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

实验主要在两个受试者上进行，沿着上述项目，并获得以下结果。（1）从生物学和形态学角度研究了致敏绵羊红细胞对HSV-1感染的FL细胞的吸附作用。几乎100%的FL细胞在感染的晚期阶段（即，e. 23小时）中HSV-1 gC抗原的出现为阳性，而约86%的它们具有血细胞吸附（HAD）活性。为了阐明为什么所有感染的细胞不显示HAD活性，FL细胞在感染的相似阶段进行了检查，通过高分辨率扫描电子显微镜，也通过免疫扫描电子显微镜。用过氧化物酶抗过氧化物酶（PAP）兔IgG和胶体金标记的羊抗兔IgG分别处理感染细胞后，所有细胞表面均清晰地标记有胶体金颗粒。HAD的形态学观察显示，红细胞表面粘附有许多微绒毛。因此，除了HSV诱导的FcR在感染细胞的表面膜上的表达（这是HAD的先决条件）之外，微绒毛在这种现象的出现中起着至关重要的作用。（2）用电镜观察人疱疹病毒6型（HHV-6）感染的人淋巴细胞和MT_4细胞，观察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的包膜病毒颗粒中未发现包覆衣壳的独特被膜，但对于位于细胞质以及细胞外的所有衣壳都清楚地证明了这一点。这一发现为提出一种可能的病毒转运机制提供了基础。e. HHV-6的排出是通过核周病毒的包膜与核膜的外层融合并将所得的细胞质核衣壳重新附着在细胞质膜上来实现的。

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.