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.

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.

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

No specific therapy is available at present for La Crosse encephalitis, and management is limited to alleviating the symptoms and balancing fluids and electrolyte levels. Intravenous ribavirin is effective against La Crosse encephalitis virus in the laboratory, and several studies in patients with severe, brain biopsy confirmed, La Crosse encephalitis are ongoing.

In a trial with 15 children being infected with La Crosse viral encephalitis were treated at certain phases with ribavirin (RBV). RBV appeared to be safe at moderate doses. At escalated doses of RBV, adverse events occurred and then the trial was discontinued. Nonetheless, this was the largest study of antiviral treatment for La Crosse encephalitis.

A vaccine has been conditionally approved for use in animals in the US. It has been shown that knockout of the NSs and NSm nonstructural proteins of this virus produces an effective vaccine in sheep as well.

West Nile virus can be sampled from the environment by the pooling of trapped mosquitoes via ovitraps, carbon dioxide-baited light traps, and gravid traps, testing blood samples drawn from wild birds, dogs, and sentinel monkeys, as well as testing brains of dead birds found by various animal control agencies and the public.

Testing of the mosquito samples requires the use of reverse-transcriptase PCR (RT-PCR) to directly amplify and show the presence of virus in the submitted samples. When using the blood sera of wild birds and sentinel chickens, samples must be tested for the presence of WNV antibodies by use of immunohistochemistry (IHC) or enzyme-linked immunosorbent assay (ELISA).

Dead birds, after necropsy, or their oral swab samples collected on specific RNA-preserving filter paper card, can have their virus presence tested by either RT-PCR or IHC, where virus shows up as brown-stained tissue because of a substrate-enzyme reaction.

West Nile control is achieved through mosquito control, by elimination of mosquito breeding sites such as abandoned pools, applying larvacide to active breeding areas, and targeting the adult population via lethal ovitraps and aerial spraying of pesticides.

Environmentalists have condemned attempts to control the transmitting mosquitoes by spraying pesticide, saying the detrimental health effects of spraying outweigh the relatively few lives that may be saved, and more environmentally friendly ways of controlling mosquitoes are available. They also question the effectiveness of insecticide spraying, as they believe mosquitoes that are resting or flying above the level of spraying will not be killed; the most common vector in the northeastern United States, "Culex pipiens", is a canopy feeder.

There are no vaccines or any other treatments specifically for Saint Louis encephalitis virus, although one study showed that early use of interferon-alpha2b may decrease the severity of complications.

Prophylaxis by vaccination, as well as preventive measures like protective clothing, tick control, and mosquito control are advised. The vaccine for KFDV consists of formalin-inactivated KFDV. The vaccine has a 62.4% effectiveness rate for individuals who receive two doses. For individuals who receive an additional dose, the effectiveness increases to 82.9%. Specific treatments are not available.

A vaccine for horses (ATCvet code: ) based on killed viruses exists; some zoos have given this vaccine to their birds, although its effectiveness is unknown. Dogs and cats show few if any signs of infection. There have been no known cases of direct canine-human or feline-human transmission; although these pets can become infected, it is unlikely they are, in turn, capable of infecting native mosquitoes and thus continuing the disease cycle.

AMD3100, which had been proposed as an antiretroviral drug for HIV, has shown promise against West Nile encephalitis. Morpholino antisense oligos conjugated to cell penetrating peptides have been shown to partially protect mice from WNV disease. There have also been attempts to treat infections using ribavirin, intravenous immunoglobulin, or alpha interferon. GenoMed, a U.S. biotech company, has found that blocking angiotensin II can treat the "cytokine storm" of West Nile virus encephalitis as well as other viruses.

A vaccine called Chimerivax-WNV is being actively researched and has undergone phase II Clinical trials in 2011.

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.

The scientific study of the genetics of MVEV has been facilitated by the construction and manipulation of an infectious cDNA clone of the virus.

There is no cure for EEE. Treatment consists of corticosteroids, anticonvulsants, and supportive measures (treating symptoms) such as intravenous fluids, tracheal intubation, and antipyretics. About four percent of humans known to be infected develop symptoms, with a total of about six cases per year in the US. A third of these cases die, and many survivors suffer permanent brain damage.

The disease is incurable once manifested, so there is no specific drug therapy for TBE. Symptomatic brain damage requires hospitalization and supportive care based on syndrome severity. Anti-inflammatory drugs, such as corticosteroids, may be considered under specific circumstances for symptomatic relief. Tracheal intubation and respiratory support may be necessary.

Prevention includes non-specific (tick-bite prevention, tick checks) and specific prophylaxis in the form of a vaccine. TBE immunoglobulin is no longer used. Tick-borne encephalitis vaccine is very effective and available in many disease endemic areas and in travel clinics.

