HTNV-derived peptides could be presented by HLA-E on HTNV-infected cells, but they prevent the recognition and interaction between HLA-E and CD94/NKG2A on CD56dimNKG2A+NK cells in the peripheral blood of HFRS patients, thus “abrogating” the inhibitory signal of NKG2A and “relieving” the cytotoxic effects of NK cells against HTNV infection (Fig 14). This evidence concerns the gene KLRD1 and hemorrhagic fever with renal syndrome.