IL2 and infection: During the infection, the patient's capillaries become engorged, and focal hemorrhages develop; ultimately, the systemic expansion of capillary leakage leads to retroperitoneal edema, which may affect the pancreas.[1] Potential mediators, which increase vascular permeability during the acute stage of HFRS, are tumor necrosis factor-alpha, interleukin-1 and interleukin-2, and nitric oxide.[18] Activation of inflammation mediators during the hypotensive stage of HFRS seems to be caused by an inflammatory cascade mediated by cytokines, immunocytes, and the complement system.