Mitterhofer A P, Tinti F, Mordenti M, Pietropaolo V, Colosimo M, Ginanni Corradini S, Chiarini F, Rossi M, Ferretti G, Brunini F, Poli L, Berloco P B, Taliani G
Department of Clinical Medicine, Nephrology and Dialysis Unit, Sapienza University of Rome, Rome, Italy.
Transplant Proc. 2011 May;43(4):1142-4. doi: 10.1016/j.transproceed.2011.02.048.
Polyomavirus-associated nephropathy (PVAN) has a predilection for kidney rather than for other solid organ transplants such as the liver. Immunosuppression is widely recognized to be a major risk factor for PVAN development. Since end-stage liver disease (ESLD) patients are immunocompromised and immunosuppression is a major cause of BK virus reactivation, we sought to evaluate BK virus replication in patients listed for liver transplantation. From April to October 2010, we enrolled 20 patients listed for liver transplantation. BK virus load was measured by quantitative real-time polymerase chain reaction on plasma and urine samples. Viremia occurred in only 1 among 20 patients. We hypothesized that in ESLD patients, the low prevalence of BK virus infection may be related to the prevalent impairment of antibacterial immunity rather than to the viral-specific one. In BK virus reactivation, not only the immunodepressive state itself, but also the specific immunologic mechanisms involved may have a role.
多瘤病毒相关性肾病（PVAN）更易发生于肾脏，而非肝脏等其他实体器官移植。免疫抑制被广泛认为是PVAN发生的主要危险因素。由于终末期肝病（ESLD）患者免疫功能低下，且免疫抑制是BK病毒再激活的主要原因，我们试图评估等待肝移植患者的BK病毒复制情况。2010年4月至10月，我们纳入了20例等待肝移植的患者。通过对血浆和尿液样本进行定量实时聚合酶链反应来检测BK病毒载量。20例患者中仅1例发生病毒血症。我们推测，在ESLD患者中，BK病毒感染的低患病率可能与普遍存在的抗菌免疫受损有关，而非病毒特异性免疫受损。在BK病毒再激活过程中，不仅免疫抑制状态本身，而且所涉及的特定免疫机制可能都发挥了作用。
