Strikingly, while direct exposure of CD16– or CD16+ monocytes to virus or TLR7/8L did not have a clear impact on CCR7 expression, exposure to infected or TNFα treated BECs upregulated CCR7 expression in both cell types, suggesting that activated endothelial cells but not the virus itself are needed for monocyte CCR7 upregulation in vitro, and perhaps in HFRS patients. Here, CCR7 is linked to hemorrhagic fever with renal syndrome.