Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJEB22539 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	ERR2116043.fastq.gz	Fastqsanger.gz
	ERR2116044.fastq.gz	Fastqsanger.gz

Items per page:

1 - 3 of 3

Similar Datasets

Complete genomes of BK Polyomavirus clinical isolates.

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

| PRJEB24289 | ENA

Diversity of BK Polyomavirus genomes

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

| PRJEB29756 | ENA

Single-cell analysis of human kidney biopsy tissue reveals epithelial and immune cell responses to BK polyomavirus infection

Project description:BK polyomavirus (BKV) infection is associated with injury and subsequent graft loss due to the extent of injury or rejection. However, the molecular mechanisms driving injury and subsequent adverse outcomes remain poorly understood. In a cross-sectional study, single-cell RNA sequencing from kidney allograft biopsies was used to assess cell type-specific responses between uninfected controls and two distinct phases of BKV infection: peaking (increasing viral blood titers) and resolving (decreasing viral titers following immunosuppression reduction). Genes upregulated in BK viral nephropathy (BKVN) were enriched for polyomavirus infection hallmarks, including ribosome biogenesis, translation, and energy restructuring. Additionally enriched pathways included wound healing, cellular stress, antigen presentation and immune signaling. Even without BKVN (peaking BK viremia alone), epithelial cells expressed signatures for wound healing, cellular stress, and extracellular matrix remodeling. In vivo tubular cell responses at single-cell resolution were validated against single cell transcriptomic data of BKV infected cells in a cell culture model. Despite similarities, in vivo tubular cells underwent metabolic adaptation favoring fatty acid oxidation and proinflammatory responses not observed in culture models likely from an absent innate and adaptive immune system. Despite lymphopenia and immunosuppressive therapies, the proportion of recipient derived intrarenal adaptive immune cells was expanded in biopsies associated with peaking viremia alongside activation of innate immune responses. Adaptive immune cells continued to have persistent inflammatory signaling and remodeling of energy metabolism during the resolving phase of infection. These novel insights into BKV-associated injury could have implications for clinical management and improved allograft outcomes

2026-02-10 | GSE317012 | 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

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

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

Project description:BK Polyomavirus Sequencing

| PRJNA1198305 | ENA

Project description:BK polyomavirus sequencing

| PRJNA670723 | ENA

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data