Hantavirus was first seen in Asia. It is called Hantavirus for the Hantaan River in Korea.

An epidemic characterized by fever and acute pulmonary edema occurred in the southwestern U.S. in 1993 and led to the recognition of Hantavirus. The endothelium of the lung is selectively and extensively infected by the virus. Other symptoms associated with the syndrome range from mild hypoxemia with stable hemodynamics to rapidly progressive respiratory failure and cardiogenic shock. The average duration of illness prior to hospitalization is 3-4 days. Severe cardiopulmonary dysfunction predicts a poor prognosis. Treatment is supportive care. Ribavirin has not been established as an effective treatment. Hantavirus chronically infect rodent reservoirs and cause no overt disease. Human infection is probably acquired via inhalation of infectious aerosols of rodent excretions (urine, saliva, feces). Persons living, working or recreating in rural areas are susceptible for exposure to Hantavirus from deer mouse excreta. Human to human spread has occurred in only one instance in Argentina in 1996. A retrospective analysis of the U.S. National Case Registry failed to identify any human to human transmission for data through 1996. Patients hospitalized with Hantavirus pulmonary syndrome are placed on Standard Precautions for the duration of hospitalization.

The mode of transmission of Hantavirus pulmonary syndrome (HPS) is inhalation of infected rodent feces. Among confirmed cases of HPS, 70% of cases are closely associated with activities in home with rodent infestation. Data suggest that disturbing or inhabiting rodent-infested structures may constitute an important risk factor.

The full clinical spectrum of HPS is yet to be identified. The dynamic of rodents and their infections is also unknown. More longitudinal studies are required on Hantavirus before we finally identify the reason the syndrome emerged in 1993.