Molecular Biology and Morphology of Cell Membranes Modified by Infection with Herpes Simplex virus

实验主要在上述项目的两个受试者上进行，取得了以下结果：(1)从生物学和形态上研究了致敏绵羊红细胞对HSV-1感染FL细胞的吸附作用。在感染后期(即23小时)，几乎100%的FL细胞呈HSV-1 GC抗原阳性，约86%的FL细胞具有血吸附(HAD)活性。为了解释为什么不是所有感染的细胞都表现出HAD活性，用高分辨率扫描电子显微镜和免疫扫描电子显微镜对处于相似感染阶段的FL细胞进行了观察。当感染细胞先用过氧化物酶-抗过氧化物酶(PAP)兔免疫球蛋白处理，再用胶体金标记的羊抗兔免疫球蛋白处理，所有细胞的表面都有明显的胶体金标记。形态观察显示，红细胞表面有大量微绒毛附着。因此，除了HSV诱导的FCR在感染细胞表面的表达(这是HAD的先决条件)外，微绒毛在这种现象的出现中起着至关重要的作用。(2)对感染人类疱疹病毒6型(HHV-6)的人淋巴细胞和MT4细胞进行了电子显微镜观察，特别是病毒颗粒与细胞膜的相互作用。虽然在核周池或核内病毒颗粒周围没有发现明显的衣壳包裹衣壳，但位于细胞质和细胞外的所有衣壳都清楚地显示出包裹衣壳。这一发现为提出一种可能的病毒传输机制提供了基础，即HHV-6的出口是通过核周病毒的包膜与核膜的外层融合并将产生的细胞质核衣壳重新包裹在细胞质膜上而实现的。

Experiments were conducted principally on two subjects along the above described project and the following results were obtained.(1)Adsorption of sensitized sheep erythrocytes to FL cells infected with HSV-1 was studied biologically and morphologically. Almost 100% of the FL cells at a late stage of infection(i. e. 23 hrs)were positive for the appearance of HSV-1 gC antigen, while about 86% of them had hemadsorption(HAD)activity. To elucidate why all the infected cells do not show HAD activity, FL cells at the similar stage of infection were examined by high-resolution scanning electron microscopy and also by immuno-scanning electron microscopy. When infected cells were treated first with peroxidaseantiperoxidase(PAP)rabbit IgG and then with goat anti-rabbit IgG labeled with colloidal gold, the surface of all the cells were clearly tagged with colloidal gold particles. Morphological observations of HAD revealed that many microvilli adhered to the surface of erythrocytes. Thus, in addition to the expression of HSV-induced FcR on the surface membrane of infected cells, which is prerequisite for HAD, microvilli play an essential role on the appearance of this phenomenon.(2)Human lymphocytes and MT4 cells infected with human herpesvirus 6(HHV-6)were examined electron microscopically, with special attention to the interaction of viral particles with cellular membranes. While the distinct tegument coating the capsids was not revealed in enveloped viral particles in the perinuclear cisternae or around intranuclear viral particles, it was clearly demonstrated for all the capsids located in the cytoplasm as well as extracellularly. This finding provides the basis for proposing a possible viral transport mechanism, i. e. the egress of HHV-6 is achieved by fusion of the envelope of a perinuclear virus with the outer lamella of the nuclear membrane and reenvelopment of the resulting cytoplasmic nucleocapsid at a cytoplasmic membrane.