Antiviral effects of 28-deacetylsendanin on herpes simplex virus-1 replication

The compound purified from the fruit of Melia azedarach exerted an antiviral effect on herpes simplex virus-1 (HSV-1) in Vero cells. It was identified as 28-deacetylsendanin (28-DAS). The 50% inhibitory concentration (IC 50) of 28-DAS was 1.46 μg/ml without cytotoxicity at 400 μg/ml on Vero cells. E...

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Bibliographic Details
Published in:Antiviral research 1999-09, Vol.43 (2), p.103-112
Main Authors: Kim, M, Kim, S.K, Park, B.N, Lee, K.H, Min, G.H, Seoh, J.Y, Park, C.G, Hwang, E.S, Cha, C.Y, Kook, Y.H
Format: Article
Language:English
Subjects:
28-Deacetylsendanin
Animals
Antibiotics. Antiinfectious agents. Antiparasitic agents
Antiviral agents
Antiviral Agents - chemistry
Antiviral Agents - pharmacology
Antiviral Agents - toxicity
Biological and medical sciences
Cercopithecus aethiops
Fruit of Melia azedarach
Furans - chemistry
Furans - pharmacology
Furans - toxicity
General pharmacology
Herpes simplex virus 1
Herpesvirus 1, Human - drug effects
Herpesvirus 1, Human - physiology
Limonins
Medical sciences
Melia azedarach
Microscopy, Electron
Pharmacognosy. Homeopathy. Health food
Pharmacology. Drug treatments
Plant Extracts - chemistry
Plants, Medicinal - chemistry
Vero Cells
Viral Proteins - biosynthesis
Virus Replication - drug effects
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Summary:The compound purified from the fruit of Melia azedarach exerted an antiviral effect on herpes simplex virus-1 (HSV-1) in Vero cells. It was identified as 28-deacetylsendanin (28-DAS). The 50% inhibitory concentration (IC 50) of 28-DAS was 1.46 μg/ml without cytotoxicity at 400 μg/ml on Vero cells. Electron microscopy showed that low electron-dense cores of newly synthesized nucleocapsids remained in swollen nuclei and no extracellular virus particles were observed at 15 h p.i. Consistent with this result, it was confirmed by a plaque assay that few infectious progeny viruses were released from the 28-DAS-treated virus-infected cells at 24 h p.i. Intracellular viruses in 28-DAS-treated virus-infected cells were 23% of untreated and infected cells. The synthesis of thymidine kinase (TK) was reduced by 28-DAS at early stage. In conclusion, 28-DAS inhibited the replication of HSV-1, reduced the synthesis of HSV-1 TK, and led to the formation of defective nucleocapsids.
ISSN:0166-3542
1872-9096
DOI:10.1016/S0166-3542(99)00037-6