Hantavirus primarily infects endothelial cells in the bloodstream. However, it also infects epithelial cells, mononuclear phagocytes (MNP), follicular dendritic cells (DC), and perhaps other types of cells .. Hantavirus causes endothelial cell infection and is responsible for two distinct illnesses with vascular permeability . Damage to the endothelium barrier induced by an overactive innate immune response is thought to be central to the pathophysiology . Hantavirus directs endothelial cell permeability by sensitizing them to the vascular permeability factor VEGF. Angiogenesis 1 and sphingosine 1-phosphate prevent Hantavirus-induced permeability . VEGF, also known as vascular permeability factor, is a critical regulator of endothelial permeability . By amplifying the response of the VEGFR2-VE-cadherin pathway, pathogenic Hantavirus degrades the fluid barrier capabilities of endothelial cell adhesion and junctions, hence increasing the cell's permeability . Hantavirus is a pathogenic response to Endothelial growth factor (VEGF) of blood vessels to increase endothelial cell permeability . Pathogenic Hantavirus, Andes virus, and New York 1 Hantavirus dramatically boost endothelial cell permeability to VEGF. In contrast, non-pathogenic Hantaviruses Prospect Hill and Tula have no effect . The N protein of the Andes virus (ANDV) increases the permeability of microvascular endothelial cells . But during hantavirus infection, the vascular endothelium remains intact, and there is no clear cytopathic impact to account for leakage and edema .