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肾移植受者中 BK 病毒的可变来源。

Variable sources of Bk virus in renal allograft recipients.

机构信息

Laboratório de Virologia, Instituto de Medicina Tropical de São Paulo, Universidade de São Paulo, Sao Paulo, Brasil.

Divisão de Moléstias Infecciosas e Parasitárias, do Hospital das Clinicas da Faculdade de Medicina da Universidade de São Paulo, Sao Paulo, Brasil.

出版信息

J Med Virol. 2019 Jun;91(6):1136-1141. doi: 10.1002/jmv.25409. Epub 2019 Feb 4.

DOI:10.1002/jmv.25409
PMID:30680753
Abstract

BK virus is the causative agent of polyomavirus-associated nephropathy, a major cause of kidney transplant failure affecting 1%-10% of recipients. Previous studies that investigated the viral source on the kidney recipient pointed that the donor is implicated in the origin of human polyomavirus BK (BKPyV) infection in recipients, but giving the low genetic variability of BKPyV this subject is still controversial. The aim of this study was to determine if BKPyV replicating in kidney recipients after transplantation is always originated from the donor. Urine and blood samples from 68 pairs of living donors and kidney recipients who underwent renal transplantation from August 2010-September 2011 were screened for BKPyV by real time polymerase chain reaction. Only three recipients presented viremia. When both donors and recipients were BKPyV positive, a larger fragment of VP1 region was obtained and sequenced to determine the level of similarity between them. A phylogenetic tree was built for the 12 pairs of sequences obtained from urine and high level of similarity among all sequences was observed, indicating that homology inferences for donor and recipient viruses must be cautiously interpreted. However, a close inspection on the donor-recipient pairs sequences revealed that 3 of 12 pairs presented considerably different viruses and 4 of 12 presented mixed infection, indicating that the source of BKPyV infection is not exclusively derived from the donor. We report that about 60% of the renal recipients shed BKPyV genetically distinct from the donor, confronting the accepted concept that the donor is the main source of recipients' infection.

摘要

BK 病毒是多瘤病毒相关性肾病的病原体,是导致 1%-10%肾移植受者移植肾失功的主要原因。既往研究表明,在受者中,供者是人类多瘤病毒 BK(BKPyV)感染的来源,但由于 BKPyV 的遗传变异性较低,这一观点仍存在争议。本研究旨在确定移植后肾移植受者中复制的 BKPyV 是否始终来源于供者。对 2010 年 8 月至 2011 年 9 月期间接受肾移植的 68 对活体供者和肾移植受者的尿液和血液样本进行了实时聚合酶链反应检测 BKPyV。仅 3 例受者出现病毒血症。当供者和受者均为 BKPyV 阳性时,获得了更大的 VP1 区片段并进行测序,以确定它们之间的相似性水平。对从尿液中获得的 12 对序列构建了系统进化树,所有序列均显示出高度相似性,表明对供者和受者病毒的同源性推断必须谨慎解释。然而,对供者-受者序列的仔细检查显示,12 对中有 3 对存在明显不同的病毒,4 对存在混合感染,表明 BKPyV 感染的来源并非完全来自供者。我们报告称,约 60%的肾移植受者排出的 BKPyV 在遗传上与供者不同,这与供者是受者感染的主要来源的公认概念相矛盾。

