Cutting edge: adenovirus E19 has two mechanisms for affecting class I MHC expression.

Article Details

Citation

Bennett EM, Bennink JR, Yewdell JW, Brodsky FM

Cutting edge: adenovirus E19 has two mechanisms for affecting class I MHC expression.

J Immunol. 1999 May 1;162(9):5049-52.

PubMed ID
10227971 [ View in PubMed
]
Abstract

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. DeltaE19, 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.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Antigen peptide transporter 1Q03518Details