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Normal human urothelial cells infected with BK polyomavirus (BKPyV) in the presence or absence of interferon gamma (IFNg)

ABSTRACT: Normal human urothelial cells infected with BK polyomavirus (BKPyV) in the presence or absence of interferon gamma (IFNg)

PROVIDER: PRJNA728925 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14509900_1.fastq.gz	Fastqsanger.gz
	SRR14509900_2.fastq.gz	Fastqsanger.gz
	SRR14509901_1.fastq.gz	Fastqsanger.gz
	SRR14509901_2.fastq.gz	Fastqsanger.gz
	SRR14509902_1.fastq.gz	Fastqsanger.gz

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Normal human urothelial cells infected with BK polyomavirus (BKPyV) in the presence or absence of interferon gamma (IFNg)

Project description:mRNAseq data for differentiated and mitotically-quiescent Normal Human Urothelial (NHU) cells at 14 days post infection (dpi) with BKPyV

2022-02-22 | GSE174244 | GEO

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.

2019-08-15 | GSE135833 | GEO

Temporal proteomic analysis of BK polyomavirus infection reveals virus-induced G2 arrest and highly effective evasion of innate immune sensing

Project description:BK polyomavirus (BKPyV) is a small DNA virus that establishes a life-long persistent infection in the urinary tract of most people. BKPyV is known to cause severe morbidity in renal transplant recipients and can lead to graft rejection. The simple 5.2 kilobase pair dsDNA genome expresses just seven known proteins, thus it relies heavily on host machinery to replicate. How the host proteome changes over the course of infection is key to understanding this host:virus interplay. Here for the first time quantitative temporal viromics has been used to quantify global changes in >9,000 host proteins in two types of primary human epithelial cell throughout 72 hours of BKPyV infection. These data demonstrate the importance both of cell cycle progression and pseudo-G2 arrest in effective BKPyV replication, along with a surprising lack of innate immune response throughout the whole virus replication cycle. BKPyV thus evades pathogen recognition to prevent activation of innate immune responses in a sophisticated manner.

2019-05-23 | PXD013940 | Pride

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

Project description:Donor-derived, metastatic urothelial cancer after kidney transplantation associated with BK polyomavirus bearing a critical deletion in the viral NCCR

2018-01-01 | GSE90778 | GEO

Diversity of BK Polyomavirus genomes

Project description:Increased diversity of BK Polyomavirus genomes detected by whole genome sequencing in transplant recipients

| PRJEB29756 | ENA

Complete genomes of BK Polyomavirus clinical isolates.

Project description:Complete BK Polyomavirus genome sequences from patients with urinary tract infections.

| PRJEB24289 | ENA

Complete genomes of BK Polyomavirus isolates CAMB-1035 and CAMB-1055

Project description:Complete BK Polyomavirus genome sequences from two patients with urinary tract infections using the Ion Torrent platform

| PRJEB22539 | ENA

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.

2021-12-27 | GSE192576 | GEO

Devosia sp. BK strain:BK

Project description:Devosia sp. BK strain:BK Genome sequencing and assembly

| PRJNA756840 | ENA

Brincidofovir (CMX001) inhibits BK polyomavirus replication in primary human urothelial cells.

Project description:BK polyomavirus (BKPyV)-associated hemorrhagic cystitis (PyVHC) complicates 5 to 15% of allogeneic hematopoietic stem cell transplantations. Targeted antivirals are still unavailable. Brincidofovir (BCV; previously CMX001) has shown inhibitory activity against diverse viruses, including BKPyV in a primary human renal tubule cell culture model of polyomavirus-associated nephropathy. We investigated the effects of BCV in BKPyV-infected and uninfected primary human urothelial cells (HUCs), the target cells of BKPyV in PyVHC. The BCV concentrations causing 50 and 90% reductions (EC50 and EC90) in the number of intracellular BKPyV genome equivalents per cell (icBKPyV) were 0.27 μM and 0.59 μM, respectively. At 0.63 μM, BCV reduced viral late gene expression by 90% and halted progeny release. Preinfection treatment for only 24 h reduced icBKPyV similarly to treatment from 2 to 72 h postinfection, while combined pre- and postinfection treatment suppressed icBKPyV completely. After investigating BCV's effects on HUC viability, mean selectivity indices at 50 and 90% inhibition (SI50 and SI90) calculated for cellular DNA replication were 2.7 and 2.9, respectively, those for mitochondrial activity were 8.9 and 10.4, those for total ATP were 8.6 and 8.2, and those for membrane integrity were 25.9 and 16.7. The antiviral and cytostatic effects, but less so the cytotoxic effects, were inversely related to cell density. The cytotoxic effects at concentrations of ≥10 μM were rapid and likely related to BCV's lipid moiety. After carefully defining the antiviral, cytostatic, and cytotoxic properties of BCV in HUCs, we conclude that a preemptive or prophylactic approach in PyVHC is likely to give the best results.

| S-EPMC4432119 | biostudies-literature

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