IFNL4 rs368234815 polymorphism does not predict risk of BK virus associated nephropathy after living‐donor kidney transplant: A case‐control study

Background BK polyoma virus (BKPyV) associated nephropathy (BKPyVAN) is a major cause of kidney graft loss in renal transplant patients. Interferons (IFNs) are an important innate immune response against viral infections and genetic polymorphisms of the IFN‐pathways can affect susceptibility and mor...

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Veröffentlicht in:Clinical transplantation 2022-07, Vol.36 (7), p.e14663-n/a
Hauptverfasser: Tanriver, Ursula, Emmerich, Florian, Hummel, Jonas Florian, Jänigen, Bernd, Panning, Marcus, Arnold, Frederic, Tanriver, Yakup
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container_end_page n/a
container_issue 7
container_start_page e14663
container_title Clinical transplantation
container_volume 36
creator Tanriver, Ursula
Emmerich, Florian
Hummel, Jonas Florian
Jänigen, Bernd
Panning, Marcus
Arnold, Frederic
Tanriver, Yakup
description Background BK polyoma virus (BKPyV) associated nephropathy (BKPyVAN) is a major cause of kidney graft loss in renal transplant patients. Interferons (IFNs) are an important innate immune response against viral infections and genetic polymorphisms of the IFN‐pathways can affect susceptibility and mortality during viral infection. Here, we investigated whether the dinucleotide polymorphism rs368234815 (ΔG/TT) in the IFNL4 gene contributed to BKPyV reactivation or BKPyVAN after living‐donor kidney transplantation. Methods This retrospective case‐control study determines the prevalence of IFNL4 variants in a Caucasian population of living‐donor kidney transplant recipients and donors and explores its association with BKPyV infection and BKPyVAN development. We included 28 recipients with BKPyV reactivation, 10 of which developed BKPyVAN and 30 BKPyV negative controls. Targeted sequencing of the IFNL4 gene from both recipients and their respective donors was performed. Results We found IFNL4 rs368234815 ΔG allele frequencies of 41.7% in BKPyV negative and 39.3% in BKPyV positive recipients (P = .85), and 41.7% and 40.4% (P>.99) in their respective donors. IFNL4 rs368234815 ΔG allele frequencies in BKPyVAN developing recipients and their respective donors were 50% and 43.7% (P = .60 and P>.99). Conclusions Our results indicate that the IFNL4 rs368234815 ΔG allele is not associated with BKPyV reactivation, nor the manifestation of BKPyVAN.
doi_str_mv 10.1111/ctr.14663
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Interferons (IFNs) are an important innate immune response against viral infections and genetic polymorphisms of the IFN‐pathways can affect susceptibility and mortality during viral infection. Here, we investigated whether the dinucleotide polymorphism rs368234815 (ΔG/TT) in the IFNL4 gene contributed to BKPyV reactivation or BKPyVAN after living‐donor kidney transplantation. Methods This retrospective case‐control study determines the prevalence of IFNL4 variants in a Caucasian population of living‐donor kidney transplant recipients and donors and explores its association with BKPyV infection and BKPyVAN development. We included 28 recipients with BKPyV reactivation, 10 of which developed BKPyVAN and 30 BKPyV negative controls. Targeted sequencing of the IFNL4 gene from both recipients and their respective donors was performed. Results We found IFNL4 rs368234815 ΔG allele frequencies of 41.7% in BKPyV negative and 39.3% in BKPyV positive recipients (P = .85), and 41.7% and 40.4% (P&gt;.99) in their respective donors. IFNL4 rs368234815 ΔG allele frequencies in BKPyVAN developing recipients and their respective donors were 50% and 43.7% (P = .60 and P&gt;.99). Conclusions Our results indicate that the IFNL4 rs368234815 ΔG allele is not associated with BKPyV reactivation, nor the manifestation of BKPyVAN.