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.

Preventing Omsk Hemorrhagic Fever consists primarily in avoiding being exposed to tick. Persons engaged in camping, farming, forestry, hunting (especially the Siberian muskrat) are at greater risk and should wear protective clothing or use insect repellent for protection. The same is generally recommended for persons at sheltered locations.

Prevention strategies include reducing the breeding of midges through source reduction (removal and modification of breeding sites) and reducing contact between midges and people. This can be accomplished by reducing the number of natural and artificial water-filled habitats and encourage the midge larvae to grow.

Oropouche fever is present in epidemics so the chances of one contracting it after being exposed to areas of midgets or mosquitoes is rare.

Oropouche Fever has no cure or specific therapy so treatment is done by relieving the pain of the symptoms through symptomatic treatment. Certain oral analgesic and anti-inflammatory agents can help treat headaches and body pains. In extreme cases of oropouche fever the drug, Ribavirin is recommended to help against the virus. This is called antiviral therapy. Treatments also consist of drinking lots of fluids to prevent dehydration.

Asprin is not a recommended choice of drug because it can reduce blood clotting and may aggravate the hemorrhagic effects and prolong recovery time.

The infection is usually self-limiting and complications are rare. This illness usually lasts for about a week but in extreme cases can be prolonged. Patients usually recover fully with no long term ill effects. There have been no recorded fatalities resulting from oropouche fever.

During 1975 and 1976, Rocio virus was responsible for several epidemics of meningoencephalitis in coastal communities in southern São Paulo, Brazil. The outbreaks affected over 1,000 people and killed about 10% of those infected, but apparently responded well to treatment for viral encephalitides. The disease progresses rapidly after onset, with patients dying within 5 days of symptoms first appearing. The disease first presents with fever, headache, vomiting, and conjunctivitis, then progresses to neurological symptoms (confusion, disorientation, etc.) and muscle weakness; about one-third of cases enter a coma, and a third of those patients die, although supportive care such as intensive nursing and symptomatic treatment might reduce the case fatality rate to 4%. Survivors show neurological and psychological after-effects (sequelae) in about 20% of cases.

The VHF viruses are spread in a variety of ways. Some may be transmitted to humans through a respiratory route. According to Soviet defector Ken Alibek, Soviet scientists concluded China may have tried to weaponise a VHF virus during the late 1980's but discontinued to do so after an outbreak . The virus is considered by military medical planners to have a potential for aerosol dissemination, weaponizaton, or likelihood for confusion with similar agents that might be weaponized.

There are currently no Food and Drug Administration-approved vaccines for the prevention of MVD. Many candidate vaccines have been developed and tested in various animal models. Of those, the most promising ones are DNA vaccines or based on Venezuelan equine encephalitis virus replicons, vesicular stomatitis Indiana virus (VSIV) or filovirus-like particles (VLPs) as all of these candidates could protect nonhuman primates from marburgvirus-induced disease. DNA vaccines have entered clinical trials. Marburgviruses are highly infectious, but not very contagious. Importantly, and contrary to popular belief, marburgviruses do not get transmitted by aerosol during natural MVD outbreaks. Due to the absence of an approved vaccine, prevention of MVD therefore relies predominantly on behavior modification, proper personal protective equipment, and sterilization/disinfection.

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.

Since marburgviruses are not spreading via aerosol, the most straightforward prevention method during MVD outbreaks is to avoid direct (skin-to-skin) contact with patients, their excretions and body fluids, or possibly contaminated materials and utensils. Patients ought to be isolated but still have the right to be visited by family members. Medical staff should be trained and apply strict barrier nursing techniques (disposable face mask, gloves, goggles, and a gown at all times). Traditional burial rituals, especially those requiring embalming of bodies, ought to be discouraged or modified, ideally with the help of local traditional healers.

There is currently no vaccine available. The primary method of disease prevention is minimizing mosquito bites, as the disease is only transmitted by mosquitoes. Typical advice includes use of mosquito repellent and mosquito screens, wearing light coloured clothing, and minimising standing water around homes (e.g. removing Bromeliads, plant pots, garden ponds). Staying indoors during dusk/dawn hours when mosquitos are most active may also be effective. Bush camping is a common precipitant of infection so particular care is required.

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.

The study of RRF has been recently facilitated by the development of a mouse model. Mice infected with RRV develop hind-limb arthritis/arthralgia which is similar to human disease. The disease in mice is characterized by an inflammatory infiltrate including macrophages which are immunopathogenic and exacerbate disease. Furthermore, mice deficient in the C3 protein do not suffer from severe disease following infection. This indicates that an aberrant innate immune response is responsible for severe disease following RRV infection.