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In rodents, hantavirus produces a chronic infection with no adverse sequelae. In humans, hantavirus produces two major clinical syndromes: hemorrhagic fever or pulmonary syndrome. European, Asian, and African rodent-borne hantaviruses cause hemorrhagic fever. The pulmonary syndrome is caused mainly by Sin Nombre virus and Andes virus in the ...
Neutralization tests, immunofluorescent assays (IFAs), and enzyme-linked immunosorbent assays (ELISAs) can be used to detect antibodies to hantavirus infection in blood, usually anti-N or anti-Gc antibodies. [3] [23] ELISA is inexpensive and can be used at any point during the illness, [5] but results may need to be confirmed by other methods.
The virus couldn't be isolated in 1976 but testing showed that an infectious agent was responsible. [21] The virus was isolated for the first time in 1978 [3] and named "KHF strain 76-118". It was propagated in cell cultures for the first time in 1981 and renamed "Hantaan virus, strain 76-118" after the Hantan river.
HPS has a much higher case fatality rate than HFRS, at 30–60%. For both HFRS and HPS, illness is the result of increased vascular permeability, decreased platelet count, and overreaction of the immune system. Individual hantavirus particles (virions) are usually spherical and vary at 70–350 nanometers in diameter.
Hantavirus pulmonary syndrome (HPS), also called hantavirus cardiopulmonary syndrome (HCPS), is a severe respiratory disease caused by hantaviruses. The main features of illness are microvascular leakage and acute respiratory distress syndrome. Symptoms occur anywhere from 1 to 8 weeks after exposure to the virus and come in three distinct phases.
The Andes virus, a hantavirus found in South America, has even been found to spread through person-to-person transmission, raising concern about hantavirus evolution in the U.S. A hantavirus infection does not always mean HPS will arise, but the majority of hantaviruses in North, Central, and South America cause HPS.