Photoreactivation of herpes simplex virus in human fibroblasts.

WHEN DNA is treated with ultraviolet light (220–300 nm) cyclobutyl pyrimidine dimers are produced between adjacent pyrimidines on a strand of DNA1. These dimers are a major cause of mutations and death in simple organisms after ultraviolet-irradiation1, and they have been implicated in the induction of skin cancer in man2,3. An important tool for assessing the deleterious effects of dimers is the photoreactivation test: the photoreactivating enzyme repairs DNA by the specific and exclusive monomerisation of dimers in a light-dependent (> 300nm) reaction4,5. If ultraviolet biological damage can be reversed by true photoenzymatic repair, then dimers have a major role in the production of that damage6. For the test to assess the role of ultraviolet-induced dimers in human carcinogenesis at least three criteria must be met: (1) human cells must possess a functional photoreactivating enzyme, (2) this enzyme must be able to monomerise dimers in DNA, and (3) the enzyme must be able to restore biological activity to ultraviolet-irradiated DNA. It has been shown that human cells meet the first two criteria7,8; we now show that human photoreactivating enzyme in fibroblasts can restore infectivity to ultraviolet-irradiated herpes simplex virus (HSV).