Since US2 and US11, showing maximum expression levels within 24 h post-infection (89), do not affect HLA-E surface expression (67) we propose that there is a sufficient time window for the formation of HLA-EpHLA−G complexes in a subset of acutely CMV-infected monocytes/macrophages before TAP inhibition through US6 sets in and HLA-E continues to be supplied with UL40-derived TAP-independent peptide ligands. This evidence concerns the gene HLA-E and infection.