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肾移植中BK病毒的供体来源及HLA C7在持续性BK病毒血症易感性中的作用。

Donor origin of BK virus in renal transplantation and role of HLA C7 in susceptibility to sustained BK viremia.

作者信息

Bohl Daniel L, Storch Gregory A, Ryschkewitsch Caroline, Gaudreault-Keener Monique, Schnitzler Mark A, Major Eugene O, Brennan Daniel C

机构信息

Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.

出版信息

Am J Transplant. 2005 Sep;5(9):2213-21. doi: 10.1111/j.1600-6143.2005.01000.x.

DOI:10.1111/j.1600-6143.2005.01000.x
PMID:16095500
Abstract

In a previous study, we performed serial BK virus (BKV), polymerase chain reaction (PCR) and detected active BKV infection in 70 (35.4%) of 198 renal transplant recipients. In the current study, pre-transplant donor and recipient samples were analyzed for BKV antibody titer and HLA alleles. Donor antibody titer was inversely proportional to onset of viruria, p<0.001, directly proportional to duration of viruria, p=0.014 and directly proportional to peak urine viral titer p=0.005. Recipient pairs receiving kidneys from the same donor were concordant for BKV infection, p=0.017, and had matched sequences of segments of the NCCR and VP1 genes that tended to vary among recipients of kidneys from different donors. We did not see an association of HLA A, B, or DR, HLA allele mismatches or total HLA mismatches and BK infection. However, all 11 recipients with sustained BK viremia received kidneys from donors lacking HLA C7, and 10 recipients also lacked C7. These findings derive from the largest and most comprehensive prospective study of BKV infection in renal transplant recipients performed to date. Our data support donor origin for early BKV infection in kidney transplant recipients, and suggest that a specific HLA C locus may be associated with failure to control BKV infection.

摘要

在先前的一项研究中,我们对198例肾移植受者进行了系列BK病毒(BKV)聚合酶链反应(PCR)检测,发现其中70例(35.4%)存在活动性BKV感染。在当前研究中,我们分析了移植前供体和受体样本的BKV抗体滴度及HLA等位基因。供体抗体滴度与病毒尿的发生呈负相关,p<0.001;与病毒尿持续时间呈正相关,p=0.014;与尿病毒滴度峰值呈正相关,p=0.005。接受同一供体肾脏的受体对BKV感染情况一致,p=0.017,且其NCCR和VP1基因片段序列匹配,而这些序列在接受不同供体肾脏的受体中往往存在差异。我们未发现HLA A、B或DR、HLA等位基因错配或总HLA错配与BK感染之间存在关联。然而,所有11例持续BK病毒血症的受者均接受了缺乏HLA C7的供体的肾脏,且其中10例受者自身也缺乏C7。这些发现来自于迄今为止对肾移植受者BKV感染进行的规模最大、最全面的前瞻性研究。我们的数据支持肾移植受者早期BKV感染源于供体,并表明特定的HLA C位点可能与无法控制BKV感染有关。

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