Murray Valley encephalitis virus (MVEV) is an enveloped, positive-sense single-stranded RNA virus of the genus Flavivirus. It is transmitted by Culex mosquitoes and causes Murray Valley encephalitis, a severe neurologic disease in humans.
Genome and Virology
MVEV has a genome of approximately 11 kilobases encoding a single open reading frame that is translated into a polyprotein. This polyprotein is co- and post-translationally cleaved into three structural proteins—capsid, premembrane/membrane and envelope—and seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B and NS5). The envelope protein binds to host cell receptors, facilitating entry via clathrin-mediated endocytosis; low pH in endosomes triggers fusion. Replication occurs on endoplasmic reticulum-derived membranes, with NS3 acting as a serine protease and helicase and NS5 functioning as the RNA-dependent RNA polymerase and methyltransferase synthesising negative-strand intermediates and new genomes. Virions assemble in the endoplasmic reticulum, mature in the Golgi and are released by exocytosis. MVEV replicates in neurons, astrocytes and endothelial cells in mammalian hosts and in midgut and salivary gland tissues of Culex mosquitoes. Genetic analyses identify several lineages, with genotype 1 responsible for human disease in Australia.
Epidemiology and Disease Burden
MVEV is maintained in an enzootic cycle involving waterbirds, especially herons and egrets, as amplifying hosts and Culex annulirostris mosquitoes as vectors. The virus is endemic in northern Australia and parts of Papua New Guinea. Human cases occur sporadically and are often associated with heavy rainfall and flooding that expand mosquito breeding and bird habitats. Major outbreaks have occurred along the Murray‑Darling River basin during the 1950s and 1974 and more recently in Western Australia in 2011 and 2021. Most human infections are asymptomatic or cause a mild febrile illness; however, a small proportion develop neuroinvasive disease characterised by headache, vomiting, altered consciousness, seizures and coma. Case fatality among encephalitis cases ranges from 20 % to 30 %, and many survivors experience long-term neurologic deficits. There is no specific antiviral therapy or licensed vaccine. Prevention relies on mosquito control, avoidance of mosquito exposure and public health alerts during periods of elevated virus activity.
Murray Valley encephalitis virus exemplifies the risk of severe disease from mosquito-borne flaviviruses in Australia. Ongoing surveillance of bird populations and mosquitoes, combined with public education and vector control, is essential to mitigate outbreaks.
Related Terms: Japanese Encephalitis Virus, West Nile Virus, Tick-Borne Encephalitis Virus, Flavivirus, Culex annulirostris