West Nile virus

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West Nile virus
West Nile Virus Image.jpg
A micrograph of the West Nile Virus, appearing in yellow
Virus classification OOjs UI icon edit-ltr.svg
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Kitrinoviricota
Class: Flasuviricetes
Order: Amarillovirales
Family: Flaviviridae
Genus: Flavivirus
Species:
West Nile virus
Ribbon representation of the NS2B/NS3 protease of West Nile virus WNVpr trans.png
Ribbon representation of the NS2B/NS3 protease of West Nile virus

West Nile virus (WNV) is a single-stranded RNA virus that causes West Nile fever. It is a member of the family Flaviviridae , from the genus Flavivirus , which also contains the Zika virus, dengue virus, and yellow fever virus. The virus is primarily transmitted by mosquitoes, mostly species of Culex . The primary hosts of WNV are birds, so that the virus remains within a "bird–mosquito–bird" transmission cycle. [1] The virus is genetically related to the Japanese encephalitis family of viruses. Humans and horses both exhibit disease symptoms from the virus, and symptoms rarely occur in other animals.

Contents

Etymology

Contrary to popular belief, West Nile virus was not named after the Nile River, rather, the West Nile district of Uganda where the virus was first isolated in 1937. [2] After its original discovery in this region, it was found in many other parts of the world. Most likely, it spread from the original West Nile district.

Structure

Like most other flaviviruses, WNV is an enveloped virus with icosahedral symmetry. [3] Electron microscope studies reveal a 45–50 nm virion covered with a relatively smooth protein shell; this structure is similar to the dengue fever virus, another Flavivirus . [3] The protein shell is made of two structural proteins: the glycoprotein E and the small membrane protein M. [4] Protein E has numerous functions including receptor binding, viral attachment, and entry into the cell through membrane fusion. [4]

The outer protein shell is covered by a host-derived lipid membrane, the viral envelope. [5] The flavivirus lipid membrane has been found to contain cholesterol and phosphatidylserine, but other elements of the membrane have yet to be identified. [6] [7] The lipid membrane has many roles in viral infection, including acting as signaling molecules and enhancing entry into the cell. [8] Cholesterol, in particular, plays an integral part in WNV entering a host cell. [9] The two viral envelope proteins, E and M, are inserted into the membrane. [4]

The RNA genome is bound to capsid (C) proteins, which are 105 amino-acid residues long, to form the nucleocapsid. The capsid proteins are one of the first proteins created in an infected cell; [5] the capsid protein is a structural protein whose main purpose is to package RNA into the developing viruses. [10] The capsid has been found to prevent apoptosis by affecting the Akt pathway. [5]

Genome

The West Nile virus genome. Modified after Guzman et al. 2010. Genome of the West Nile Virus.gif
The West Nile virus genome. Modified after Guzman et al. 2010.

WNV is a positive-sense, single-stranded RNA virus. Its genome is approximately 11,000 nucleotides long and is flanked by 5′ and 3′ non-coding stem loop structures. [13] The coding region of the genome codes for three structural proteins and seven nonstructural (NS) proteins, proteins that are not incorporated into the structure of new viruses. The WNV genome is first translated into a polyprotein and later cleaved by virus and host proteases into separate proteins (i.e. NS1, C, E). [14]

Structural proteins

Structural proteins (C, prM/M, E) are capsid, precursor membrane proteins, and envelope proteins, respectively. [13] The structural proteins are located at the 5′ end of the genome and are cleaved into mature proteins by both host and viral proteases.[ citation needed ]

Structural ProteinFunction
CCapsid protein; encloses the RNA genome, packages RNA into immature virions. [10] [15]
prM/MViruses with M protein are infectious: the presence of M protein allows for the activation of proteins involved in viral entry into the cell. prM (precursor membrane) protein is present on immature virions, by further cleavage by furin to M protein, the virions become infectious. [16]
EA glycoprotein that forms the viral envelope, binds to receptors on the host cell surface in order to enter the cell. [17]

Nonstructural proteins

Nonstructural proteins consist of NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5. These proteins mainly assist with viral replication or act as proteases. [15] The nonstructural proteins are located near the 3′ end of the genome.

