Mechanism of inhibition of herpes simplex virus replication by delta 7-prostaglandin A1 and delta 12-prostaglandin J2.
We studied the effect of prostaglandins (PGs) A1, delta 7-A1, A2, D2, E1, E2, F2 alpha, J2 and delta 12-J2 on the replication of herpes simplex virus type 2 (HSV-2). Of nine PGs we tested, delta 7-PGA1 was found to have the most potent inhibitory effect; 50% inhibitory dose (ID50) was 0.35 microgram/ml in the plaque reduction assays and HSV-2 induced protein synthesis was strongly suppressed at 0.5 microgram/ml whereas at this dose, the protein synthesis of uninfected cells was not inhibited. Dot blot hybridization analysis revealed that delta 7-PGA1 and delta 12-PGJ2 inhibited the primary transcription of HSV-2. Thus we suggest that those PGs are primarily active at the level of mRNA synthesis.
D002472:Cell Transformation, Viral / Q000187:drug effects; D004261:DNA Replication / Q000187:drug effects*; D005347:Fibroblasts; D006801:Humans; D007700:Kinetics; D015230:Prostaglandin D2 / Q000031:analogs & derivatives*; D011453:Prostaglandins / Q000494:pharmacology*; D011455:Prostaglandins A, Synthetic / Q000494:pharmacology*; D011457:Prostaglandins D / Q000494:pharmacology*; D018139:Simplexvirus / Q000187:drug effects / Q000235:genetics*; D013329:Structure-Activity Relationship; D014779:Virus Replication / Q000187:drug effects
D011453:Prostaglandins; D011455:Prostaglandins A, Synthetic; D011457:Prostaglandins D; C040810:9-deoxy-9,10-didehydro-12,13-didehydro-13,14-dihydroprostaglandin D2; C048481:9-oxo-15-hydroxy-delta 7,10,13-prostatrienoic acid methyl ester; D015230:Prostaglandin D2