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Journal of Virology, April 2000, p. 3852-3858, Vol. 74, No. 8
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Adeno-Associated Virus Type 5 (AAV5) but Not AAV2 Binds to the Apical Surfaces of Airway Epithelia and Facilitates Gene Transfer

Joseph Zabner,1,* Michael Seiler,1 Robert Walters,1,2 Robert M. Kotin,3 Wendy Fulgeras,4 Beverly L. Davidson,1 and John A. Chiorini3,4

Departments of Internal Medicine1 and Physiology & Biophysics,2 University of Iowa College of Medicine, Iowa City, Iowa 52242, and Laboratory of Molecular Hematology, National Heart, Lung, and Blood Institute,3 and Gene Therapeutics Branch, National Institute for Dental and Craniofacial Research,4 National Institutes of Health, Bethesda Maryland 20892

Received 12 November 1999/Accepted 18 January 2000

In the genetic disease cystic fibrosis, recombinant adeno-associated virus type 2 (AAV2) is being investigated as a vector to transfer CFTR cDNA to airway epithelia. However, earlier work has shown that the apical surface of human airway epithelia is resistant to infection by AAV2, presumably as a result of a lack of heparan sulfate proteoglycans on the apical surface. This inefficiency can be overcome by increasing the amount of vector or by increasing the incubation time. However, these interventions are not very practical for translation into a therapeutic airway-directed vector. Therefore, we examined the efficiency of other AAV serotypes at infecting human airway epithelia. When applied at low multiplicity of infection to the apical surface of differentiated airway epithelia we found that a recombinant AAV5 bound and mediated gene transfer 50-fold more efficiently than AAV2. Furthermore, in contrast to AAV2, AAV5-mediated gene transfer was not inhibited by soluble heparin. Recombinant AAV5 was also more efficient than AAV2 in transferring beta -galactosidase cDNA to murine airway and alveolar epithelia in vivo. These data suggest that AAV5-derived vectors bind and mediate gene transfer to human and murine airway epithelia, and the tropism of AAV5 may be useful to target cells that are not permissive for AAV2.

* Corresponding author. Mailing address: University of Iowa College of Medicine, 500 EMRB, Iowa City, IA 52242. Phone: (319) 353-5511. Fax: (319) 335-7623. E-mail: Joseph-Zabner{at}uiowa.edu.

Journal of Virology, April 2000, p. 3852-3858, Vol. 74, No. 8
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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