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Animal: DNA Viruses |
The Children’s Hospital of Philadelphia, Division of Immunologic and Infectious Diseases, Abramson 1202, 3516 Civic Center Boulevard, Philadelphia, PA 19104, USA1
The Wistar Institute, Philadelphia, PA 19104, USA2
The Institute for Human Gene Therapy, University of Pennsylvania Medical Center, Philadelphia, PA 19104, USA3
Author for correspondence: Christopher Cohen. Fax +1 215 590 2025. e-mail Cohenc{at}email.chop.edu
A replication-defective form of chimpanzee adenovirus type 68 (C68) has been developed to circumvent problems posed by widespread preexisting immunity to common human adenovirus vectors. To investigate the determinants of C68 tropism, its interaction with the coxsackievirus and adenovirus receptor (CAR) was studied. Although CHO cells were resistant to transduction by C68 as well as by adenovirus type 5 (Ad5), CHO cells expressing either human or murine CAR were transduced readily. C68 transduction, like Ad5 transduction, was blocked when cells were exposed to anti-CAR antibody or when virus was exposed to a soluble form of the CAR extracellular domain. These results indicate that gene delivery by C68 occurs by a CAR-dependent mechanism.
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