The La Crosse encephalitis virus is a type of arbovirus called a bunyavirus. The Bunyavirales are mainly arboviruses.

Most cases of LAC encephalitis occur in children under 16 years of age. LAC virus is a zoonotic pathogen cycled between the daytime-biting treehole mosquito, "Aedes triseriatus", and vertebrate amplifier hosts (chipmunks, tree squirrels) in deciduous forest habitats. The virus is maintained over the winter by transovarial transmission in mosquito eggs. If the female mosquito is infected, she may lay eggs that carry the virus, and the adults coming from those eggs may be able to transmit the virus to chipmunks and to humans.

Anyone bitten by a mosquito in an area where the virus is circulating can get infected with LACV. The risk is highest for people who live, work or recreate in woodland habitats, because of greater exposure to potentially infected mosquitoes.

People reduce the chance of getting infected with LACV by preventing mosquito bites. There is no vaccine or preventive drug.

Prevention measures against LACV include reducing exposure to mosquito bites. Use repellent such as DEET and picaridin, while spending time outside, especially at during the daytime - from dawn until dusk. "Aedes triseriatus" mosquitoes that transmit (LACV) are most active during the day. Wear long sleeves, pants and socks while outdoors. Ensure all screens are in good condition to prevent mosquitoes from entering your home. "Aedes triseriatus" prefer treeholes to lay eggs in. Also, remove stagnant water such as old tires, birdbaths, flower pots, and barrels.

Mosquitoes, primarily from the genus "Culex", become infected by feeding on birds infected with the Saint Louis encephalitis virus. Infected mosquitoes then transmit the Saint Louis encephalitis virus to humans and animals during the feeding process. The Saint Louis encephalitis virus grows both in the infected mosquito and the infected bird, but does not make either one sick. Only infected mosquitoes can transmit Saint Louis encephalitis virus. Once a human has been infected with the virus it is not transmissible from that individual to other humans.

Viral encephalitis is a type of encephalitis caused by a virus.

It is unclear if anticonvulsants used in people with viral encephalitis would prevent seizures.

Infection with Japanese encephalitis confers lifelong immunity. There are currently three vaccines available: SA14-14-2, IC51 (marketed in Australia and New Zealand as JESPECT and elsewhere as IXIARO) and ChimeriVax-JE (marketed as IMOJEV). All current vaccines are based on the genotype III virus.

A formalin-inactivated mouse-brain derived vaccine was first produced in Japan in the 1930s and was validated for use in Taiwan in the 1960s and in Thailand in the 1980s. The widespread use of vaccine and urbanization has led to control of the disease in Japan, Korea, Taiwan, and Singapore. The high cost of this vaccine, which is grown in live mice, means that poorer countries have not been able to afford to give it as part of a routine immunization program.

The most common adverse effects are redness and pain at the injection site. Uncommonly, an urticarial reaction can develop about four days after injection. Vaccines produced from mouse brain have a risk of autoimmune neurological complications of around 1 per million vaccinations. However where the vaccine is not produced in mouse brains but in vitro using cell culture there is little adverse effects compared to placebo, the main side effects are headache and myalgia.

The neutralizing antibody persists in the circulation for at least two to three years, and perhaps longer. The total duration of protection is unknown, but because there is no firm evidence for protection beyond three years, boosters are recommended every three years for people who remain at risk. Furthermore, there is also no data available regarding the interchangeability of other JE vaccines and IXIARO.

In September 2012 the Indian firm Biological E. Limited has launched an inactivated cell culture derived vaccine based on SA 14-14-2 strain which was developed in a technology transfer agreement with Intercell and is a thiomersal-free vaccine.

Arbovirus encephalitis refers to encephalitis that is caused by arbovirus infection.

There are many types of arboviral encephalitides found in the United States.

Examples include:

- California encephalitis

- Japanese encephalitis

- St. Louis encephalitis

- Tick-borne encephalitis

- West Nile fever

- Murray Valley encephalitis

It is transmitted by the bite of several species of infected ticks, including "Ixodes scapularis", "I. ricinus" and "I. persulcatus", or (rarely) through the non-pasteurized milk of infected cows.

TBE is caused by tick-borne encephalitis virus, a member of the genus "Flavivirus" in the family Flaviviridae. It was first isolated in 1937. Three virus sub-types are described: European or Western tick-borne encephalitis virus, Siberian tick-borne encephalitis virus, and Far-Eastern tick-borne encephalitis virus (formerly known as Russian spring summer encephalitis virus).

Russia and Europe report about 5,000–7,000 human cases annually.

The former Soviet Union conducted research on tick borne diseases, including the TBE viruses.

