Japanese encephalitis virus

General information and Symptoms
Originally named Japanese B encephalitis virus in order to aid in distinguishing this species of encephalitis with an agent causing Von Economo's type A encephalitis species, it has since been modified to a more simple name without the B. Japanese encephalitis (JE) is a virus that infects the central nervous system, which consists of the brain and spinal cord. It may range from mild to acute infection. Mild Symptoms include flu-like illness that may include: A severe infection symptoms may include mild symptoms as well as: As the infection progresses without treatment it may reach an acute level. When such a high level of infection occurs, there are serious side affects which include moderate brain damage ,varying degrees of paralysis, as well as seizures and death.
 * Headaches
 * Agitation
 * Fatigue
 * Nausea
 * Vomiting
 * Chills
 * Fever
 * Rapid onset
 * Stupor
 * Disorientation
 * Coma
 * Tremors
 * Occasional convlusions (occurs more often in infants)
 * Spastic paralysis
 * Flaccid paralysis (occurs in rare instances)

Transmission and Epidemiology
Japanese encephalitis virus is considered an arthropod virus called an arbovirus. The vector that spreads this arbovirus is a mosquito. The Culicine mosquito from the genus Culex are responsible for many diseases such as Dengue fever, Yellow fever, Venezuelan equine encephalitis, as well as the Japanese encephalitis. Their eggs are laid in still water that is either clean water or contaminated with organic waste. These eggs are also resistant to dessication for several months. The first reported suspicion of JE was within the last century and first documented in horses as well as humans in Japan, which explains the origin of it's name. The virus was first isolated from human brain tissue in rabbits in 1924. The specific species of Culex mosquitos linked to the JE virus is the C. ''tritaeniorhynchus'.' Infection into a healthy human begins with an infected mosquito. This mosquito lands on a human's skin and bites the victim, this transmits the virus into the bloodstream and is able to cause viraemia, the virus being spread intially from the bite site which allows it access to the rest of the body through the circulatory system. The way a mosquito can be infected with the virus is from feeding on infected humans, horses, and cattle. These are all hosts that are dead-end and due to high rates of fatality do not transmit the disease as readily, however, swine are largely asymptomatic hosts. The only exception is the high abnormalities and abortions of fetal swine in pregnant sows. Due to their lack of symptoms mosquitos are more likely to feed on a seemingly healthy pig. This causes the mosquito to be contaminated and become a vector. Infection in humans occur in the cochlea of the ear. The species that is most significant in the JE virus, C. tritaeniorhynchus, typically feeds on bovine animals. Despite suggestions of the spraying of pesticides to kill mosquito vectors and moving swine herds to more rural areas away from humans there is a belief among many that Japanese encephilitis will not be eliminated because the natural host for this virus is a bird. JE is the most prevalent of viral encephalitis in Asia with 30,000-50,000 cases reported each year, of those cases fatalities fall between 0.3-60%. There is a high risk of contracting this virus in rural areas that are endemic locations. Some cities have had success in conquering major epidemic outbreaks of JE, such as Thailand, Taiwan, Japan, China, and Korea. They have done this with vaccinations. While these countries, to a certain extent, have successfully contained this virus, some still have periodic outbreaks. The countries that fall into this category are Malaysia, Myanmar, India, Nepal, Cambodia, and Vietnam. Despite JE occuring mostly in Asia, 1998 was the first report of 2 fatal cases of JE on the mainland of northern Australia.

Ecology


Structure and Metabolism
JE is an enveloped virus that has positive sense single stranded RNA genome (+ssRNA). The outer envelope aids in the viral entry to cell through its composition, it is composed of (E) protein which is a protective antigen. The structure is packaged in a capsid formed by the capsid protein. genome encodes the structure proteins: This type of the encephalitis virus causes rapid and significant build up of viral proteins. 
 * NS1
 * NS2 a and b
 * NS3 (a putative helicase)
 * N4a
 * NS4b
 * NS5 (a viral polymerase)

Pathology
Japanese Encephalitis is antigenically linked to several other flaviviruses and belongs to the family Flaviviridae. An Antigen is a substance that causes that causes the body to illicit an immune response such as the production of antibody through the introduction of a foreign substance such as a virus or bacteria into the body. In the autopsies performed on 20 persons who died in the 1924 encephalitis epidemic of Tokyo, Nagano, and Shikoku districts of Japan there were 9 cases of acute, 8 subacute cases, and 3 chronic cases. An acute case typically lasts between 1-2 weeks, subacute would be 2 or more weeks while chronic cases are several months to several years with some permanent sequelae. In this study both qualitative and quantitative approaches were used. The focus of this study was the inflammatory changes of the central nervous system (CNS). In acute cases there were areas of degenerative tissue, severe damage of the nerve cells, neuronophagia which is the phagocytosis of infected neurons, perivascular cuffing, and injury to the parenchyma. The grey matter of the brain is where all these changes occur. Lesions are usually found in the diencephalon and mesencephalon, then the next highest frequency are found in the brain stem, cerebral cortex and the cerebellum. There may also be slight changes seen in the leptomeninges of the spinal cord. In subacute cases, changes are found to be less than that of acute cases. the inflammation is still found in the mesencephalon, diencephalon and brain stem but is rare found in the cerebral cortex, cerebellum, meninges, and spinal cord. The most dominant changes in this stage is degeneration, even to the point of loss, of nerve cells and proliferation of glial cells. Lesions also are more localized. Hylalin thrombus formation, a blood clot, may be found in both acute and subacute stages. Chronic stages localized nercosis or softening is seen in the mesencephalon, diencephalon, and brain stem but is most often in the substantia nigra. There is also degeneration of nervous tissue that may lead to complete loss, fibrous thickening of the vascular walls, and marked post-inflammatory organization. Overall, there are cellular changes in the reticulo-endothelial system of the visceral organs. Studies have shown that the cells seem to be undergoing karyolysis or autolysis (cell suicide). Karyolysis is the chromatin matter dissolution by DNAase by a dying cell. Autolysis and karyolysis are most often seen in acute cases.