Ross River virus is endemic to parts of Australia and Papua New Guinea, and was observed in an outbreak in the South Pacific during 1979-1980. It was named following the isolation of an arbovirus from mosquitoes trapped beside Ross River, near Townsville, Queensland, in 1959, and the subsequent identification of this virus as the one responsible for cases of epidemic polyarthritis in Queensland and New South Wales. Outbreaks as long ago as 1928 are now attributed to Ross River virus.
Ross River fever is also known as Ross River virus infection or Ross River virus disease, since not all patients experience symptoms of fever. A review of a number of studies concluded that between 20% and 60% of patients experience fever. Similarly, the name epidemic polyarthritis fell out of use because arthritic symptoms are not observed in all patients; the same review found that between 83% and 98% of patients experienced joint pain. Other symptoms include rash. Although there is some (mostly) anecdotal evidence of long-term chronic effects due to Ross River virus, particularly joint pain, patients can typically expect to recover within a month after the onset of symptoms.
In rural and regional areas of Australia, the continued prevalence of Ross River virus is thought to be supported by 'reservoir' hosts such as large marsupial mammals, but antibodies to Ross River virus have been found in a wide variety of placental and marsupial mammals, and also in a number of bird species. It is not presently known what reservoir hosts support Ross River virus in metropolitan areas such as Brisbane.
The Southern Saltmarsh mosquito (Aedes camptorhyncus) which is known to carry the Ross River virus was discovered in New Zealand in 1998, and there is an ongoing eradication program by the New Zealand Ministry of Health, involving spraying the insectide Bti on infested areas. As of June 2007 there have been no reported cases of Ross River Virus that arose in New Zealand.
The study of RRV induced disease in the laboratory has been recently facilited by a mouse model. Inbred mice infected with RRV develop hind-limb arthritis/arthralgia which is similar to human disease. The disease in mice, similar to humans, is characterized by an inflammatory infiltrate including macrophages which are immunopathlogic and excaberate disease. Furthermore, recent data indicate that the serum component, C3, directly contributes to disease since mice deficient in the C3 protein do not suffer from severe disease following infection. Taken together, this indicates that an aberrant innate immune response is responsible for severe disease following RRV infection.