole genome sequencing at the single molecule level reveals emerging viral populations in Progressive Multifocal Leucoencephalopathy

Project description:JC polyomavirus (circular genome) contains two opposite coding regions separated by the regulator non-coding control region (NCCR). NCCR rearrangements and missense mutations in the viral capsid protein VP1 gene differentiate JCV prototype genomes recovered from PML lesions from archetype urine strains. To further investigate the emerging variability of JCV populations in PML, we deep sequenced JCV whole genome recovered from CNS and/or urine samples from HIV- and non HIV-infected PML patients, using single-molecule real-time sequencing (PacBio, Paciﬁc Biosciences). Phylogenetic analysis showed that PML strains distributed among 6 of 7 known genotypes. Whole genome single molecule sequencing provides insight in the genesis of JCV neurotropic populations.

2022-01-12 | E-MTAB-11077 | biostudies-arrayexpress

JC Polyomavirus Infection of Primary Human Renal Epithelial Cells Is Controlled by a Type I IFN-Induced Response

Project description:JC polyomavirus (JCPyV) established a persistent infection, but BK polyomavirus (BKPyV) killed the cells in 15 days. To identify the cellular factors responsible for controlling JCPyV infection and promoting viral persistence, we profiled the transcriptomes of JCPyV- and BKPyV-infected cells at several time points postinfection. We found that interferon-stimulated genes (ISGs) were only activated in the JCPyV and not in the BKPyV-infected cells.

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Ischemia-reperfusion injury and immunosuppressants promote polyomavirus replication through common molecular mechanisms

Project description:Background Immunosuppressants and renal ischemia-reperfusion injury (IRI) are risk factors for BK polyomavirus infection after kidney transplantation. However, the mechanism remains unclear. Methods We used a model of mouse polyomavirus (MPyV) infection to investigate the mechanism of IRI and immunosuppressants to promote polyomavirus replication. Results After primary infection, MPyV established persistent infection in the kidneys until week 9 and subsequently were significantly increased by IRI or immunosuppressants treatment individually. In IRI group, viral loads peaked on day 3 in the left kidney, which were significantly higher than that in the right kidney and the control group, and then gradually decreased. In immunosuppressants group, viral loads increased on day 3 without significant difference between left and right kidney, which were significantly higher than that in the control group, and then maintained at high levels. Protein-protein interaction network analysis screened complement C3, EGFR, and FN1 as core genes. Pathway enrichment analysis based on the IRI or immunosuppressants related genes selected by WGCNA indicated that NF-?B signaling pathway was the main pathway involved in promoting MPyV replication. We further confirmed our findings using published datasets GSE47199 and GSE75693. Conclusions Our study demonstrated that IRI and immunosuppressants promote polyomavirus replication through common molecular mechanisms.

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