Vera-Sempere Francisco J, Rubio Luis, Felipe-Ponce Vanesa, García Ana, Mayordomo Fernando, Sánchez-Plumed Jaime, Beneyto Isabel, Ramos David, Zamora Isabel, Simón José
Laboratory of Molecular Pathology, Service of Pathology, University Hospital La Fe, University Medical School, Valencia, Spain.
Clin Transplant. 2006 Nov-Dec;20(6):706-11. doi: 10.1111/j.1399-0012.2006.00539.x.
BK virus (BKV) reactivation arises from immunocompromised conditions and can produce a tubulointerstitial nephropathy (BKVN) in kidney transplant recipients (KTR). Approximately 5% of KTR develop BKVN, and about 45% of these lose their graft. Therefore, using molecular tools to test for BKV may be helpful in early detection. A series of 125 Spanish KTR, originating from a single transplant center, were studied in relation to BKV infection in the first post-transplant year. First, we carried out a urinary cytological study, looking for decoy cells as a possible marker of virus replication. Secondly, in all positive cytological samples and in some negative cytological samples (selected at random), we performed qualitative polymerase chain reaction (PCR) assays in serum and urine amplifying two different genome regions (LT and VP1). A transcription control region (TCR)-BK polymorphism sequence analysis was also performed in those BK PCR positive cases. Twenty-three of 125 (18.4%) KTR presented decoy cells in at least one urinary cytological sample. Molecular studies revealed that 10 of 125 (8%) KTR were BK PCR-serum positive cases (seven LT+/VP1- and three LT+/VP1+); and 13 of 40 (32.5%) KTR were BK PCR-urine positive cases (five LT+/VP1- and eight LT+/VP1+). When we compared PCR-urine and cytological results in 40 KTR, only 15% (six cases) revealed simultaneous positivity in both studies. In the context of clinical graft dysfunction, three patients demonstrated BK DNA presence in the renal biopsy. Finally, sequence analysis of the TCR was performed in 13 BK-PCR positive cases determining the AS, JL, WW, and WW-like viral variants. TCR sequence analysis, allows us to demonstrate the possible implication of the donor in BK infection studying four BK-PCR positive patients paired by donor.
BK病毒（BKV）再激活源于免疫功能低下状态，可在肾移植受者（KTR）中引发肾小管间质性肾病（BKVN）。约5%的KTR会发生BKVN，其中约45%会失去移植肾。因此，使用分子工具检测BKV可能有助于早期发现。对来自单个移植中心的125例西班牙KTR在移植后的第一年进行了与BKV感染相关的研究。首先，我们进行了尿细胞学研究，寻找作为病毒复制可能标志物的诱饵细胞。其次，在所有阳性细胞学样本和一些阴性细胞学样本（随机选择）中，我们对血清和尿液进行了定性聚合酶链反应（PCR）检测，扩增两个不同的基因组区域（LT和VP1）。对那些BK PCR阳性病例还进行了转录控制区（TCR）-BK多态性序列分析。125例KTR中有23例（18.4%）在至少一份尿细胞学样本中出现了诱饵细胞。分子研究表明，125例KTR中有10例（8%）为BK PCR血清阳性病例（7例LT+/VP1-和3例LT+/VP1+）；40例KTR中有13例（32.5%）为BK PCR尿液阳性病例（5例LT+/VP1-和8例LT+/VP1+）。当我们比较40例KTR的PCR尿液和细胞学结果时，只有15%（6例）在两项研究中均显示同时阳性。在临床移植肾功能障碍的情况下，3例患者在肾活检中显示存在BK DNA。最后，对13例BK-PCR阳性病例进行了TCR序列分析，确定了AS、JL、WW和WW样病毒变体。TCR序列分析使我们能够通过研究4例由供体配对的BK-PCR阳性患者来证明供体在BK感染中的可能作用。
