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J Biol Chem, Vol. 274, Issue 15, 10219-10226, April 9, 1999
,
From the Departments of Internal Medicine, Howard Hughes Medical
Institute, Physiology and Biophysics, University of Iowa College of
Medicine, Iowa City, Iowa 52242, the Recent identification of two receptors for the
adenovirus fiber protein, coxsackie B and adenovirus type 2 and 5 receptor (CAR), and the major histocompatibility complex (MHC) Class I Division of
Immunologic and Infectious Diseases, Children's Hospital of
Philadelphia, Philadelphia, Pennsylvania 19104, and the ¶ Dana
Farber Cancer Institute, Boston, Massachusetts 02115
-2 domain allows the molecular basis of adenoviral infection to be
investigated. Earlier work has shown that human airway epithelia are
resistant to infection by adenovirus. Therefore, we examined the
expression and localization of CAR and MHC Class I in an in vitro model of well differentiated, ciliated human airway
epithelia. We found that airway epithelia express CAR and MHC Class I. However, neither receptor was present in the apical membrane; instead, both were polarized to the basolateral membrane. These findings explain
the relative resistance to adenovirus infection from the apical
surface. In contrast, when the virus was applied to the basolateral
surface, gene transfer was much more efficient because of an
interaction of adenovirus fiber with its receptors. In addition, when
the integrity of the tight junctions was transiently disrupted, apically applied adenovirus gained access to the basolateral surface and enhanced gene transfer. These data suggest that the receptors required for efficient infection are not available on the apical surface, and interventions that allow access to the basolateral space
where fiber receptors are located increase gene transfer efficiency.
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