Project/Area Number |
02670194
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
Virology
|
Research Institution | Okayama University |
Principal Investigator |
NII Shiro Okayama University Medical School, Department of Virology, Professor, 医学部, 教授 (40029757)
|
Co-Investigator(Kenkyū-buntansha) |
ARAO Yujiro Okayama University Medical School, Department of Virology, Research Associate (, 医学部, 助手 (40151146)
YOSHIDA Mariko Okayama University Medical School, Department of Virology, Research Associate, 医学部, 助手 (20144743)
YAMADA Masao Okayama University Medical School, Department of Virology, Assistant Professor, 医学部, 講師 (40166731)
|
Project Period (FY) |
1990 – 1991
|
Project Status |
Completed (Fiscal Year 1991)
|
Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1991: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1990: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
Keywords | HSV-1 / Hemadsorption / Human Herpesvirus 6 / Fc receptor / Microvilli / Tegument / テグメント / hemadsorption / 糖蛋白 / microvilli |
Research Abstract |
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.
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