Nonstructural ProteinFunction
NS1NS1 is a cofactor for viral replication, specifically for regulation of the replication complex. [18]
NS2ANS2A has a variety of functions: it is involved in viral replication, virion assembly, and inducing host cell death. [19]
NS2BA cofactor for NS3 and together forms the NS2B-NS3 protease complex. [15] Contains transmembrane domains which bind the protease to intracellular membranes.
NS3A serine protease that is responsible for cleaving the polyprotein to produce mature proteins; it also acts as a helicase. [13]
NS4ANS4A is a cofactor for viral replication, specifically regulates the activity of the NS3 helicase. [20]
NS4BInhibits interferon signaling. [21]
NS5The largest and most conserved protein of WNV, NS5 acts as a methyltransferase and a RNA polymerase, though it lacks proofreading properties. [15] [22]

Life cycle

Once WNV has successfully entered the bloodstream of a host animal, the envelope protein, E, binds to attachment factors called glycosaminoglycans on the host cell. [17] These attachment factors aid entry into the cell, however, binding to primary receptors is also necessary. [23] Primary receptors include DC-SIGN, DC-SIGN-R, and the integrin αvβ3. [24] By binding to these primary receptors, WNV enters the cell through clathrin-mediated endocytosis. [25] As a result of endocytosis, WNV enters the cell within an endosome.[ citation needed ]

The acidity of the endosome catalyzes the fusion of the endosomal and viral membranes, allowing the genome to be released into the cytoplasm. [26] Translation of the positive-sense single-stranded RNA occurs at the endoplasmic reticulum; the RNA is translated into a polyprotein which is then cleaved by both host and viral proteases NS2B-NS3 to produce mature proteins. [27]

In order to replicate its genome, NS5, a RNA polymerase, forms a replication complex with other nonstructural proteins to produce an intermediary negative-sense single-stranded RNA; the negative-sense strand serves as a template for synthesis of the final positive-sense RNA. [23] Once the positive-sense RNA has been synthesized, the capsid protein, C, encloses the RNA strands into immature virions. [24] The rest of the virus is assembled along the endoplasmic reticulum and through the Golgi apparatus, and results in non-infectious immature virions. [27] The E protein is then glycosylated and prM is cleaved by furin, a host cell protease, into the M protein, thereby producing an infectious mature virion. [13] [27] The mature viruses are then secreted out of the cell.[ citation needed ]

Phylogeny

Phylogenetic tree of West Nile viruses based on sequencing of the envelope gene during complete genome sequencing of the virus Phylogenetic tree of West Nile viruses.gif
Phylogenetic tree of West Nile viruses based on sequencing of the envelope gene during complete genome sequencing of the virus

WNV is one of the Japanese encephalitis antigenic serocomplex of viruses, together with Japanese encephalitis virus, Murray Valley encephalitis virus, Saint Louis encephalitis virus and some other flaviviruses. [29] Studies of phylogenetic lineages have determined that WNV emerged as a distinct virus around 1000 years ago. [30] This initial virus developed into two distinct lineages. Lineage 1 and its multiple profiles is the source of the epidemic transmission in Africa and throughout the world. Lineage 2 was considered an African zoonosis. However, in 2008, lineage 2, previously only seen in horses in sub-Saharan Africa and Madagascar, began to appear in horses in Europe, where the first known outbreak affected 18 animals in Hungary. [31] Lineage 1 West Nile virus was detected in South Africa in 2010 in a mare and her aborted fetus; previously, only lineage 2 West Nile virus had been detected in horses and humans in South Africa. [32] Kunjin virus is a subtype of West Nile virus endemic to Oceania. A 2007 fatal case in a killer whale in Texas broadened the known host range of West Nile virus to include cetaceans. [33]

Since the first North American cases in 1999, the virus has been reported throughout the United States, Canada, Mexico, the Caribbean, and Central America. There have been human cases and equine cases, and many birds are infected. The Barbary macaque, Macaca sylvanus , was the first nonhuman primate to contract WNV. [34] Both the American and Israeli strains are marked by high mortality rates in infected avian populations; the presence of dead birds—especially Corvidae—can be an early indicator of the arrival of the virus.[ citation needed ]

Host range and transmission

Culex pipiens mosquitoes are a vector for WNV. Pipiens feeding.jpg
Culex pipiens mosquitoes are a vector for WNV.

