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High Levels of Enhanced Reactivation of Herpes Simplex Virus in Skin Fibroblasts from Various Hereditary Cancer-prone Syndromes¹

Laboratory for Molecular Carcinogenesis, Sylvius Laboratories, 2300 RA Leiden, The Netherlands

The dose response of the enhanced reactivation (ER) of herpes simplex virus type 1 has been studied in UV-irradiated normal human skin fibroblasts and fibroblasts from the following hereditary cancer-prone syndromes: retinoblastoma, aniridia, polyposis coli, neurofibromatosis type 1 and 2, dysplastic nevus syndrome, Von Hippel-Lindau syndrome, multiple endocrine neoplasia type 2, and Bloom's syndrome. Surprisingly, much higher levels of ER were observed in all these genetically heterogeneous hereditary disorders than in normal human skin fibroblasts. These results suggest that loss of one allele of putative tumor suppressor genes may activate cellular processes that result in the induction of the ER response, and they support our previous observation suggesting that ER may somehow be related to the process of carcinogenesis (P. J. Abrahams et al., Cancer Res., 48: 6054–6057, 1988).

¹ This work was supported by the J. A. Cohen Institute, Interuniversity Research Institute for Radiopathology and Radiation Protection, and by EEC Contract Bi.7-034.

Received 7/ 9/91. Accepted 10/18/91.

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