EYE INFECTION OF CYTOMEGALOVIRUS

人类的许多巨细胞病毒 (CMV) 眼部疾病 眼部机会性感染，主要发生在 免疫抑制个体。 随着免疫抑制的数量 近年来患者增加主要是由于获得性 免疫缺陷综合症（艾滋病），巨细胞病毒已成为致病因子 对于一种重要的眼部疾病。 然而，CMV 眼病的发病机制 目前对感染的了解还很少。 针对十个严重 CMV 眼部感染的性质，甚至增加 CMV 发病率 艾滋病患者的眼部感染，对艾滋病患者眼部感染的严格评估 CMV在人眼感染中的作用及综合研究 迫切需要了解该疾病的性质。 我们对小鼠巨细胞病毒（MCMV）眼部感染的初步研究清楚 研究表明，与人类一样，完整的宿主细胞免疫是 保护小鼠免受感染的重要因素 和 MCMV 复发。 因此，作为我们最初的努力 评估宿主细胞免疫对发病机制的影响 CMV眼部感染，以下一系列实验是 提议： 1）小鼠各种细胞免疫成分的作用，即 辅助性 T 细胞（L3T4 细胞）、抑制性 T 细胞（Lyt-2 细胞）、 自然杀伤细胞和巨噬细胞在诱导病毒血症中的作用 MCMV全身感染期间的原发性眼部感染将 被研究。 2) MCMV在眼睛和巨噬细胞潜伏期的建立 将检查原发感染后的位置 眼组织中的病毒基因组将通过以下方法确定 共培养方法和 DNA-DNA 杂交技术 MCMV-DNA 探针。 3) 可能在体内负责的细胞免疫成分 眼睛中潜伏 MCMV 的重新激活将通过以下方式识别 评估每种免疫选择性耗竭的效果 潜伏病毒重新激活的成分。 拟议的研究将为我们提供迄今为止无法获得的信息 关于 CMV 眼部感染，这将为我们提供一些线索 了解该疾病的发病机制，也将有助于 我们正在寻找有效的预防和预防手段 治疗人类巨细胞病毒感染。

Many ocular diseases of cytomegalovirus (CMV) in humans are opportunistic infections of the eye and occur predominantly in immunosuppressed individuals. As the number of immunosuppressed patients increases in recent years due largely to acquired immunodeficiency syndrome (AIDS), CMV has become the causal agent for an important eye disease. Yet, the pathogenesis of CMV eye infection is poorly understood at present. In view of ten serious nature of CMV eye infection and even increasing incidence of CMV eye infection among AIDS patients, a critical assessment of the role of CMV in human eye infection as well as a comprehensive study of the nature of the disease are urgently needed. Our preliminary studies on murine CMV (MCMV) eye infection clearly showed that as in humans, the intact host cellular immunity is an important factor for the protection of the mouse from the infection and recurrence of MCMV. Therefore, as our initial efforts to evaluate the effect of host cellular immunity on the pathogenesis of CMV eye infection, the following series of experiments is proposed: 1) Roles of various cellular immune components of the mouse, namely helper T cells (L3T4+ cells), suppressor T cells (Lyt-2+ cells), natural killer cells and macrophages in the induction of viremia and primary eye infection during systemic infection of MCMV will be studied. 2) The establishment of latency of MCMV in the eye and macrophages following primary infection will be examined, and the location of the virus genomes in the eye tissues will be determined by means of co-culture method and DNA-DNA hybridization techniques with MCMV-DNA probes. 3) Cellular immune components which may be responsible for in vivo reactivation of latent MCMV in the eye will be identified by evaluating the effect of selective depletion of each immune component on the reactivation of the latent virus. The proposed study will provide us hitherto unavailable information on CMV eye infection which will shed some light on our understanding of pathogenesis of the disease and also will assist us in the search for effective means for the prevention and treatment of CMV infections in humans.