In this review we will focus mainly on zoonotic encephalitis caused by arthropod-borne viruses (arboviruses) of the families Flaviviridae (genus Flavivirus) and Togaviridae (genus Alphavirus) which are important in both humans and pets animals. Specifically, we will focus on alphaviruses (Eastern equine encephalitis virus, Western equine encephalitis virus, Venezuelan equine encephalitis virus) and flaviviruses (Japanese encephalitis virus and West Nile virus). Most of these viruses were originally found in tropical regions such as Africa and South America or in some regions of Asia. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay However, they have spread widely and currently cause diseases throughout the world. Global warming, increased urbanization and population size in tropical regions, faster transportation, and the rapid spread of arthropod vectors contribute to the continued spread of arboviruses into new geographic areas causing reemerging or recrusting diseases. Most re-emerging arboviruses have also emerged as agents of zoonotic diseases and have created serious public health problems and epidemics. “Zoonosis” is defined as a disease or infection transmitted naturally from vertebrate animals to humans. Zoonotic diseases can be transmitted through direct or indirect contact. Transmission of an infectious agent from a vertebrate animal to a human via an arthropod vector is an example of indirect transmission of a zoonotic disease. Viruses that maintain cycles of transmission between reservoirs of vertebrate animals as the main amplifying hosts and insects as the primary vectors are known as arboviruses (arthropod-borne viruses). Arboviruses must replicate in arthropod vectors, such as mosquitoes, ticks, midges, or sandflies, before transmission. Female mosquitoes acquire the virus while feeding on the blood of an infected animal, and the virus replicates in the epithelial cells of the mesenteron. Virus released from mesenteric epithelial cells infects salivary glands after secondary amplification in other cells and tissues. Some arboviruses can infect salivary glands without secondary amplification in other cells and tissues. Subsequently, the virus released from the salivary gland epithelium is transmitted during blood feeding of the vertebrate host. Arboviruses are included in several taxonomic families, including Flaviviridae (genus Flavivirus), Bunyaviridae (genus Nairovirus, Orthobunyavirus, Phlebovirus, and Tospovirus), Togaviridae (genus Alphavirus), Rhabdoviridae (genus Vesiculovirus), Orthomyxoviridae (genus Thogotovirus), and Reoviridae (genus Orbivirus and Coltivirus) Many of the important zoonotic arboviruses belong to the Togaviridae and Flaviviridae families [2]. However, there are many other clinically important human and animal arboviruses belonging to the family Bunyaviridae, such as the Crimean-Congo hemorrhagic fever virus (tick-transmitted) in the genus Nairovirus and the Toscana virus (transmitted by sandflies) and the sandfly virus of the Rift Valley (transmitted by mosquitoes) in the genus Phlebovirus. Colorado tick fever virus of the family Reoviridae (genus Coltivirus) is also an important human arbovirus. Arboviruses are maintained in complex life cycles involving non-human primate/vertebrate hosts and primary arthropod vectors. Mosquitoes are the most important vectors transmitting zoonotic viruses. Different species of mosquitoes (Culex spp., Aedes spp., etc.) can act as vectors of the same virus in different vertebrate hosts adepending on the different geographical and ecological positions. Ticks, sandflies (Phlebotomus spp.) and midges (Culicoides spp.) are also important vectors of some arboviruses. Vertical transmission (transovarial and transstadial) occurs in some arthropod vectors as they transmit some arboviruses from parent arthropods to daughter arthropods. This type of transmission occurs primarily in tick-borne encephalitis viruses (TBEV) but has also been reported in some mosquito-borne viruses. For example, La Crosse virus, one of the most important viruses among the agents causing California encephalitis, is transmitted by its main vector, Aedes triseriatus, not only transovarially and transstadially but also sexually. The best-known arboviruses were first isolated in tropical regions such as Africa and South America and in some Asian countries. However, the geographic distribution and frequency of arboviral disease epidemics have expanded significantly worldwide in recent decades. Several factors such as changes in viral genetics, host and/or vector populations, and climate changes have facilitated the expansion and transmission of arboviruses resulting in the emergence/reemergence of arboviral disease outbreaks in new regions of the