Meningitis is a very common in children. Newborns can develop herpes virus infections through contact with infected secretions in the birth canal. Other viral infections are acquired by breathing air contaminated with virus-containing droplets exhaled by an infected person. Arbovirus infections are acquired from bites by infected insects (called epidemic encephalitis). Viral central nervous system infections in newborns and infants usually begin with fever. The inability of infants to communicate directly makes it difficult to understand their symptoms. Newborns may have no other symptoms and may initially not otherwise appear ill. Infants older than a month or so typically become irritable and fussy and refuse to eat. Vomiting is common. Sometimes the soft spot on top of a newborn's head (fontanelle) bulges, indicating an increase in pressure on the brain. Because irritation of the meninges is worsened by movement, an infant with meningitis may cry more, rather than calm down, when picked up and rocked. Some infants develop a strange, high-pitched cry. Infants with encephalitis often have seizures or other abnormal movements. Infants with severe encephalitis may become lethargic and comatose and then die. To make the diagnosis of meningitis or the diagnosis of encephalitis, doctors do a spinal tap (lumbar puncture) to obtain cerebrospinal fluid (CSF) for laboratory analysis in children.

Viral encephalitis can occur either as a direct effect of an acute infection, or as one of the sequelae of a latent infection. The majority of viral cases of encephalitis have an unknown cause, however the most common identifiable cause of viral encephalitis is from herpes simplex infection. Other causes of acute viral encephalitis are rabies virus, poliovirus, and measles virus.

Additional possible viral causes are arbovirus (St. Louis encephalitis, West Nile encephalitis virus), bunyavirus (La Crosse strain), arenavirus (lymphocytic choriomeningitis virus) and reovirus (Colorado tick virus). The Powassan virus is a rare cause of encephalitis.

The majority of infections result in mild illness, including fever and headache. When infection is more severe the person may experience headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions and spastic paralysis. Fatality ranges from . Aged people are more likely to have a fatal infection.

It can be caused by a bacterial infection, such as bacterial meningitis, or may be a complication of a current infectious disease syphilis (secondary encephalitis).

Certain parasitic or protozoal infestations, such as toxoplasmosis, malaria, or primary amoebic meningoencephalitis, can also cause encephalitis in people with compromised immune systems. Lyme disease or "Bartonella henselae" may also cause encephalitis.

Other bacterial pathogens, like "Mycoplasma" and those causing rickettsial disease, cause inflammation of the meninges and consequently encephalitis. A non-infectious cause includes acute disseminated encephalitis which is demyelinated.

Herpesviral Encephalitis can be treated with high-dose intravenous acyclovir. Without treatment, HSE results in rapid death in approximately 70% of cases; survivors suffer severe neurological damage. When treated, HSE is still fatal in one-third of cases, and causes serious long-term neurological damage in over half of survivors. Twenty percent of treated patients recover with minor damage. Only a small population of survivors (2.5%) regain completely normal brain function. Indeed, many amnesic cases in the scientific literature have etiologies involving HSE. Earlier treatment (within 48 hours of symptom onset) improves the chances of a good recovery. Rarely, treated individuals can have relapse of infection weeks to months later. There is evidence that aberrant inflammation triggered by herpes simplex can result in granulomatous inflammation in the brain, which responds to steroids. While the herpes virus can be spread, encephalitis itself is not infectious. Other viruses can cause similar symptoms of encephalitis, though usually milder (Herpesvirus 6, varicella zoster virus, Epstein-Barr, cytomegalovirus, coxsackievirus, etc.).

Types of encephalitis in humans include:

- Arbovirus encephalitis

- La Crosse encephalitis

- Enterovirus

- California encephalitis virus

- Japanese encephalitis

- St. Louis encephalitis

- Eastern equine encephalitis virus

- Western equine encephalitis virus

- Venezuelan equine encephalitis virus

- Murray Valley encephalitis virus

- Tick-borne meningoencephalitis

- Powassan encephalitis

- West Nile virus

- Herpes simplex

- Human herpesvirus 6

- Varicella zoster virus

- Rabies

- HIV

- H5N1 encephalitis

- Nipah virus encephalitis

- Lymphocytic choriomeningitis, which also causes encephalitis

Many viral infections of the central nervous system occur in seasonal peaks or as epidemics, whereas others, such as herpes simplex encephalitis, are sporadic. In endemic areas it is mostly a disease of children, but as the disease spreads to new regions, or nonimmune travelers visit endemic regions, nonimmune adults are also affected.

Herpesviral encephalitis is encephalitis due to herpes simplex virus.

