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ABSTRACT: Characterization of BK viruses in serum and urine from kidney transplant recipients with polyomavirus nephropathy

PROVIDER: PRJNA450104 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7001611_1.fastq.gz	Fastqsanger.gz
	SRR7001611_2.fastq.gz	Fastqsanger.gz
	SRR7001612_1.fastq.gz	Fastqsanger.gz
	SRR7001612_2.fastq.gz	Fastqsanger.gz
	SRR7001613_1.fastq.gz	Fastqsanger.gz

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

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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.

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Project description:Gene expression data was analyzed to map with urine proteomics data gene expression data from kidney biopsies from kidney transplant patients with and without acute rejection, chronic allograft nephropathy and BK virus nephritis was used to study gene expression changes during acute rejection, chronic allograft nephropathy and bk virus nephropathy. Samples labeled STA16, STA22, STA14, and STA18 were included in the CAN vs no-CAN analysis as no-CAN samples as they also qualified as non-CAN samples.

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Project description:Kidney transplant injury processes are associated with molecular changes in renal tissue, primarily related to immune cell activation and infiltration. How these processes are reflected by molecular alterations in circulating immune cells is poorly understood. We performed RNA-sequencing on 384 biobanked blood samples from four transplant centers, taken at time of a kidney allograft biopsy, selected for their phenotype (acute T cell- and antibody-mediated rejection, polyomavirus-associated nephropathy, and control). We performed differential expression analysis and pathway analysis per phenotype. In peripheral blood, differentially expressed genes in rejection vs. no rejection samples demonstrated upregulation of glucocorticoid receptor and NOD-like receptor signaling pathways. Pathways enriched in antibody-mediated rejection were strongly immune-specific, whereas pathways enriched in T cell-mediated rejection were less immune related. Differentially expressed genes in polyoma viremia and polyomavirus-associated nephropathy were similar and demonstrated upregulation of mitochondrial dysfunction and interferon signaling pathways. Our results highlight the immune activation pathways in peripheral blood leukocytes at time of antibody-mediated rejection and polyomavirus nephropathy and provide a framework for future therapeutic interventions.

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Project description:Post-Kidney Transplant Urine Microbiome Characterization

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Project description:<p>In this study, we investigated the role of the gut microbiota on the development of complications in kidney transplant recipients. We collected serial fecal specimens from 168 kidney transplant recipients within the first 3 months after transplantation. We performed 16S rRNA gene sequencing of the V4-V5 hypervariable region and examined whether the relative gut abundance of pathogenic bacteria was associated with future development of complications like bacteriuria and urinary tract infections. In a subset of samples, we performed metagenomic sequencing of stool and urine supernatant specimens to determine strain level analysis. </p>

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Project description:Mouse kidney parvovirus (MKPV) is a member of the provisional Chapparvovirus group that causes renal disease in immune-compromised mice, with a disease course reminiscent of polyomavirus-associated nephropathy in immune-suppressed kidney transplant patients. Here we map four MKPV transcripts, created by alternative splicing, to a common transcription initiation region, and use mass spectrometry to identify “p10” and “p15” as novel chapparvovirus accessory proteins produced in MKPV-infected kidneys. p15 and a splicing dependent putative accessory protein NS2 are conserved in all near-complete tetrapod chapparvovirus genomes currently available (from mammals, birds and a reptile). In contrast, p10 may be encoded only by viruses with >60% amino acid identity to MKPV. We show that MKPV is kidney-tropic and that the bat chapparvovirus DrPV-1 and a primate chapparvovirus,CKPV, are also found in the kidneys of their hosts. We propose, therefore, that chapparvoviruses with >60% VP1 amino acid identity to MKPV be classified into a genus Nephro-tropic chapparvoviruses dubbed Nephroparvovirus, which is consistent with nomenclature for the genus Erythroparvovirus.

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