Murray Valley encephalitis virus

Murray Valley encephalitis virus
Virus classification
Group:	Group IV ((+)ssRNA)
Family:	Flaviviridae
Genus:	Flavivirus
Species:	Murray Valley encephalitis virus

Murray Valley encephalitis virus
Classification and external resources
ICD-9	062.4

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.

Vector

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.^[1] The major mosquito vector is Culex annulirostris. Human infection occurs only through bites from infected mosquitoes; the virus cannot be transmitted from person to person.^[2]

History

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.^[3][4]

Epidemics usually occur due to either infected birds or mosquitoes migrating from endemic areas to non-endemic areas.^[2]

Presentation

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, 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.^[2] Of those who contract MVE, one-quarter die from the disease.^[5]

Clone

The scientific study of the genetics of MVEV has been facilitated by the construction and manipulation of an infectious cDNA clone of the virus. ^[6] Mutations in the envelope gene have been linked to the attenuation of disease in mouse models of infection.

References

1. ^ Marshall ID, Brown BK, Keith K, Gard GP, Thibos E (1982). "Variation in arbovirus infection rates in species of birds sampled in a serological survey during an encephalitis epidemic in the Murray Valley of South-eastern Australia, February 1974". Aust J Exp Biol Med Sci 60 (5): 471–8. doi:10.1038/icb.1982.52. PMID 6299259. 
2. ^ ^{a b c} "Murray Valley encephalitis virus infection - Fact Sheet". Department of Health and Ageing. http://www.health.gov.au/internet/main/Publishing.nsf/Content/health-arbovirus-pdf-fsmurrayvalley.htm. Retrieved 2008-08-28. ^{[dead link]}
3. ^ French EL (1952). "Murray Valley encephalitis isolation and characterization of the aetiological agent". Med. J. Aust. 1 (4): 100–3. PMID 14909902. 
4. ^ Burnet FM (1952). "Murray Valley encephalitis.". Am J Public Health Nations Health 42 (12): 1519–21. doi:10.2105/AJPH.42.12.1519. PMC 1526305. PMID 13007862. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1526305. 
5. ^ "Deadly mosquito disease suspected". ABC News (Australia). May 15, 2009. http://www.abc.net.au/news/stories/2009/05/15/2572025.htm. Retrieved 2009-05-16. 
6. ^ Hurrelbrink RJ, Nestorowicz A, McMinn PC (1 December 1999). "Characterization of infectious Murray Valley encephalitis virus derived from a stably cloned genome-length cDNA". J. Gen. Virol. 80 (12): 3115–25. PMID 10567642. http://vir.sgmjournals.org/cgi/pmidlookup?view=long&pmid=10567642.