Abstract
Abstract The cell-surface presentation of viral antigens by MHC class I molecules to CD8+ T-cells is critical for eliminating virus-infected cells. In turn, viruses have evolved numerous strategies to interfere with the generation and presentation of class I antigens. Human adenoviruses (Ads) comprise more than 70 different types classified into seven species (A to G); Ad infections cause diseases of the respiratory track (species B, C, and E), eyes (species D), and gastrointestinal track (species F). Ads encode the E3-19K protein that targets MHC class I molecules for retention in the endoplasmic reticulum of infected cells, thereby suppressing cell-surface presentation of Ad-derived antigens. In recent years, we determined the x-ray structures of Ad2 (species C) and Ad4 (species E) E3-19K bound to HLA-A2, which together with biochemical and functional data allowed to explain the mechanism of immunomodulation. Interestingly, in comparison to other Ads, species F Ads lack a gene for the common E3-19K protein and instead have two unique and uncharacterized genes, E3-19.4K and -31.6K. We are using a biochemical and functional approach to investigate how species F Ads modulate various cell surface immune proteins, including MHC I molecules, and what role of E3-19.4K and -31.6K proteins play in these effects.
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