world. Extensive tropical urbanization and faster and greater movements of humans and animals by modern transportation have helped vectors to be in closer contact with vertebrate host reservoirs, increasing the potential for transmission. The introduction of West Nile virus to the New World and the emergence of Japanese encephalitis virus (JEV) in Australia are some notable examples of recent unexpected emerging/reemerging zoonotic diseases. Epidemics/epizootics in humans and domestic animals usually occur when the enzootic virus is introduced into rural environments or comes into close contact with humans via a bridging vector. Usually, humans and domestic animals develop clinical disease but do not develop a sufficient level of viremia to infect arthropods, so they are considered dead-end hosts and do not contribute to the transmission cycle. However, some arboviruses such as dengue fever (DF), yellow fever, and chikungunya viruses (CHIKV) cause high levels of viremia in humans and can be transmitted from person to person by mosquitoes (urban cycle). In this review, we will mainly focus on the transmission and epidemiology of mosquito-borne arboviruses, especially alphaviruses and flaviviruses that are pathogenic to humans and domestic animals, thus increasing the importance for public health and l 'economy. Although these viruses, with the exception of JEV, are not currently circulating on the Korean Peninsula, there is a great possibility that other viruses will emerge when a competent vector and vertebrate host populations are temporally and spatially together in a permissive environment.AlphavirusesAlphaviruses (formerly arboviruses of group A) are single-stranded, enveloped, positive-sense RNA viruses that belong to the Alphavirus genus of the Togaviridae family. The alphavirus genome ranges between 11 and 12 kb in length and is composed of a non-segmented single-stranded RNA with a 7-methylguanosine tail and a poly-A tail at the 5'- and 3'-terminus, respectively. It encodes four nonstructural proteins responsible for genome replication and protein processing and generates a subgenomic mRNA (26S). The five structural proteins (C, E3, E2, 6K, and E1) are translated from the 26S subgenomic mRNA. Alphaviruses are widely distributed throughout the world. They have been classified as belonging to the New and Old alphavirusesWorld: New World alphaviruses (eg, Eastern equine encephalitis virus [EEEV], Western equine encephalitis virus [WEEV], and Venezuelan equine encephalitis virus [VEEV]) are distributed in the Americas and cause encephalitis in humans, while Old World alphaviruses (e.g., Sindbis virus [SINV], CHIKV, O'nyong-nyong virus [ONNV], Ross River virus [RRV], Barmah Forest virus [ BFV] and Semliki Forest virus [ SFV]), characterized by fever, rashes, and arthritis, are found in Europe, Asia, Australia, and parts of Africa. However, RRV, SINV, and CHIKV have occasionally been associated with encephalitis. The alphavirus serogroups can be divided into seven antigenically related complexes: Barmah Forest, Eastern Equine Encephalitis (EEE), Middleburg, Ndumu, Semliki Forest, Equine Venezuelanencephalitis (VEE), and Western Equine Encephalitis (WEE). All clinically relevant alphaviruses are transmitted by mosquitoes. More than one mosquito species is usually involved in the alphavirus transmission cycle. The survival of alphaviruses in a given geographic region depends on the presence of competent vectors (mosquitoes) and vertebrate hosts that develop a low pathogenicity viremic infection. Important amplification hosts are birds (for SINV, SFV, EEEV and WEEV), rodents (for RRV, VEEV, BFV) and monkeys (for CHIKV, ONNV and Mayaro fever virus). EEEV is a zoonotic virus transmitted by mosquitoes and originating in birds. In North America, EEEV is an important cause of disease in domestic animals and humans. The disease is serious in horses, pigs, dogs and some bird species. EEEV was first isolated in 1933 from the brains of affected horses during a widespread epidemic in the northeastern United States, New Jersey and Virginia. However, horse deaths have recently been reported further north along the east coast of the United States (New Hampshire and Maine) and Canada. In 1936, South American EEEV was first isolated from a horse in Argentina. The EEEV strains present in South and North America are antigenically and genetically different from each other and also differ in human pathogenicity. There are four lineages (I, II, III and IV) of EEEV based on their antigenicity and distribution in various geographical regions. Viruses of the closely related North American EEEV (NA-EEEV) lineage occurring in the United States, Canada, and the Caribbean are the most virulent to horses and humans. In contrast, infection