Journal
VIROLOGY
Volume 403, Issue 1, Pages 1-16Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2010.04.007
Keywords
Activation; Endocytosis; Endosomes; FAK; Src; HPV16; Infection; Phosphorylation
Categories
Funding
- H.M. Bligh Cancer Research Laboratory of RFUMS, ACS-IL [07-34, 09-15]
- NIH/NRSA [1 F31 AI081515-01A1]
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Human papillomavirus type 16 (HPV16) is the major causative agent of cervical cancer. Studies regarding the early binding and signaling molecules that play a significant role in infection are still lacking. The current study analyzes the role of heparan sulfate, integrins, and the signaling molecule FAK in HPV16 infection of human adult keratinocytes cell line (HaCaTs). Our data demonstrate that infection requires the binding of viral particles to heparan sulfate followed by activation of focal adhesion kinase through an integrin. Infections were reduced in the presence of the FAK inhibitor, TAE226. TAE226 was observed to inhibit viral entry to the early endosome a known infectious route. These findings suggest that FAK can serve as a novel target for antiviral therapy. (C) 2010 Elsevier Inc. All rights reserved.
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