Cytomegaloviruses (CMV), in common with other Herpesviruses, establish lifelong persistence in their hosts. These highly host-specific viruses each encode viral genes that interfere with antigen presentation to CD8+ T cells, although the molecular mechanisms by which this end is achieved differ for human and murine CMVs. In each case, there has been a presumption that these genes are necessary for virus persistence in the host. However, recent data in the murine model casts doubt on that presumption. Here, we review the molecular mechanisms of interference with the class I pathway, and the published data regarding functional significance, with a focus on the murine model.
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