The natural hosts for WNV are birds and mosquitoes. [35] Over 300 different species of bird have been shown to be infected with the virus. [36] [37] Some birds, including the American crow (Corvus brachyrhynchos), blue jay (Cyanocitta cristata) and greater sage-grouse (Centrocercus urophasianus), are killed by the infection, but others survive. [38] [39] The American robin (Turdus migratorius) and house sparrow (Passer domesticus) are thought to be among the most important reservoir species in N. American and European cities. [40] [41] Brown thrashers (Toxostoma rufum), gray catbirds (Dumetella carolinensis), northern cardinals (Cardinalis cardinalis), northern mockingbirds (Mimus polyglottos), wood thrushes (Hylocichla mustelina) and the dove family are among the other common N. American birds in which high levels of antibodies against WNV have been found. [38]

WNV has been demonstrated in a large number of mosquito species, but the most significant for viral transmission are Culex species that feed on birds, including Culex pipiens , C. restuans , C. salinarius , C. quinquefasciatus , C. nigripalpus , C. erraticus and C. tarsalis . [38] Experimental infection has also been demonstrated with soft tick vectors, but is unlikely to be important in natural transmission. [38] [42]

WNV has a broad host range, and is also known to be able to infect at least 30 mammalian species, including humans, some non-human primates, [43] horses, dogs and cats. [35] [36] [40] [44] Some infected humans and horses experience disease but dogs and cats rarely show symptoms. [36] Reptiles and amphibians can also be infected, including some species of crocodiles, alligators, snakes, lizards and frogs. [44] [45] [46] [47] Mammals are considered incidental or dead-end hosts for the virus: they do not usually develop a high enough level of virus in the blood (viremia) to infect another mosquito feeding on them and carry on the transmission cycle; some birds are also dead-end hosts. [38]

In the normal rural or enzootic transmission cycle, the virus alternates between the bird reservoir and the mosquito vector. It can also be transmitted between birds via direct contact, by eating an infected bird carcass or by drinking infected water. [41] Vertical transmission between female and offspring is possible in mosquitoes, and might potentially be important in overwintering. [48] [49] In the urban or spillover cycle, infected mosquitoes that have fed on infected birds transmit the virus to humans. This requires mosquito species that bite both birds and humans, which are termed bridge vectors. [41] [50] [51] The virus can also rarely be spread through blood transfusions, organ transplants, or from mother to baby during pregnancy, delivery, or breastfeeding. [50] Unlike in birds, it does not otherwise spread directly between people. [52]

Disease

Humans

This section is an excerpt from West Nile fever.[ edit ]
West Nile virus Em wnvirus j7908i.jpg
West Nile virus

West Nile fever is an infection by the West Nile virus, which is typically spread by mosquitoes. [53] In about 80% of infections people have few or no symptoms. [54] About 20% of people develop a fever, headache, vomiting, or a rash. [53] In less than 1% of people, encephalitis or meningitis occurs, with associated neck stiffness, confusion, or seizures. [53] Recovery may take weeks to months. [53] The risk of death among those in whom the nervous system is affected is about 10 percent. [53]

West Nile virus (WNV) is usually spread by mosquitoes that become infected when they feed on infected birds, which often carry the disease. [53] Rarely the virus is spread through blood transfusions, organ transplants, or from mother to baby during pregnancy, delivery, or breastfeeding, [53] but it otherwise does not spread directly between people. [55] Risks for severe disease include being over 60 years old and having other health problems. [53] Diagnosis is typically based on symptoms and blood tests. [53]

There is no human vaccine. [53] The best way to reduce the risk of infection is to avoid mosquito bites. [53] Mosquito populations may be reduced by eliminating standing pools of water, such as in old tires, buckets, gutters, and swimming pools. [53] When mosquitoes cannot be avoided, mosquito repellent, window screens, and mosquito nets reduce the likelihood of being bitten. [53] [55] There is no specific treatment for the disease; pain medications may reduce symptoms. [53]

The virus was discovered in Uganda in 1937, and was first detected in North America in 1999. [53] [55] WNV has occurred in Europe, Africa, Asia, Australia, and North America. [53] In the United States thousands of cases are reported a year, with most occurring in August and September. [56] It can occur in outbreaks of disease. [55] Severe disease may also occur in horses, for which a vaccine is available. [55] A surveillance system in birds is useful for early detection of a potential human outbreak. [55]

Horses

Severe disease may also occur in horses. [52] Several vaccines for these animals are now available. [57] [52] Before the availability of veterinary vaccines, around 40% of horses infected in North America died. [38]

