EYE INFECTIONS BY TYPE 2 HERPES SIMPLEX VIRUS

新生儿疱疹脉络膜视网膜炎的发病机制是 人们对此知之甚少。我们对新生兔子的初步研究揭示了 A)感染了2型单纯疱疹病毒的单个核细胞 (2)单纯疱疹病毒2型，而不是游离单纯疱疹病毒2型，会引起视网膜脉络膜炎； 诱导单个核细胞正常免疫球蛋白Fc受体； 感染HSV-2的单个核细胞需要正常的免疫球蛋白才能诱导 新生兔眼部损伤的情况。基于这些观察， 与其他研究人员一样，下列致病过程 新生儿视网膜脉络膜炎的发展被提出如下： HSV-2感染诱导单个核细胞正常免疫球蛋白Fc受体 细胞。免疫球蛋白与Fc受体的结合改变了 单纯疱疹病毒感染的单个核细胞表面，并导致包裹性 视网膜和脉络膜毛细血管中的细胞。被诱骗的人 然后，感染HSV的单个核细胞在该部位发起感染，并 会导致视网膜脉络膜炎。 为了检查这一提议的致病过程的有效性，以下是 将进行一系列实验：a)亚种群 作为HSV-2主要携带者的单个核细胞能够 将确定新生兔是否发生视网膜脉络膜炎；b) 将研究HSV-2与单个核细胞的相互作用，以及 将对HSV诱导的单个核细胞上的Fc受体进行鉴定；c) 免疫球蛋白与单纯疱疹病毒Fc受体结合对小鼠血管内皮细胞功能的影响 单纯疱疹病毒感染单个核细胞与视网膜脉络膜炎的关系 将会被评估。最后，(D)单纯疱疹病毒特异性抗体和 将对感染HSVG的单个核细胞上的抗病毒药物进行测试。 如果这一假设的正确性得到证实，我们的调查将 有重要的医学意义：a)致病过程 新生儿疱疹病毒性视网膜脉络膜炎将得到澄清，并有效 将找到预防和治疗这种疾病的方法；b) Fc受体在疱疹发病机制中的生物学作用 将会发现视网膜脉络膜炎；及c) 研究将有助于我们对其发病机制的理解。 由其他病毒引起的新生儿视网膜脉络膜炎，如 水痘-带状疱疹、巨细胞病毒、麻疹和风疹病毒。

The pathogenic mechanism for herpetic chorioretinitis in the neonate is poorly understood. Our preliminary studies in the newborn rabbit revealed that a) mononuclear cells infected with type 2 herpes simplex virus (HSV-2), rather than free HSV-2, produce retinochoroiditis; b) HSV-2 induced Fc receptors for normal IgG on mononuclear cells; and c) mononuclear cells infected with HSV-2 required normal IgG for the induction of the ocular lesion in the newborn rabbits. Based on these observations, as well as those of other researchers, the following pathogenic process for the development of retinochoroiditis in the neonate is proposed: Following infection, HSV-2 induces Fc receptors for normal IgG on the mononuclear cells. The binding of IgG to the Fc receptors changes the nature of the cell surface of HSV-infected mononuclear cells and leads to the entrapment of the cell in the capillaries of the retina and choroid. The entrapped HSV-infected mononuclear cell then initiates infection at the site and produces retinochoroiditis. To examine the validity of this proposed pathogenic process, the following series of experiments will be carried out: a) subpopulations of mononuclear cells which are major carriers of HSV-2 and are capable of producing retinochoroiditis in the newborn rabbits will be determined; b) the interaction between HSV-2 and mononuclear cells will be studied, and HSV-induced Fc receptors on the mononuclear cells will be characterized; c) the effects of binding of IgG to HSV-induced Fc receptors on the HSV-infected mononuclear cells and on the induction of retinochoroiditis will be evaluated. Finally, (d) the effect of HSV-specific antibody and of the antiviral agents on the HSVG-infected mononuclear cells will be tested. If the validity of this hypothesis can be proven, our investigation will have important medical implications: a) The pathogenic process for neonatal herpetic retinochoroiditis will be clarified, and an effective means of preventing and treating the disease will be found; b) the biological role of Fc receptors in the pathogenesis of herpetic retinochoroiditis will be identified; and c) the findings of this investigation will shed some light in our understanding of pathogenesis of retinochoroiditis in the newborn produced by other viruses, such as varicella-zoster, cytomegalo, measles and rubella viruses.