Jäger M, Prang N, Mitterer M, Larcher C, Huemer H P, Reischl U, Wolf H, Schwarzmann F
Institut für Medizinische Mikrobiologie und Hygiene, Universität Regensburg, Germany.
Br J Haematol. 1996 Dec;95(4):626-36. doi: 10.1046/j.1365-2141.1996.d01-1969.x.
In rare cases Epstein-Barr virus (EBV) leads to chronic active infection (CAEBV) which is characterized by persistant symptoms of infectious mononucleosis. Previously we described a case of persisting polyclonal B-cell lymphocytosis (PPBL) that was associated with CAEBV. Using reverse transcription and polymerase chain reaction we showed that in late passages of a spontaneous cell line, SM, latent EB viral genes such as EBNA1, EBNA2, EBNA3A/3B/ 3C, LMP1 and LMP2A were active. The master gene of the lytic cycle, BZLF1, was silent. This indicated that there was no general defect in immortalization and establishing latency by this CAEBV isolate SM. We obtained virus from the standard immortalizing strain B95-8 and the CAEBV strain SM from latently infected LCL quantified the number of virus particles by competitive PCR and demonstrated that the impaired capacity to immortalize umbilical cord blood lymphocytes was a virus strain-specific property, and was not due to an incapability to infect purified CD19+ B lymphocytes. Transcription of latency- and immortalization-associated genes such as EBNA1, EBNA2 and LMP2A was reduced, in contrast to a strongly enhanced activity of the master gene of the lytic cycle, BZLF1. A scenario for an antagonistic regulation of lytic and latent cycle genes is presented and a role for the pathogenesis of CAEBV is discussed.
在罕见情况下，爱泼斯坦-巴尔病毒（EBV）会导致慢性活动性感染（CAEBV），其特征为传染性单核细胞增多症的持续症状。此前我们描述了一例与CAEBV相关的持续性多克隆B细胞淋巴细胞增多症（PPBL）病例。通过逆转录和聚合酶链反应，我们发现，在自发细胞系SM的后期传代中，潜伏性EB病毒基因如EBNA1、EBNA2、EBNA3A/3B/3C、LMP1和LMP2A是活跃的。裂解周期的主导基因BZLF1是沉默的。这表明，该CAEBV分离株SM在永生化和建立潜伏状态方面不存在普遍缺陷。我们从标准永生化菌株B95-8和来自潜伏感染的LCL的CAEBV菌株SM中获取病毒，通过竞争性PCR对病毒颗粒数量进行定量，并证明永生化脐带血淋巴细胞能力受损是病毒株特异性的特性，并非由于无法感染纯化的CD19+B淋巴细胞。与裂解周期主导基因BZLF1的活性强烈增强相反，EBNA1、EBNA2和LMP2A等潜伏和永生化相关基因的转录减少。本文提出了裂解和潜伏周期基因拮抗调节的一种情况，并讨论了其在CAEBV发病机制中的作用。
