Usage of heparan sulfate, integrins, and FAK in HPV16 infection.
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.
Abban
Cynthia Y
CY
School of Graduate and Postdoctoral Studies, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, USA.
Meneses
Patricio I
PI
D002460:Cell Line; D051417:Focal Adhesion Kinase 1 / Q000378:metabolism*; D006497:Heparan Sulfate / Q000378:metabolism*; D054884:Host-Pathogen Interactions; D052162:Human papillomavirus 16 / Q000472:pathogenicity*; D006801:Humans; D039503:Integrin alpha6 / Q000378:metabolism*; D015603:Keratinocytes / Q000821:virology; D009025:Morpholines / Q000494:pharmacology; D053585:Virus Attachment; D053586:Virus Internalization
D051417:Focal Adhesion Kinase 1; D006497:Heparan Sulfate; D039503:Integrin alpha6; D009025:Morpholines; C524632:TAE226; C496050:PTK2 protein, human