The effect of prostaglandins on the multiplication and cell-to-cell spread of herpes simplex virus type 2 in vitro.
Herpes simplex virus type 2 (HSV-2) after infecting an individual has the ability to remain latent in nervous tissues. The factors that control herpesvirus infection, latency, and reactivation are poorly understood. Fever, menstruation, emotional stress, exposure to sunlight, and surgical resection have been associated with activation of latent herpes. The situations which activate latent herpes are associated with a local or systemic rise in prostaglandins. The data presented show that prostaglandin F2 alpha (PGF2 alpha) and E2 (PGE2) enhanced cell-to-cell spread of HSV-2 in an in vitro model. Ibuprofen, a prostaglandin inhibitor, suppressed HSV-2 multiplication as well as cell-to-cell spread. Prostaglandins may play an important role in herpesvirus infections and latency.
D015237:Dinoprost; D015232:Dinoprostone; D007052:Ibuprofen / Q000494:pharmacology; D011453:Prostaglandins / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology; D011460:Prostaglandins F / Q000494:pharmacology; D018139:Simplexvirus / Q000502:physiology*; D010948:Viral Plaque Assay; D014779:Virus Replication / Q000187:drug effects*
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D015237:Dinoprost; D015232:Dinoprostone; D007052:Ibuprofen