1987 Fiscal Year Final Research Report Summary
ELUCIDATION OF MECHANISMS AND THERAPY IN RECURRENT HERPETIC KERATITIS
| Project/Area Number |
61570843
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Ophthalmology
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| Research Institution | OSAKA UNIVERSITY |
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Principal Investigator |
SHIMOMURA YOSHIKAZU OSAKA UNIERSITY MEDICAL SCHOOL, ASSISTANT, 医学部, 助手 (20162737)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO YASUNORI OSAKA UNIVERSITY MEDICAL SCHOOL, ASSISTANT, 医学部, 助手 (10183691)
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| Project Period (FY) |
1986 – 1987
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| Keywords | HSV-1 / Reactivation / Epinephrine / Receptor / Iontophoresis / Glycoprotein D / 潜伏感染 |
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| Research Abstract |
1. IN VESTIGATION ABOUT MECHANISMS OF HSV-1 REACTIVATION
(1) IN VITRO EXPERIMENT ----- IT WAS DEMONSTRATED THAT EPINEPHRINE DID NOT REACTIVATE HSV-1.
(2) IN VIVO EXPERIMENT ----- IT WAS DEMONSTRATED THAT 1 <micrn>G/ML EPINEPHRINE REACTIVATED HSV-1 USING HSV-1 LATENTLY INFECTED MICE GANGLIA. ALPHA AND BETA RECEPTORS PRESENT IN GANGLIA MIGHT BE RELATED TO THE VIRUS REACTIVATION PROCESS.
2. INHIBITION OF HSV-1 LATENCY BY INTERFERON
TRIGEMINAL GANGLIA WERE TAKEN FROM THE KILLED MOUSE TO INVESTIGATE HSV-1 LATENCY 28 DAYS POSTINOCULATION. THE EFFICIENCIES OF REDUCING HSV-1 LATENCY WERE 67% WITH IONTOPHORESIS 13% WITH SYSTEMIC ADMINISTRATION, AND 17% WITH EYE DROPS. IONTOPHORESIS GROUP SHOWED A STATISTICALLY SIGNIFICANT DIFFERENCE FROM THE OTHER GROUPS. THE RESULTS INDICATED THAT HSV-1 LATENCY IN THE TRIGEMINAL GANGLIA WERE DECREASED WHEN INTERFERON WAS DELIVERED IN HIGHER CONCENTRATION INTO THE EYE BY IONTOPHORESIS.
3. THERAPEUTIC EFFECTS OF VACCINE FOR MOUSE HERPETIC KERATITIS
IT WAS DEMONSTRATED THAT HERPES SIMPLEX VIRUS GLYCOPROTEIN D SIGNIFICANTLY PREVENTED THE DEVELOPMENT OF KERATITIS AS WELL AS THE ESTABLISHMENT OF GANGLIONIC LATENCY. AND IT WAS FOUND THAT GLYCOPROTEIN D DID NOT INDUCE THE CELLULAR IMMUNITY SUCH AS KILLER T CELL OR DELAYED TYPE HYPERSENSITIVITY, BUT INDUCED THE HUMORAL IMMUNITY.
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