We have investigated the antiviral activity of the photoactivatable compound gilvocarcin (GV), an antitumor agent which is closely related to psoralen. GV binds to DNA in the presence of near UV radiation (UVA, 320- 400nm) through cycloaddition, blocks DNA replication, and causes DNA strand breaks. GV has been shown to be toxic to bacteria and mammalian cells at picomolar levels in the presence of UVA. GV was considered to be an ideal treatment of the inactivation of viruses which contaminate transfusable blood products, since viral nucleic acid would be targeted, thereby eliminating most damage to platelets and red blood cells which are anucleate. We evaluated the effectiveness of GV and UVA for inactivation of several viruses, including the bacterial viruses phi X174, T7, PRD1 and phi 6, and herpes simplex virus, type 1 (HSV). Some inactivation of the bacterial viruses was observed with UVA radiation alone (exposures <26 kJ/m2). Additional, photosensitized inactivation was observed only with phi 6 and T7 at 2uM GV. HSV was photosensitive at concentrations of GV three orders of magnitude lower (1nM). The survival curves for all three viruses displayed multicomponent kinetics, indicating that 80-90% of these viruses constituted sensitive populations). At present there is no explanation for the wide range of sensitivities. The lack of inactivation of two viruses, phiX174 and PRD1, suggests that GV is not appropriate to photoinactivate viruses in blood products. These data were presented at the annual meeting of the American Society for Photobiology, June, 1991. A manuscript will be submitted to Photochemistry and Photobiology.
