These data likely will have to be complemented by other studies directed at understanding the impact of other components of the antigen processing pathway that are known to differ between the two species. This includes the lack of ERAP2 in mice, and incompatibilities between humanMHC molecules and the murine peptide loading complex. Also, the difference in mouse and human self, which, due to the requirement for self-tolerance, leads to differences in TCR repertoire, may have to be taken into account. Finally, genomic and proteomic tools will permit to study host influences on viral protein expression, or host specific viral immune evasion mechanisms, which will also affect the epitope repertoire in a species specific manner. In conclusion, our detailed analysis of the binding specificity of the murine transporters allows for a sensitive comparison between peptide selection by mouse and human TAP, and demonstrates that epitopes recognized by murine CTLs are selected for increased TAP affinity. This work provides a key step towards the complete and differential description of human and murine antigen processing events. Epstein-Barr virus is a human herpesvirus, which has been categorized as the first known human tumor virus. This virus is widespread and persists in all infected individuals as a lifelong, usually asymptomatic and latent infection in the B-cell compartment. Acute infection with EBV can cause infectious mononucleosis, and its latent state can evolve to yield several B-cell lymphomas, nasopharyngeal carcinoma and gastric cancer, and other more sporadic malignancies. Although EBV has been studied extensively at the molecular level in vitro, conditions of virus latency, virus-associated diseases and their TWS119 GSK-3 inhibitor pathogenesis are difficult to study in the human population due to individual variations in genetics, environment and behaviour. EBV is highly species-specific in that it infects human and certain primate cells, only. Much effort has gone into establishing a suitable animal model for EBV but even the most advanced models, i.e. humanized mice show considerable limits. Experimental infections of mice with an EBV-related murine herpesvirus termed MHV68 share certain features of EBV��s pathogenesis and latency but MHV68 does not encode homologues of EBV latency-associated or transforming genes. These EBV genes include the latent membrane proteins 1 and LMP2a as well as the EBV nuclear antigens 2, and EBNA1, among others. All of these latent gene products have intrinsic activating characteristics and thereby contribute to growth transformation of human B cells, an accepted in vitro model, which partially reflects EBV��s contributions to viral oncogenesis. A mouse model that embodies SB431542 ALK inhibitor multiple features of EBV��s infection would be most desirable to understand EBV��s contribution to viral latency and tumor development.