| Project/Area Number |
61570225
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Virology
|
|---|
| Research Institution | TOHOKU UNIVERSITY |
|---|
Principal Investigator |
SEKIZAWA Tsuyoshi Research Associate, Tohoku University School of Medicine, 医学部付属病院, 助手 (50150264)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TSUKAMOTO Tetsuro Research Associate, Tohoku University School of Medicine, 医学部付属病院, 助手 (20171978)
TAKASE Sadao Associate Professor, Tohoku University School of Medicine, 医学部, 助教授 (60004983)
NAKAMURA Shozo Research Associate, Tohoku University School of Medicine, 医学部, 助手 (80108498)
|
|---|
| Project Period (FY) |
1986 – 1987
|
| Project Status |
Completed (Fiscal Year 1987)
|
| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1987: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1986: ¥1,400,000 (Direct Cost: ¥1,400,000)
|
|---|
| Keywords | Herpes simplex virus / latency / reactivation / butyrate / Ricin / 潜伏感染除去 / 特発性動眠神経麻痺 / New entity / Herpes simplex virus / n-butyrate / 運動ニューロン / 動眼神経マヒ |
|---|
| Research Abstract |
We found enhancing effect of butyrate on in vitro reactivation of herpes simplex virus(HSV) in latently infected trigeminal ganglia of mice. Such enhancement was not seen when 5-Aza cytidine and 12-o-tetradecanolyphorbol-13-acetate(TPA) were use. For the study of mechanism(s) of enhanced reactivation by butyrate, we used protein inhibitors, cycloheximide and puromycin in the presence or absence of butyrate. These protein inhibitors had reversal(inhibitory) effect on butyrate induced enhancement of HSV reactivation, indicating that enhanced reactivation by butyrate might be due to such protein-inhibitors-sensitive protein(s), not due to direct action of this compound. It is suggested that our studies provide the mechanisms of HSV reactivation and of occurrence of diseases in central nervous system like encephalitis. In another study, we could eliminate HSV latency by intradermal injection of Ricin by the route of virus-inoculated site. This is important since once established there has been no effective way to eliminate HSV latency, having only way toward potential hazard for occurrence of reactivated infection. Thus, success of this treatment in an experimental model gives strategies for therapy of HSV infection. Apart from such underlying studies, we reported two cases of idiopathic oculomotor (3rd cranial) nerve palsy associated with HSV infection as a new clinical entity. Mechanisms of occurrence of this palsy were induced by the idea based on the reactivation in the trigeminal ganglia followed by spread to oculomotor nucleus in central gray via mesencephalic unclear tract of trigeminal nerve and/or reactivation in the oculomotor nucleus harbouring HSV latency in experimental animals.
|
