Immune responses to Epstein-Barr virus: molecular interactions in the virus evasion of CD8+ T cell immunity

Abstract

Persistent viruses have mechanisms for modulating the host immune responses that are essential for achieving a lifelong virus-host balance while minimizing the viral pathogenicity. Here we review some of the immune-modulating mechanisms evolved by the ubiquitous but potentially oncogenic Epstein-Barr virus, with particular emphasis on the molecular mechanisms of genes interfering with HLA class I antigen presentation.

Fig. 1

Schematic comparing the modulation of HLA-I antigen presentation by (A) HCMV and (B) EBV gene products.

Fig. 2

Residues in BGLF5 that, when mutated, affect both DNase and host-shutoff function (D203S; red), or selectively affect DNase (S280L; blue) or shutoff functions (K231M; yellow). The purple shaded regions of the BGLF5 cartoon structure represent the DNase catalytic core. The green shaded regions are the non-catalytic core domains mainly comprising the N-terminal domains, where in mutations selective for shutoff function are clustered in the KSHV SOX protein . The structure of the BGLF5 protein was taken from PDB ID: 2W45 (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article).