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Conference Paper: Quantitative and genotypic analysis of polyoma BK viruria during hemorrhagic cystitis complicating bone marrow transplantation

TitleQuantitative and genotypic analysis of polyoma BK viruria during hemorrhagic cystitis complicating bone marrow transplantation
Authors
Issue Date2001
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
The 43rd Annual Meeting of American Society of Hematology (ASH 2001), Orlando, FL., 7-11 December 2001. In Blood, 2001, v. 98 n. 6, p. 1971-1978 How to Cite?
AbstractPolyoma BK virus (BKV) is frequently identified in the urine of bone marrow transplantation (BMT) patients with hemorrhagic cystitis (HC). However, viruria is common even in asymptomatic patients, making a direct causative role of BKV difficult to establish. This study prospectively quantified BK viruria and viremia in 50 BMT patients to define the quantitative relationship of BKV reactivation with HC. Adenovirus (ADV) was similarly quantified as a control. More than 800 patient samples were quantified for BKV VP1 gene with a real-time quantitative polymerase chain reaction. Twenty patients (40%) developed HC, 6 with gross hematuria (HC grade 2 or higher) and 14 with microscopic hematuria (HC grade 1). When compared with asymptomatic patients, patients with HC had significantly higher peak BK viruria (6 x 10(12) versus 5.7 x 10(7) genome copies/d, P <.001) and larger total amounts of BKV excreted during BMT (4.9 x 10(13) versus 7.7 x 10(8) genome copies, P <.001). There was no detectable increase in BK viremia. Binary logistic regression analysis showed that BK viruria was the only risk factor, with HC not related to age, conditioning regimen, type of BMT, and graft-versus-host disease. Furthermore, the levels of ADV viruria in patients with or without HC were similar and comparable with those of BK viruria in patients without HC, suggesting that the significant increase in BK viruria in HC patients was not due to background viral reactivation or damage to the urothelium. BK viruria was quantitatively related to the occurrence of HC after BMT.
Persistent Identifierhttp://hdl.handle.net/10722/102250
ISSN
2015 Impact Factor: 11.841
2015 SCImago Journal Rankings: 6.395

 

DC FieldValueLanguage
dc.contributor.authorLeung, AYH-
dc.contributor.authorSuen, CK-
dc.contributor.authorLie, AKW-
dc.contributor.authorLiang, RHS-
dc.contributor.authorYuen, KY-
dc.contributor.authorKwong, YL-
dc.date.accessioned2010-09-25T20:23:04Z-
dc.date.available2010-09-25T20:23:04Z-
dc.date.issued2001-
dc.identifier.citationThe 43rd Annual Meeting of American Society of Hematology (ASH 2001), Orlando, FL., 7-11 December 2001. In Blood, 2001, v. 98 n. 6, p. 1971-1978-
dc.identifier.issn0006-4971-
dc.identifier.urihttp://hdl.handle.net/10722/102250-
dc.description.abstractPolyoma BK virus (BKV) is frequently identified in the urine of bone marrow transplantation (BMT) patients with hemorrhagic cystitis (HC). However, viruria is common even in asymptomatic patients, making a direct causative role of BKV difficult to establish. This study prospectively quantified BK viruria and viremia in 50 BMT patients to define the quantitative relationship of BKV reactivation with HC. Adenovirus (ADV) was similarly quantified as a control. More than 800 patient samples were quantified for BKV VP1 gene with a real-time quantitative polymerase chain reaction. Twenty patients (40%) developed HC, 6 with gross hematuria (HC grade 2 or higher) and 14 with microscopic hematuria (HC grade 1). When compared with asymptomatic patients, patients with HC had significantly higher peak BK viruria (6 x 10(12) versus 5.7 x 10(7) genome copies/d, P <.001) and larger total amounts of BKV excreted during BMT (4.9 x 10(13) versus 7.7 x 10(8) genome copies, P <.001). There was no detectable increase in BK viremia. Binary logistic regression analysis showed that BK viruria was the only risk factor, with HC not related to age, conditioning regimen, type of BMT, and graft-versus-host disease. Furthermore, the levels of ADV viruria in patients with or without HC were similar and comparable with those of BK viruria in patients without HC, suggesting that the significant increase in BK viruria in HC patients was not due to background viral reactivation or damage to the urothelium. BK viruria was quantitatively related to the occurrence of HC after BMT.-
dc.languageeng-
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/-
dc.relation.ispartofBlood-
dc.subject.meshBK Virus - genetics - isolation & purification-
dc.subject.meshBone Marrow Transplantation - adverse effects-
dc.subject.meshCystitis - diagnosis - etiology - virology-
dc.subject.meshHematuria - diagnosis - etiology - virology-
dc.subject.meshPapillomavirus Infections - diagnosis - etiology - virology-
dc.subject.meshUrine - virology-
dc.titleQuantitative and genotypic analysis of polyoma BK viruria during hemorrhagic cystitis complicating bone marrow transplantation-
dc.typeConference_Paper-
dc.identifier.emailLeung, AYH: ayhleung@hku.hk-
dc.identifier.emailLie, AKW: akwlie@hku.hk-
dc.identifier.emailLiang, RHS: rliang@hku.hk-
dc.identifier.emailYuen, KY: kyyuen@hku.hk-
dc.identifier.emailKwong, YL: ylkwong@hku.hk-
dc.identifier.authorityLeung, AYH=rp00265-
dc.identifier.authorityLiang, RHS=rp00345-
dc.identifier.authorityYuen, KY=rp00366-
dc.identifier.authorityKwong, YL=rp00358-
dc.identifier.doi10.1182/blood.V98.6.1971-
dc.identifier.pmid11535537-
dc.identifier.hkuros66907-
dc.identifier.volume98-
dc.identifier.issue6-
dc.identifier.spage1971-
dc.identifier.epage1978-
dc.publisher.placeUnited States-
dc.customcontrol.immutablesml 170111-

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