Since we observed increased expression of the endothelial adhesion marker CD62L on CD16-expressing monocytes (IMs and NCMs) and CCR7 on all monocyte subsets in patients with acute HFRS caused by PUUV, we investigated the consequences of in vitro exposure to PUUV-Suonenjoki strain (shown to have wild-type properties [30]) of bead-enriched CD16+ (IMs and NCMs) and CD16– (CMs) monocytes (Fig 7A). This evidence concerns the gene SELL and hemorrhagic fever with renal syndrome.