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CUTTING EDGE |
,
*
The G. W. Hooper Foundation, Department of Microbiology and Immunology, and Departments of
Biopharmaceutical Sciences and
Pharmaceutical Chemistry, University of California, San Francisco, CA 94143; and
§
Laboratories of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD, 20892
1 This work was supported by National Institutes of Health Grants GM38093 and GM57657 (to F.M.B.), Training Grant GM07175-23 (to E.M.B.), and by a scholarship from Achievement Rewards for College Scientists (ARCS) Foundation (to E.M.B.).
Viral strategies for immune evasion include inhibition of
various steps in the class I MHC assembly pathway. Here, we demonstrate
that adenovirus produces one gene product with a dual function in this
regard. It is well established that adenovirus E19 binds class I
molecules and retains them in the endoplasmic reticulum (ER). However,
E19 also delays the expression of class I alleles to which it cannot
tightly bind. Here, we show that E19 binds TAP and acts as a tapasin
inhibitor, preventing class I/TAP association. 
E19, an E19 mutant
lacking the ER-retention signal, delays maturation of class I
molecules, indicating that E19’s inhibition of class I/TAP interaction
is sufficient to delay class I expression. These data identify tapasin
inhibition as a novel mechanism of viral immune evasion and suggest
that, through this secondary mechanism, adenovirus can affect Ag
presentation by MHC alleles that it can only weakly affect by direct
retention.
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