相似文献

1
Variable sources of Bk virus in renal allograft recipients.肾移植受者中 BK 病毒的可变来源。
J Med Virol. 2019 Jun;91(6):1136-1141. doi: 10.1002/jmv.25409. Epub 2019 Feb 4.
2
Impact of donor BK polyomavirus replication on recipient infections in living donor transplantation.供体BK多瘤病毒复制对活体供体移植中受体感染的影响。
Transpl Infect Dis. 2018 Aug;20(4):e12917. doi: 10.1111/tid.12917. Epub 2018 Jun 11.
3
Impact of HPyV9 and TSPyV coinfection on the development of BK polyomavirus viremia and associated nephropathy after kidney transplantation.人乳头瘤病毒 9 型和 TSPyV 合并感染对肾移植后 BK 多瘤病毒血症及相关肾病发展的影响。
J Med Virol. 2019 Jun;91(6):1142-1147. doi: 10.1002/jmv.25397. Epub 2019 Jan 21.
4
Prevalence of polyoma BK virus infection among living-donor renal transplant recipients.活体供肾肾移植受者中多瘤BK病毒感染的患病率。
Transpl Infect Dis. 2016 Aug;18(4):529-37. doi: 10.1111/tid.12557. Epub 2016 Jul 29.
5
Early fulminant BK polyomavirus-associated nephropathy in two kidney transplant patients with low neutralizing antibody titers receiving allografts from the same donor.两名接受同一供体同种异体移植物的肾移植患者,由于低中和抗体滴度而发生早期暴发性 BK 多瘤病毒相关性肾病。
Virol J. 2020 Jan 10;17(1):5. doi: 10.1186/s12985-019-1275-9.
6
Impact of Pretransplant Donor BK Viruria in Kidney Transplant Recipients.移植前供体 BK 病毒尿症对肾移植受者的影响。
J Infect Dis. 2019 Jul 2;220(3):370-376. doi: 10.1093/infdis/jiz114.
7
Pretransplantation Donor-Recipient Pair Seroreactivity Against BK Polyomavirus Predicts Viremia and Nephropathy After Kidney Transplantation.移植前供体-受体对BK多瘤病毒的血清反应性可预测肾移植后的病毒血症和肾病。
Am J Transplant. 2017 Jan;17(1):161-172. doi: 10.1111/ajt.13880. Epub 2016 Jul 8.
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Stabilization of renal function after the first year of follow-up in kidney transplant recipients treated for significant BK polyomavirus infection or BK polyomavirus-associated nephropathy.肾移植受者在接受显著BK多瘤病毒感染或BK多瘤病毒相关性肾病治疗后的第一年随访期后肾功能的稳定情况。
Transpl Infect Dis. 2017 Jun;19(3). doi: 10.1111/tid.12681. Epub 2017 Apr 17.
9
Urine Donor-Derived Cell-Free DNA Helps Discriminate BK Polyomavirus-Associated Nephropathy in Kidney Transplant Recipients With BK Polyomavirus Infection.尿源无细胞 DNA 有助于区分肾移植受者 BK 多瘤病毒感染相关肾病
Front Immunol. 2020 Aug 19;11:1763. doi: 10.3389/fimmu.2020.01763. eCollection 2020.
10
Viral Origin, Clinical Course, and Renal Outcomes in Patients With BK Virus Infection After Living-Donor Renal Transplantation.活体供肾肾移植术后BK病毒感染患者的病毒起源、临床病程及肾脏转归
Transplantation. 2016 Apr;100(4):844-53. doi: 10.1097/TP.0000000000001066.

引用本文的文献

1
Outcomes of Living Kidney Donor Candidates and Living Kidney Recipient Candidates with JC Polyomavirus and BK Polyomavirus Viruria.携带JC多瘤病毒和BK多瘤病毒病毒尿症的活体肾供体候选者及活体肾受体候选者的结局
Int J Nephrol. 2021 Aug 19;2021:8010144. doi: 10.1155/2021/8010144. eCollection 2021.
2
Non-permissive human conventional CD1c+ dendritic cells enable trans-infection of human primary renal tubular epithelial cells and protect BK polyomavirus from neutralization.非许可性人类常规CD1c+树突状细胞可实现对人原代肾小管上皮细胞的转染,并保护BK多瘤病毒免受中和。
PLoS Pathog. 2021 Feb 16;17(2):e1009042. doi: 10.1371/journal.ppat.1009042. eCollection 2021 Feb.
3
Beyond Cytomegalovirus and Epstein-Barr Virus: a Review of Viruses Composing the Blood Virome of Solid Organ Transplant and Hematopoietic Stem Cell Transplant Recipients.
超越巨细胞病毒和爱泼斯坦-巴尔病毒:实体器官移植和造血干细胞移植受者血液病毒组中病毒的综述。
Clin Microbiol Rev. 2020 Aug 26;33(4). doi: 10.1128/CMR.00027-20. Print 2020 Sep 16.