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Journal of Virology, July 2008, p. 6288-6298, Vol. 82, No. 13
0022-538X/08/$08.00+0     doi:10.1128/JVI.00569-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Bovine Papillomavirus Type 1: from Clathrin to Caveolin{triangledown}

Valerie Laniosz,1 Kirsten A. Holthusen,2 and Patricio I. Meneses1,2*

School of Graduate and Postdoctoral Studies, Department of Microbiology and Immunology, H. M. Bligh Cancer Research Laboratory,1 Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois 600642

Received 13 March 2008/ Accepted 10 April 2008

Viruses may infect cells through clathrin-dependent, caveolin-dependent, or clathrin- and caveolin-independent endocytosis. Bovine papillomavirus type 1 (BPV1) entry into cells has been shown to occur by clathrin-dependent endocytosis, a pathway that involves the formation of clathrin-coated pits and fusion to early endosomes. Recently, it has been demonstrated that the closely related JC virus can enter cells in clathrin-coated vesicles and subsequently traffic to caveolae, the organelle where vesicles of the caveolin-dependent pathway deliver their cargo. In this study, we use immunofluorescence staining of BPV1 pseudovirions to show that BPV1 overlaps with the endosome marker EEA1 early during infection and later colocalizes with caveolin-1. We provide evidence through the colocalization of BPV1 with transferrin and cholera toxin B that BPVl trafficking may not be restricted to the clathrin-dependent pathway. Disrupting the entry of caveolar vesicles did not affect BPV1 infection; however, we show that blocking the caveolar pathway postentry results in a loss of BPV1 infection. These data indicate that BPV1 may enter by clathrin-mediated endocytosis and then utilize the caveolar pathway for infection, a pattern of trafficking that may explain the slow kinetics of BPV1 infection.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, 2.351, North Chicago, IL 60064. Phone: (847) 578-3000, ext. 7775. Fax: (847) 578-3349. E-mail: patricio.meneses{at}rosalindfranklin.edu

{triangledown} Published ahead of print on 16 April 2008.

Journal of Virology, July 2008, p. 6288-6298, Vol. 82, No. 13
0022-538X/08/$08.00+0     doi:10.1128/JVI.00569-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Laniosz, V., Dabydeen, S. A., Havens, M. A., Meneses, P. I. (2009). Human Papillomavirus Type 16 Infection of Human Keratinocytes Requires Clathrin and Caveolin-1 and Is Brefeldin A Sensitive. J. Virol. 83: 8221-8232 [Abstract] [Full Text]  
  • Conway, M.J., Meyers, C. (2009). Replication and Assembly of Human Papillomaviruses. JDR 88: 307-317 [Abstract] [Full Text]  
  • Smith, J. L., Campos, S. K., Wandinger-Ness, A., Ozbun, M. A. (2008). Caveolin-1-Dependent Infectious Entry of Human Papillomavirus Type 31 in Human Keratinocytes Proceeds to the Endosomal Pathway for pH-Dependent Uncoating. J. Virol. 82: 9505-9512 [Abstract] [Full Text]  


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