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Viruses 2015, 7(11), 5813-5830;

Cleavage of the HPV16 Minor Capsid Protein L2 during Virion Morphogenesis Ablates the Requirement for Cellular Furin during De Novo Infection

Department of Microbiology and Immunology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Academic Editor: Andrew Mehle
Received: 21 August 2015 / Revised: 23 October 2015 / Accepted: 29 October 2015 / Published: 11 November 2015
(This article belongs to the Section Animal Viruses)
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Infections by high-risk human papillomaviruses (HPV) are the causative agents for the development of cervical cancer. As with other non-enveloped viruses, HPVs are taken up by the cell through endocytosis following primary attachment to the host cell. Through studies using recombinant pseudovirus particles (PsV), many host cellular proteins have been implicated in the process. The proprotein convertase furin has been demonstrated to cleave the minor capsid protein, L2, post-attachment to host cells and is required for infectious entry by HPV16 PsV. In contrast, using biochemical inhibition by a furin inhibitor and furin-negative cells, we show that tissue-derived HPV16 native virus (NV) initiates infection independent of cellular furin. We show that HPV16 L2 is cleaved during virion morphogenesis in differentiated tissue. In addition, HPV45 is also not dependent on cellular furin, but two other alpha papillomaviruses, HPV18 and HPV31, are dependent on the activity of cellular furin for infection. View Full-Text
Keywords: human papillomavirus (HPV); HPV16; furin; PACS; J0101 human papillomavirus (HPV); HPV16; furin; PACS; J0101

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Cruz, L.; Biryukov, J.; Conway, M.J.; Meyers, C. Cleavage of the HPV16 Minor Capsid Protein L2 during Virion Morphogenesis Ablates the Requirement for Cellular Furin during De Novo Infection. Viruses 2015, 7, 5813-5830.

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