Schwarzmann F, Jäger M, Prang N, Wolf H
Institut fur Medizinische Mikrobiologie und Hygiene, D-93053 Regensburg, Germany.
Int J Mol Med. 1998 Jan;1(1):137-42. doi: 10.3892/ijmm.1.1.137.
Uncontrolled replication of a virus, which is harmful to the host is also disadvantageous to the virus. Most viruses cannot compete with the various immune mechanisms and become eliminated in the course of infection. Therefore, only the time between infection and eradication remains for these viruses to proliferate. A few viruses, like the Herpesviruses or the papillomaviruses, however, have developed a sophisticated strategy for persisting lifelong, usually asymptomatically in the host, hiding from the immune system and producing infectious progeny at the same time. This strategy depends on a separation of latency and the lytic replication, either by time due to differentiation-dependent mechanisms or by spatial separation as the result of different host cell types. Both are true for the Epstein-Barr virus (EBV). B cells and epithelial cells have a pivotal role in the life cycle of the virus. The former can become latently infected and are thought to be the virus reservoir in vivo, whereas the latter were shown to be permissive for lytic replication. However, replication of EBV in vivo is controlled primarily by host immune mechanisms selecting for cells that are not permissive for viral replication as the result of a particular set of transcription factors. These factors control the activity of the regulatory immediate-early genes and, in addition, lytic and latent cycle regulatory genes negatively interfere with each other and thus link cellular and viral gene regulatory mechanisms. Disturbance of both the immune surveillance as well as viral gene regulation may result in EBV-associated disease.
对宿主有害的病毒不受控制的复制对病毒自身也不利。大多数病毒无法与各种免疫机制抗衡，在感染过程中被清除。因此，对于这些病毒来说，只有感染到被根除之间的这段时间可以用来增殖。然而，一些病毒，如疱疹病毒或乳头瘤病毒，已经形成了一种复杂的策略，能够在宿主体内终身潜伏，通常不表现出症状，躲避免疫系统同时产生有传染性的后代。这种策略依赖于潜伏期和裂解性复制的分离，要么是由于依赖分化的机制在时间上分离，要么是由于不同宿主细胞类型导致的空间分离。对于爱泼斯坦-巴尔病毒（EBV）来说，这两种情况都存在。B细胞和上皮细胞在病毒的生命周期中起关键作用。前者可被潜伏感染，被认为是病毒在体内的储存库，而后者被证明允许裂解性复制。然而，EBV在体内的复制主要受宿主免疫机制控制，宿主通过一组特定的转录因子选择那些不允许病毒复制的细胞。这些因子控制调节性立即早期基因的活性，此外，裂解周期和潜伏周期调节基因相互负向干扰，从而将细胞和病毒基因调节机制联系起来。免疫监视以及病毒基因调节的紊乱都可能导致EBV相关疾病。
