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Journal of Virology, May 2006, p. 4580-4590, Vol. 80, No. 9
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.9.4580-4590.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

E2 Proteins from High- and Low-Risk Human Papillomavirus Types Differ in Their Ability To Bind p53 and Induce Apoptotic Cell Death

Joanna L. Parish,1,{dagger} Anna Kowalczyk,1 Hsin-Tien Chen,1 Geraldine E. Roeder,1 Richard Sessions,1 Malcolm Buckle,2 and Kevin Gaston1*

Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom,1 Enzymologie et Cinétique Structurale, LBPA (UMR 8113 du CNRS), Ecole Normale Supérieur de Cachan, 61 Avenue du President Wilson, 94235 Cachan, France2

Received 5 August 2005/ Accepted 2 February 2006

The E2 proteins from oncogenic (high-risk) human papillomaviruses (HPVs) can induce apoptotic cell death in both HPV-transformed and non-HPV-transformed cells. Here we show that the E2 proteins from HPV type 6 (HPV6) and HPV11, two nononcogenic (low-risk) HPV types, fail to induce apoptosis. Unlike the high-risk HPV16 E2 protein, these low-risk E2 proteins fail to bind p53 and fail to induce p53-dependent transcription activation. Interestingly, neither the ability of p53 to activate transcription nor the ability of p53 to bind DNA, are required for HPV16 E2-induced apoptosis in non-HPV-transformed cells. However, mutations that reduce the binding of the HPV16 E2 protein to p53 inhibit E2-induced apoptosis in non-HPV-transformed cells. In contrast, the interaction between HPV16 E2 and p53 is not required for this E2 protein to induce apoptosis in HPV-transformed cells. Thus, our data suggest that this high-risk HPV E2 protein induces apoptosis via two pathways. One pathway involves the binding of E2 to p53 and can operate in both HPV-transformed and non-HPV-transformed cells. The second pathway requires the binding of E2 to the viral genome and can only operate in HPV-transformed cells.

* Corresponding author. Mailing address: Department of Biochemistry, University of Bristol, Bristol BS8 1TD, United Kingdom. Phone: 44 117 954 6852. Fax: 44 117 928 8274. E-mail: kevin.gaston{at}bristol.ac.uk.

{dagger} Present address: University of Massachusetts Medical School, 364 Plantation Street, Worcester MA 01605.

Journal of Virology, May 2006, p. 4580-4590, Vol. 80, No. 9
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.9.4580-4590.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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