Herpes virus infection and repair in cells pretreated with gilvocarcin V or merocyanine 540 and radiation

• Published in: Journal of photochemistry and photobiology. B, Biology Biology, 1994-04, Vol.23 (1), p.57-62
• Main Authors: Lytle, C.D., Routson, L.B., Prodouz, K.N.
• Format: Article
• Language: English
• Subjects: Aminoglycosides; Animals; Anti-Bacterial Agents - toxicity; Antiviral Agents - toxicity; Biological and medical sciences; Cell Line; Cercopithecus aethiops; Coumarins; Dose-Response Relationship, Radiation; Enhanced virus reactivation; Gilvocarcin V; Glycosides; herpes simplex virus; Herpes virus; Host capacity; Kidney; Medical sciences; Merocyanine 540; Photoradiation therapy and photosensitizing agent; Photosensitizing Agents - toxicity; Pyrimidinones - toxicity; Simplexvirus - drug effects; Simplexvirus - physiology; Simplexvirus - radiation effects; Treatment with physical agents; Treatment. General aspects; Tumors; Ultraviolet Rays; Viral Plaque Assay
• ISSN: 1011-1344; 1873-2682
• DOI: 10.1016/1011-1344(93)06980-H

Pretreatment of mammalian cells with certain genotoxic agents decreases the ability of the cell monolayers to support virus plaque formation but enhances repair of UV-irradiated virus. This study was made to determine whether these phenomena extend to pretreatments with light and photosensitizers, including one dye that primarily affects cell membranes. Confluent CV-1 monkey kidney fibroblast monolayers were pretreated with either gilvocarcin V (GV) or merocyanine 540 (MC540) and light of appropriate wavelengths and infected with control or UV-irradiated herpes simplex virus (HSV). GV phototreatment is known to affect cells at the DNA level, and MC540 at the membrane level. UV radiation served as a positive control pretreatment. Phototoxic concentrations of GV and MC540 were determined via the capacity of pretreated cell monolayers to support plaque formation by unirradiated HSV. Parallel monolayer pretreatment and subsequent infection by UV-irradiated HSV demonstrated that both types of phototreatments enhanced virus survival, but the dose responses and time courses were different. The DNA-damaging GV phototreatment mimicked the effect of UV-irradiating the cells and produced delayed enhanced repair of UV-irradiated virus. However, the MC540-phototreatment produced enhancement of virus survival with a bimodal dose response pattern for immediate infection, suggesting a different route for affecting repair of damaged virus.