</description><identifier>ISSN: 0902-0063</identifier><identifier>EISSN: 1399-0012</identifier><identifier>DOI: 10.1111/ctr.14663</identifier><identifier>PMID: 35368114</identifier><language>eng</language><publisher>Denmark</publisher><subject>allograft rejection ; BK virus ; IFNL4 polymorphisms ; living‐donor kidney transplant ; polyomavirus associated nephropathy</subject><ispartof>Clinical transplantation, 2022-07, Vol.36 (7), p.e14663-n/a</ispartof><rights>2022 The Authors. published by John Wiley &amp; Sons Ltd.</rights><rights>This article is protected by copyright. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3203-fce62bcd514df00dda8efad07192f1fbd30b3f9cf9dd7c017e3f796444ac68313</cites><orcidid>0000-0002-4806-2548 ; 0000-0001-9401-8815 ; 0000-0002-4573-8856</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fctr.14663$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fctr.14663$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35368114$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tanriver, Ursula</creatorcontrib><creatorcontrib>Emmerich, Florian</creatorcontrib><creatorcontrib>Hummel, Jonas Florian</creatorcontrib><creatorcontrib>Jänigen, Bernd</creatorcontrib><creatorcontrib>Panning, Marcus</creatorcontrib><creatorcontrib>Arnold, Frederic</creatorcontrib><creatorcontrib>Tanriver, Yakup</creatorcontrib><title>IFNL4 rs368234815 polymorphism does not predict risk of BK virus associated nephropathy after living‐donor kidney transplant: A case‐control study</title><title>Clinical transplantation</title><addtitle>Clin Transplant</addtitle><description>Background BK polyoma virus (BKPyV) associated nephropathy (BKPyVAN) is a major cause of kidney graft loss in renal transplant patients. Interferons (IFNs) are an important innate immune response against viral infections and genetic polymorphisms of the IFN‐pathways can affect susceptibility and mortality during viral infection. Here, we investigated whether the dinucleotide polymorphism rs368234815 (ΔG/TT) in the IFNL4 gene contributed to BKPyV reactivation or BKPyVAN after living‐donor kidney transplantation. Methods This retrospective case‐control study determines the prevalence of IFNL4 variants in a Caucasian population of living‐donor kidney transplant recipients and donors and explores its association with BKPyV infection and BKPyVAN development. We included 28 recipients with BKPyV reactivation, 10 of which developed BKPyVAN and 30 BKPyV negative controls. Targeted sequencing of the IFNL4 gene from both recipients and their respective donors was performed. Results We found IFNL4 rs368234815 ΔG allele frequencies of 41.7% in BKPyV negative and 39.3% in BKPyV positive recipients (P = .85), and 41.7% and 40.4% (P&gt;.99) in their respective donors. IFNL4 rs368234815 ΔG allele frequencies in BKPyVAN developing recipients and their respective donors were 50% and 43.7% (P = .60 and P&gt;.99). Conclusions Our results indicate that the IFNL4 rs368234815 ΔG allele is not associated with BKPyV reactivation, nor the manifestation of BKPyVAN.</description><subject>allograft rejection</subject><subject>BK virus</subject><subject>IFNL4 polymorphisms</subject><subject>living‐donor kidney transplant</subject><subject>polyomavirus associated nephropathy</subject><issn>0902-0063</issn><issn>1399-0012</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><recordid>eNp1kcFu1DAQhi0EotvCgRdAc4TDtnbs9Sbc2hUtFSuQUDlHXnvMmiZx8DhFufEInHhAngTDFm7MZUajT59G8zP2TPBTUerM5nQqlNbyAVsI2TRLzkX1kC14w6sya3nEjok-l60WevWYHcmV1LUQasF-XF--2ypIVBaVVLVYwRi7uY9p3AfqwUUkGGKGMaELNkMKdAvRw8VbuAtpIjBE0QaT0cGA4z7F0eT9DMZnTNCFuzB8-vntu4tDTHAb3IAz5GQGGjsz5FdwDtYQFsLGIafYAeXJzU_YI286wqf3_YR9vHx9s3mz3L6_ut6cb5dWVlwuvUVd7axbCeU8586ZGr1xfC2aygu_c5LvpG-sb5xbWy7WKP260UopY3UthTxhLw7eMcUvE1Ju-0AWu3IbxonaSivdKKHquqAvD6hNkSihb8cUepPmVvD2dwxtiaH9E0Nhn99rp12P7h_59-8FODsAX0OH8_9N7ebmw0H5C1s9lbU</recordid><startdate>202207</startdate><enddate>202207</enddate><creator>Tanriver, Ursula</creator><creator>Emmerich, Florian</creator><creator>Hummel, Jonas Florian</creator><creator>Jänigen, Bernd</creator><creator>Panning, Marcus</creator><creator>Arnold, Frederic</creator><creator>Tanriver, Yakup</creator><scope>24P</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4806-2548</orcidid><orcidid>https://orcid.org/0000-0001-9401-8815</orcidid><orcidid>https://orcid.org/0000-0002-4573-8856</orcidid></search><sort><creationdate>202207</creationdate><title>IFNL4 