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Cervical/vaginal dysplasias of Transgenic Mice Harbouring Human Papillomavirus Type 16 E6–E7 Genes

Toshiyuki Sasagawa^1,

¹ Department of Tumor Virology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita-Osaka 565,
and² Department of Obstetrics and Gynecology, Osaka University Medical School, 2-2 Yamadaoka, Suita-Osaka 565, Japan

Half of the female transgenic mice harbouring human papillomavirus type 16 (HPV-16) E6–E7 genes under control of the mouse mammary tumour virus promoter, developed malignant tumours, including salivary gland carcinomas, lymphomas and skin histiocytomas. Although the E6–E7 genes are aetiological factors for human anogenital carcinoma, the transgenic mice produced no tumours in the anogenital tract. We investigated cytological and histological changes in the anogenital tract of the same transgenic mice. Seventeen (77%) of 22 transgenic mice developed dysplastic and/or hyperplastic changes in the cervix and vagina. HPV-16 E6–E7 mRNA signals were observed in the genital lesions, while they were not detected in the normal cervices and vaginas of transgenic mice and control mice by RNA in situ hybridization analysis. RNA/PCR analysis using poly(A)⁺ RNA showed that only a full-length E6–E7 RNA was expressed in three scraped cell samples from dysplasia, whereas full-length and spliced E6–E7 transcripts were in three cell samples from dysplasia/hyperplasia. These results suggest that expression of both E6 and E7 genes of HPV-16 is important for inducing dysplastic and hyperplastic changes in the genital epithelium.

Present address: ICRF Tumour Virus Group, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, U.K.

Received 7 April 1994; accepted 24 June 1994.