of horses or humans with genetically and antigenically diverse, enzootic viral strains in Central and South America (lines II, III, and IV [SA-EEEV]) rarely results in significant clinical disease. Lineage II strains are distributed along the coasts of South and Central America, lineage III in the Amazon basin, and lineage IV in Brazil. In North America, EEEV is enzootic from the East and Gulf Coasts to inland sites (Texas) [36,37]. NA-EEEV strains are genetically highly conserved, with only one major lineage (lineage I) since first isolation in 1933. Most EEE epidemics in North America occur in late summer to early fall , often associated with heavy rain. Epidemics in horses are common and often accompanied by high mortality rates. 80-90% of infected horses develop the acute, lethal disease, and approximately 66% of survivors develop severe neurologic sequelae. During EEE outbreaks or epidemics, horses do not serve as amplifying hosts but tend to be the first to develop clinical signs and often serve as an indicator of the onset of an outbreak or epidemic. Therefore, rapid detection of EEEV in equine samples is critical for the control of disease outbreaksin humans, horses and other animal species. NA-EEEV strains are responsible for the majority of human cases. Human infections are generally asymptomatic, but some progress to severe encephalitis accompanied by a high mortality rate or disabling sequelae. The disease is generally more severe in older adults and infants. Although only a few cases of EEEV infection in humans have been reported annually since the 1960s, the high mortality rate and severe neurologic sequelae in infected patients make EEEV an important human pathogen. In South America, enzootic EEEVs are widely distributed in most tropical forest areas, the Amazon basin in Brazil, and northern Argentina. In these regions, EEEV is primarily an equine pathogen, and equine cases can occur year-round. However, human EEEV infections have rarely been detected, even during major equine epizootics. In temperate regions of South America (e.g., Argentina), EEEV infections often occur during the summer. EEEV transmission cycle The EEEV transmission cycle in North America is maintained between passerines as reservoir/amplifier hosts and the ornithophilic mosquito, Culisetamelanura, as the primary enzootic vector in marshland habitats. Furthermore, studies have shown that C. melanura, considered so far a bridging vector in human and equine infections, can also serve as a main epizootic vector. Mosquito species such as C. pescator, C. erraticus, and Uranotaenia sapphirina can also serve as enzootic vectors in some regions of the southeastern United States. These mosquitoes are known to feed on reptiles and amphibians. Recently, it has been suggested that snakes play a role in the enzootic transmission cycle of EEEV as overwintering hosts. EEEV infections in birds are generally asymptomatic; however, diseases with high viremia and high mortality rate have been reported in chukar partridges, pheasants, egrets, glossy ibises (Plegadis falcinellus), turtle doves, house sparrows, psittacine birds, ratites (emus, ostriches), African penguins, chickens (<14 days), pigeons, Peking ducks and whooping cranes. Passerine birds develop extremely high levels of viremia, sufficient to infect both enzootic vectors and a variety of bridging vectors (e.g. Aedes and Coquillettidia) that transmit the virus by the enzootic cycle to humans and horses. In pheasants, EEEV is transmitted through feather picking and cannibalism. Humans and equids are dead-end hosts as they do not develop sufficient viremia to transmit the virus. In South America, the reservoirs and amplification hosts involved in the enzootic transmission cycle of EEEV are not yet known. However, seroprevalence and experimental studies suggest that the Culex subgenus (Melanoconion) and rodents/marsupials may serve as major enzootic vectors and reservoirs, respectively, and may play a more important role in the enzootic transmission of EEEVs in South America. The virus primarily causes disease in horses, and occasional cases of encephalitis have also been reported in sheep, cattle, deer, South American camelids (llamas and alpacas), and pigs. Furthermore, infections have been observed in dogs, goats, bats and small mammals including rodents. EEEV vaccine There is a formalin-inactivated vaccine based on a NA-EEEV (PE-6) strain used in horses and emus, however it does not work. do not induce significant neutralizing anti-E2 antibodies against SA-EEEV. The vaccine is used in laboratory workers to protect them from accidental exposure. A similar formalin-inactivated vaccine is available for horses. There is currently no specific therapy for EEE. The virus.