rs368234815 polymorphism does not predict risk of BK virus associated nephropathy after living‐donor kidney transplant: A case‐control study</title><author>Tanriver, Ursula ; Emmerich, Florian ; Hummel, Jonas Florian ; Jänigen, Bernd ; Panning, Marcus ; Arnold, Frederic ; Tanriver, Yakup</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3203-fce62bcd514df00dda8efad07192f1fbd30b3f9cf9dd7c017e3f796444ac68313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>allograft rejection</topic><topic>BK virus</topic><topic>IFNL4 polymorphisms</topic><topic>living‐donor kidney transplant</topic><topic>polyomavirus associated nephropathy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tanriver, Ursula</creatorcontrib><creatorcontrib>Emmerich, Florian</creatorcontrib><creatorcontrib>Hummel, Jonas Florian</creatorcontrib><creatorcontrib>Jänigen, Bernd</creatorcontrib><creatorcontrib>Panning, Marcus</creatorcontrib><creatorcontrib>Arnold, Frederic</creatorcontrib><creatorcontrib>Tanriver, Yakup</creatorcontrib><collection>Wiley_OA刊</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tanriver, Ursula</au><au>Emmerich, Florian</au><au>Hummel, Jonas Florian</au><au>Jänigen, Bernd</au><au>Panning, Marcus</au><au>Arnold, Frederic</au><au>Tanriver, Yakup</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IFNL4 rs368234815 polymorphism does not predict risk of BK virus associated nephropathy after living‐donor kidney transplant: A case‐control study</atitle><jtitle>Clinical transplantation</jtitle><addtitle>Clin Transplant</addtitle><date>2022-07</date><risdate>2022</risdate><volume>36</volume><issue>7</issue><spage>e14663</spage><epage>n/a</epage><pages>e14663-n/a</pages><issn>0902-0063</issn><eissn>1399-0012</eissn><abstract>Background BK polyoma virus (BKPyV) associated nephropathy (BKPyVAN) is a major cause of kidney graft loss in renal transplant patients. Interferons (IFNs) are an important innate immune response against viral infections and genetic polymorphisms of the IFN‐pathways can affect susceptibility and mortality during viral infection. Here, we investigated whether the dinucleotide polymorphism rs368234815 (ΔG/TT) in the IFNL4 gene contributed to BKPyV reactivation or BKPyVAN after living‐donor kidney transplantation. Methods This retrospective case‐control study determines the prevalence of IFNL4 variants in a Caucasian population of living‐donor kidney transplant recipients and donors and explores its association with BKPyV infection and BKPyVAN development. We included 28 recipients with BKPyV reactivation, 10 of which developed BKPyVAN and 30 BKPyV negative controls. Targeted sequencing of the IFNL4 gene from both recipients and their respective donors was performed. Results We found IFNL4 rs368234815 ΔG allele frequencies of 41.7% in BKPyV negative and 39.3% in BKPyV positive recipients (P = .85), and 41.7% and 40.4% (P&gt;.99) in their respective donors. IFNL4 rs368234815 ΔG allele frequencies in BKPyVAN developing recipients and their respective donors were 50% and 43.7% (P = .60 and P&gt;.99). Conclusions Our results indicate that the IFNL4 rs368234815 ΔG allele is not associated with BKPyV reactivation, nor the manifestation of BKPyVAN.</abstract><cop>Denmark</cop><pmid>35368114</pmid><doi>10.1111/ctr.14663</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-4806-2548</orcidid><orcidid>https://orcid.org/0000-0001-9401-8815</orcidid><orcidid>https://orcid.org/0000-0002-4573-8856</orcidid><oa>free_for_read</oa></addata></record>
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subjects allograft rejection
BK virus
IFNL4 polymorphisms
living‐donor kidney transplant
polyomavirus associated nephropathy
title IFNL4 rs368234815 polymorphism does not predict risk of BK virus associated nephropathy after living‐donor kidney transplant: A case‐control study
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