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Identification of potential key protein interaction networks of BK virus nephropathy in patients receiving kidney transplantation.

ABSTRACT: We aim to identify the key protein interaction networks and implicated pathways of BK virus nephropathy (BKVN) via bioinformatic methods. The microarray data GSE75693 of 30 patients with stable kidney transplantation and 15 with BKVN were downloaded and analyzed by using the limma package to identify differentially expressed genes (DEGs). Then the gene ontology (GO) functional enrichment analysis and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were done to investigate the molecular function (MF), biological process (BP), cellular components (CC) and pathways of DEGs. Finally, protein-protein interactions (PPIs) were constructed, and the hub proteins were identified. As a result, 249 up-regulated genes and 253 down-regulated genes of BKVN patients were selected based on criteria of P?>?0.01 and fold change?>2.0. GO and KEGG showed that DEGs were mainly located in nucleus and cytosol, and were implicated in the immune responses. In the PPI analysis, 26 up-regulated and 8 down-regulated proteins composed the pivotal interaction network. CXCL10, EGF and STAT1 were identified as hub proteins in BKVN. In conclusion, CXCL10, EGF and STAT1 may induce kidney injuries by promoting inflammation and prohibiting reparation of tissue damage in BKVN.

SUBMITTER: Jia L

PROVIDER: S-EPMC5864740 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

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Identification of potential key protein interaction networks of BK virus nephropathy in patients receiving kidney transplantation.

Jia Linpei L Fu Wenjing W Jia Rufu R Wu Leiyun L Li Xiaoxia X Jia Qiang Q Zhang Hongliang H

Scientific reports 20180322 1

We aim to identify the key protein interaction networks and implicated pathways of BK virus nephropathy (BKVN) via bioinformatic methods. The microarray data GSE75693 of 30 patients with stable kidney transplantation and 15 with BKVN were downloaded and analyzed by using the limma package to identify differentially expressed genes (DEGs). Then the gene ontology (GO) functional enrichment analysis and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were done to investigate the ...[more]

PMID: 29567951

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Project description:BACKGROUND:BK Polyomavirus (BKPyV) causes premature graft failure in 1 to 15% of kidney transplant (KT) recipients. High-level BKPyV-viruria and BKPyV-DNAemia precede polyomavirus-associated nephropathy (PyVAN), and guide clinical management decisions. In most cases, BKPyV appears to come from the donor kidney, but data from biopsy-proven PyVAN cases are lacking. Here, we report the early fulminant course of biopsy-proven PyVAN in two male KT recipients in their sixties, receiving kidneys from the same deceased male donor. CASE PRESENTATIONS:Both recipients received intravenous basiliximab induction, and maintenance therapy consisting of tacrolimus (trough levels 3-7?ng/mL from time of engraftment), mycophenolate mofetil 750?mg bid, and prednisolone. At 4?weeks post-transplant, renal function was satisfactory with serum creatinine concentrations of 106 and 72??mol/L in recipient #1 and recipient #2, respectively. Plasma BKPyV-DNAemia was first investigated at 5 and 8?weeks post-transplant being 8.58?×?104 and 1.12?×?106 copies/mL in recipient #1 and recipient #2, respectively. Renal function declined and biopsy-proven PyVAN was diagnosed in both recipients at 12?weeks post-transplant. Mycophenolate mofetil levels were reduced from 750?mg to 250?mg bid while tacrolimus levels were kept below 5?ng/mL. Recipient #2 cleared BKPyV-DNAemia at 5.5?months post-transplant, while recipient #1 had persistent BKPyV-DNAemia of 1.07?×?105 copies/mL at the last follow-up 52?weeks post-transplant. DNA sequencing of viral DNA from early plasma samples revealed apparently identical viruses in both recipients, belonging to genotype Ib-2 with archetype non-coding control region. Retrospective serological work-up, demonstrated that the donor had high BKPyV-IgG-virus-like particle ELISA activity and a high BKPyV-genotype I neutralizing antibody titer, whereas both KT recipients only had low neutralizing antibody titers pre-transplantation. By 20?weeks post-transplant, the neutralizing antibody titer had increased by >?1000-fold in both recipients, but only recipient #2 cleared BKPyV-DNAemia. CONCLUSIONS:Low titers of genotype-specific neutralizing antibodies in recipients pre-transplant, may identify patients at high risk for early fulminant donor-derived BKPyV-DNAemia and PyVAN, but development of high neutralizing antibody titers may not be sufficient for clearance.

Dataset Information

Identification of potential key protein interaction networks of BK virus nephropathy in patients receiving kidney transplantation.

Publications

Identification of potential key protein interaction networks of BK virus nephropathy in patients receiving kidney transplantation.

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