Given the remarkably strong cytotoxic lymphocyte-responses of hantavirus-infected patients, with up to 50% of their peripheral blood CD8 T cells responding during the acute phase of infection and a unique NK cell-profile including highly elevated levels of activated NK cells present up to 60 days after symptom debut in many of the patients [7]–[9], it has been suggested that cytotoxic lymphocytes are directly involved in the HFRS/HCPS-pathogenesis by causing increased vascular permeability by killing hantavirus-infected endothelial cells [1], [6]. This evidence concerns the gene CD8A and hemorrhagic fever with renal syndrome.