Reactivation of murine cytomegalovirus by cyclophosphamide
Reactivation of murine cytomegalovirus by cyclophosphamide
复制标题
环磷酰胺重新激活小鼠巨细胞病毒
作者：
D. Mayo;J. Armstrong;M. Ho
移植受者中巨细胞病毒（CMV）感染的高患病率是众所周知的，但我们对所涉及的危险因素的了解并不完整。人们认为免疫抑制的作用可能是最重要的。在开始环磷酰胺治疗后前瞻性随访的一系列风湿病患者中，很大一部分 (43%) 出现了 CMV 感染，如病毒尿和血清学反应所示1。由于大多数这些感染出现在最初血清反应呈阳性的患者中，因此我们认为它们代表了潜伏感染（本文定义为通过标准噬菌斑测定无法检测到病毒的感染）或隐性感染的重新激活。据推测，移植受者也会因免疫抑制而重新激活。肾移植受者 CMV 感染的另一个危险因素是将肾脏从 CMV 血清阳性供体转移到血清阴性受者 2,3。我们使用小鼠巨细胞病毒 (MCMV) 模型来更好地了解涉及这组疱疹样病毒潜伏和重新激活的因素，并表明同种异体移植会增强受者的慢性 MCMV 感染4。我们在此提出对小鼠模型的进一步观察，表明潜伏的 MCMV 感染可以通过环磷酰胺治疗重新激活，并且潜伏感染的脾细胞的转移可以导致受体感染。我们还展示了免疫抑制在后一种情况中的作用。
THE high prevalence of cytomegalovirus (CMV) infection in transplant recipients is well known but our understanding of the risk factors involved is incomplete. It is thought that the role of immunosuppression is probably paramount. In a series of rheumatologic patients followed prospectively after initiation of cyclophosphamide therapy, a significant proportion (43%) developed CMV infection as evidenced by viruria and serologic response1. Since most of these infections were seen in initially seropositive patients, we believe that they represent reactivations of latent (herein defined as an infection in which no virus can be detected by standard plaque assays) or inapparent infection. Presumably, reactivation by immunosuppression also occurs in transplant recipients. Another risk factor for CMV infection in renal transplant recipients is the transfer of kidneys from donors seropositive for CMV into seronegative recipients2,3. We are using the mouse cytomegalovirus (MCMV) model for better understanding of the factors involved in latency and reactivation of this group of herpeslike viruses and have shown that allografting will enhance chronic MCMV infection in the recipients4. We present here further observations on the mouse model, showing that latent MCMV infection can be reactivated by treatment with cyclophosphamide and that the transfer of latently infected spleen cells can lead to infections in recipients. We also show a role for immunosuppression in the latter situation.