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Background  Human papillomavirus type 16 (HPV-16) E5 protein co-operates with epidermal growth factor to stimulate mitogenesis of murine fibroblasts. Currently, little is known about which viral amino acids are involved in this process. Using sequence variants of HPV-16 E5 we have investigated their effects upon E5 transcription, cell-cycling and cell-growth of murine fibroblasts.    Results  We demonstrate that: (i) introduction of Thr 64  into the reference E5 sequence of HPV-16 abrogates mitogenic activity: both were poorly transcribed in NIH-3T3 cells; (ii) substitution of Leu 44 Val 65  or, Thr 37 Leu 44 Val 65  into the HPV-16 E5 reference backbone resulted in high transcription in NIH-3T3 cells, enhanced cell-cycle progression and high cell-growth; and, (iii) inclusion of Tyr 8  into the Leu 44 Val 65  backbone inhibited E5 induced cell-growth and repression of p21 expression, despite high transcription levels.    Conclusion  The effects of HPV-16 E5 variants upon mitosis help to explain why Leu 44 Val 65  HPV-16 E5 variants are most prevalent in 'wild' pathogenic viral populations in the UK.

Analyses of variant human papillomavirus type-16 E5 proteins for their ability to induce mitogenesis of murine fibroblasts