The primary site of infection is the lung, where the virus elicits an inflammatory response enabling widespread dissemination to vascular endothelial cells. This leads to severe vascular permeability, capillary leak, noncardiogenic pulmonary edema, hypoxia, lactic acidosis, elevated systemic vascular resistance, and myocardial depression. The proximate cause of death in patients is usually cardiogenic shock. The disease comprises four clinical phases: prodrome, pulmonary edema and shock, diuresis, and convalescence. During the prodromal phase, patients present with nonspecific complaints almost indistinguishable from influenza. Headache and abdominal pain may be quite prominent and can progress over the next 7 to 10 days and include nonproductive cough and dyspnea. Patients will be febrile, tachycardic, tachypneic, and hypoxic, which heralds the development of worsening respiratory failure and hypotension. Patients who survive the shock phase enter the diuretic phase with rapid (24-48 h) resolution of respiratory and hemodynamic abnormalities. Patients then enter the convalescent phase of the illness, which typically lasts for a few months, but some patients have taken up to 2 years for full recovery.