HERPES VIRUS PRODUCTION IN MONKEY KIDNEY AND HUMAN SKIN CELLS TREATED WITH ANGELICIN OR 8‐METHOXYPSORALEN PLUS 365 nm LIGHT

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Abstract
—At an cquimolar concentration of 50 μM the bifunctional furocoumarin, 8‐methoxypsoralen (8‐MOP), is about 36 times more efficient in inhibiting the colony forming ability of CV‐I monkey kidney cells than the monofunctional furocoumarin angelicin. In contrast 8‐MOP is only 7.5 times more efficient than angelicin for the inhibition of herpes simplex virus (HSV) production in CV‐1 cells. This latter factor seems to reflect differences in photoreactivity of the two compounds with host cell DNA.A substantial recovery of HSV production was seen when cells were infected at different time intervals after treatment with angelicin‐plus‐light, whereas recovery was very limited after 8‐MOP plus light treatment. The recovery process was slow as compared to that observed after UV (254 nm)‐irradiation.The repair capacities of treated normal and xeroderma pigmentosum (group A) skin fibroblasts were estimated by measuring HSV production and unscheduled DNA synthesis. XP‐A cells repaired angelicin induced damage less efficiently than did normal cells. Neither cell type showed any repair activity after 8‐MOP plus light treatment.

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