Herpes simplex encephalitis (HSE) is a viral infection of the human central nervous system. It is estimated to affect at least 1 in 500,000 individuals per year and some studies suggest an incidence rate of 5.9 cases per 100,000 live births. The majority of cases of herpes encephalitis are caused by herpes simplex virus-1 (HSV-1), the same virus that causes cold sores. 57% of American adults are infected with HSV-1, which is spread through droplets, casual contact, and sometimes sexual contact, though most infected people never have cold sores. About 10% of cases of herpes encephalitis are due to HSV-2, which is typically spread through sexual contact. About 1 in 3 cases of HSE result from primary HSV-1 infection, predominantly occurring in individuals under the age of 18; 2 in 3 cases occur in seropositive persons, few of whom have history of recurrent orofacial herpes. Approximately 50% of individuals who develop HSE are over 50 years of age.

While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60–90 days to recover. People with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple long term (>1+ years) somatic complaints such as tremor, and dysfunction in motor skills and executive functions. People with milder illness are just as likely as people with more severe illness to experience adverse outcomes. Recovery is marked by a long convalescence with fatigue. One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease.

Risk factors independently associated with developing a clinical infection with WNV include a suppressed immune system and a patient history of organ transplantation. For neuroinvasive disease the additional risk factors include older age (>50+), male sex, hypertension, and diabetes mellitus.

A genetic factor also appears to increase susceptibility to West Nile disease. A mutation of the gene "CCR5" gives some protection against HIV but leads to more serious complications of WNV infection. Carriers of two mutated copies of "CCR5" made up 4.0 to 4.5% of a sample of West Nile disease sufferers, while the incidence of the gene in the general population is only 1.0%.

There is no specific treatment for Japanese encephalitis and treatment is supportive, with assistance given for feeding, breathing or seizure control as required. Raised intracranial pressure may be managed with mannitol. There is no transmission from person to person and therefore patients do not need to be isolated.

A breakthrough in the field of Japanese encephalitis therapeutics is the identification of macrophage receptor involvement in the disease severity. A recent report of an Indian group demonstrates the involvement of monocyte and macrophage receptor CLEC5A in severe inflammatory response in Japanese Encephalitis infection of the brain. This transcriptomic study provides a hypothesis of neuroinflammation and a new lead in development of appropriate therapeutic against Japanese encephalitis.

There is currently no established treatment.

Half of all cases results in permanent neurological damage and 10-15% result in death.

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 lifelong 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.

Of those who contract MVE, one-quarter die from the disease.

MVEV is a mosquito-borne virus that is maintained in a bird-mosquito-bird cycle. Water birds from the order Ciconiiformes, 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; the virus cannot be transmitted from person to person.

The mortality rate of the virus largely depends on the immune status of the infected dogs. Puppies experience the highest mortality rate, where complications such as pneumonia and encephalitis are more common. In older dogs that develop distemper encephalomyelitis, vestibular disease may present. Around 15% of canine inflammatory central nervous system diseases are a result of CDV.

A preceding antigenic challenge can be identified in approximately two-thirds of people. Viral infections thought to induce ADEM include influenza virus, enterovirus, measles, mumps, rubella, varicella zoster, Epstein Barr virus, cytomegalovirus, herpes simplex virus, hepatitis A, and coxsackievirus; while the bacterial infections include Mycoplasma pneumoniae, Borrelia burgdorferi, Leptospira, and beta-hemolytic Streptococci. The only vaccine proven to induce ADEM is the Semple form of the rabies vaccine, but hepatitis B, pertussis, diphtheria, measles, mumps, rubella, pneumococcus, varicella, influenza, Japanese encephalitis, and polio vaccines have all been implicated. The majority of the studies that correlate vaccination with ADEM onset use small samples or case studies. Large scale epidemiological studies (e.g., of MMR vaccine or smallpox vaccine) do not show increased risk of ADEM following vaccination. In rare cases, ADEM seems to follow from organ transplantation. An upper bound for the risk of ADEM from measles vaccination, if it exists, can be estimated to be 10 per million, which is far lower than the risk of developing ADEM from an actual measles infection, which is about 1 per 1,000 cases. For a rubella infection, the risk is 1 per 5,000 cases. Some early vaccines, later shown to have been contaminated with host animal CNS tissue, had ADEM incident rates as high as 1 in 600.

The disease can be prevented in horses with the use of vaccinations. These vaccinations are usually given together with vaccinations for other diseases, most commonly WEE, VEE, and tetanus. Most vaccinations for EEE consist of the killed virus. For humans there is no vaccine for EEE so prevention involves reducing the risk of exposure. Using repellent, wearing protective clothing, and reducing the amount of standing water is the best means for prevention