Murray Valley encephalitis virus

Murray Valley encephalitis virus (MVEV) is a zoonotic flavivirus endemic to northern Australia and Papua New Guinea. It is the causal agent of Murray Valley encephalitis (previously known as Australian encephalitis) and in humans can cause permanent neurological disease or death. MVEV is related to Kunjin virus which has a similar ecology but has a lower morbidity rate.

MVEV is a mosquito-borne virus that is maintained in a bird-mosquito-bird cycle. Water birds from the Ciconiiformes order, including herons and cormorants, provide the natural reservoir for MVEV. The major mosquito vector is Culex annulirostris. Human infection occurs only through bites from infected mosquitoes, it cannot be transmitted from person to person.

The first epidemics of MVE occurred in 1917 and 1918 in Southeastern Australia following years of high rainfall. The virus was isolated from human samples in 1951 during an epidemic in the Murray Valley, Australia. Epidemics usually occur due to either infected birds or mosquitoes migrating from endemic areas to non-endemic areas

The majority of MVEV infections are sub-clinical, i.e. do not produce disease symptoms, although some people may experience a mild form of the disease with symptoms such as fever, headaches, nausea and vomiting and only a very small number of these cases go on to develop MVE. In fact, serological surveys which measure the level of anti-MVEV antibodies within the population estimate that only 1 in 800-1000 of all infections result in clinical disease. The incubation period following exposure to the virus is around 1 to 4 weeks. Following infection, a person will have life-long immunity to the virus. When a patient appears to show MVE symptoms and has been in an MVE-endemic area during the wet season (November to July), when outbreaks usually occur, MVE infection must be confirmed by laboratory diagnosis, usually by detection of a significant rise of MVE-specific antibodies in the patient's serum.

The scientific study of the genetics of MVEV has been facilitated by the construction and manipulation of an infectious cDNA clone of the virus (Hurrelbrink et al., 1999). Mutations in the envelope gene have been linked to the attenuation of disease in mouse models of infection.