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Journal of Virology, November 2002, p. 10914-10920, Vol. 76, No. 21
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.21.10914-10920.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Modulation of the Cell Division Cycle by Human Papillomavirus Type 18 E4

Tomomi Nakahara,{dagger} Akiko Nishimura,{ddagger} Masakazu Tanaka, Takaharu Ueno, Akinori Ishimoto, and Hiroyuki Sakai*

Laboratory of Gene Analysis, Department of Viral Oncology, Institute for Virus Research, Kyoto University, Sakyo-Ku, Kyoto 606-8507, Japan

Received 11 March 2002/ Accepted 20 July 2002

The life cycle of human papillomaviruses (HPVs) is tightly coupled to the differentiation program of their host epithelial cells. HPV E4 gene expression is first observed in the parabasal layers of squamous epithelia, suggesting that the E4 gene product contributes to the mechanism of differentiation-dependent virus replication, although its biological function remains unclear. We analyzed the effect of HPV type 18 E4 on cell proliferation and found that E4 expression induced cell cycle arrest at the G2/M boundary. The functional region of E4 necessary for the growth arrest activity was located in the central portion of the molecule, and this activity was independent of the E4-mediated collapse of cytokeratin intermediate filament structures.

* Corresponding author. Mailing address: Laboratory of Gene Analysis, Department of Viral Oncology, Institute for Virus Research, Kyoto University, Sakyo-Ku, Kyoto 606-8507, Japan. Phone: 81-75-751-4010. Fax: 81-75-751-3995. E-mail: hsakai{at}virus.kyoto-u.ac.jp.

{dagger} Present address: McArdle Laboratory for Cancer Research, University of Wisconsin—Madison, Madison, WI 53706.

{ddagger} Present address: Department of Pathology, Harvard Medical School, Boston, MA 02115.

Journal of Virology, November 2002, p. 10914-10920, Vol. 76, No. 21
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.21.10914-10920.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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