Recent reports implicate two DNA tumour viruses, herpes simplex virus type 2 (HSV-2) and human papillomavirus types 16 or 18 (HPV-16 and -18), in the pathogenesis of cervical cancer. Previous studies have indicated that primary human fibroblasts transfected with HPV-16 and HSV-2 morphological transforming region III (mtr III) are more aneuploid than fibroblasts immortalized with HPV-16 and that HSV-2 DNA sequences are retained in transformed cells. Since HSV-2 and HPV typically infect cells of epithelial origin, the interactions of these viruses with respect to morphological transformation were examined in human keratinocytes. HPV-16- or HPV-18-immortalized keratinocytes (FEPL and FEA cells, respectively) were transfected with fragments derived from HSV-2 mtr III. When compared to their normal counterparts, FEPL cells and FEA cells transfected with mtr III fragments grew to higher saturation densities and were morphologically transformed. FEPL cells transformed by HSV-2 were capable of growth in soft agar and, when injected into mice, lesions developed at the site of injection. Histological examination of the lesions revealed a benign mass which was composed of squamous epithelial cells that were producing keratin. In contrast, immortalized keratinocytes (FEPL or FEA) or FEA cells transfected with HSV-2 did not produce these lesions. These observations suggest that sequences within mtr III can alter the growth properties of human keratinocytes immortalized by HPV-16 or HPV-18.


Article metrics loading...

Loading full text...

Full text loading...


Most cited this month Most Cited RSS feed

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error