Epidemiology

According to the Center for Disease Control, infection with West Nile Virus is seasonal in temperate zones. Climates that are temperate, such as those in the United States and Europe, see peak season from July to October. Peak season changes depending on geographic region and warmer and humid climates can see longer peak seasons. [58] All ages are equally likely to be infected but there is a higher amount of death and neuroinvasive West Nile Virus in people 60–89 years old. [58] People of older age are more likely to have adverse effects.[ citation needed ]

There are several modes of transmission, but the most common cause of infection in humans is by being bitten by an infected mosquito. Other modes of transmission include blood transfusion, organ transplantation, breast-feeding, transplacental transmission, and laboratory acquisition. These alternative modes of transmission are extremely rare. [59]

Prevention

Prevention efforts against WNV mainly focus on preventing human contact with and being bitten by infected mosquitoes. This is twofold, first by personal protective actions and second by mosquito-control actions. When a person is in an area that has WNV, it is important to avoid outdoor activity, and if they go outside they should use a mosquito repellent with DEET. [59] A person can also wear clothing that covers more skin, such as long sleeves and pants. Mosquito control can be done at the community level and include surveillance programs and control programs including pesticides and reducing mosquito habitats. This includes draining standing water. Surveillance systems in birds is particularly useful. [60] If dead birds are found in a neighborhood, the event should be reported to local authorities. This may help health departments do surveillance and determine if the birds are infected with West Nile Virus. [61]

Despite the commercial availability of four veterinary vaccines for horses, no human vaccine has progressed beyond phase II clinical trials. [57] [50] [62] Efforts have been made to produce a vaccine for human use and several candidates have been produced but none are licensed to use. [59] [62] The best method to reduce the risk of infections is avoiding mosquito bites. [50] This may be done by eliminating standing pools of water, such as in old tires, buckets, gutters, and swimming pools. [50] Mosquito repellent, window screens, mosquito nets, and avoiding areas where mosquitoes occur may also be useful. [50] [52]

Climate change

Global distribution of West Nile Virus from the CDC Global distribution of West Nile virus-CDC.gif
Global distribution of West Nile Virus from the CDC

Like other tropical diseases which are expected to have increased spread due to climate change, there is concern that changing weather conditions will increase West Nile Virus spread. Climate change will affect disease rates, ranges, and seasonality and affects the distribution of West Nile Virus. [63]

Projected changes in flood frequency and severity can bring new challenges in flood risk management, allowing for increased mosquito populations in urban areas. [64] Weather conditions affected by climate change including temperature, precipitation and wind may affect the survival and reproduction rates of mosquitoes, suitable habitats, distribution, and abundance. Ambient temperatures drive mosquito replication rates and transmission of WNV by affecting the peak season of mosquitoes and geographic variations. For example, increased temperatures can affect the rate of virus replication, speed up the virus evolution rate, and viral transmission efficiency. Furthermore, higher winter temperatures and warmer spring may lead to larger summer mosquito populations, increasing the risk for WNV. Similarly, rainfall may also drive mosquito replication rates and affect the seasonality and geographic variations of the virus. Studies show an association between heavy precipitation and higher incidence of reported WNV. Likewise, wind is another environmental factor that serves as a dispersal mechanism for mosquitoes. [63]

Mosquitoes have extremely wide environmental tolerances and a nearly ubiquitous geographical distribution, being present on all major land masses except Antarctica and Iceland. Nevertheless, changes in climate and land use on ecological timescales can variously expand or fragment their distribution patterns, raising consequent concerns for human health. [65]

See also

Related Research Articles

<span class="mw-page-title-main">West Nile fever</span> Human disease caused by West Nile virus infection

West Nile fever is an infection by the West Nile virus, which is typically spread by mosquitoes. In about 80% of infections people have few or no symptoms. About 20% of people develop a fever, headache, vomiting, or a rash. In less than 1% of people, encephalitis or meningitis occurs, with associated neck stiffness, confusion, or seizures. Recovery may take weeks to months. The risk of death among those in whom the nervous system is affected is about 10 percent.

<i>Hepadnaviridae</i> Family of viruses

Hepadnaviridae is a family of viruses. Humans, apes, and birds serve as natural hosts. There are currently 18 species in this family, divided among 5 genera. Its best-known member is hepatitis B virus. Diseases associated with this family include: liver infections, such as hepatitis, hepatocellular carcinomas, and cirrhosis. It is the sole accepted family in the order Blubervirales.

<i>Flavivirus</i> Genus of viruses

Flavivirus, renamed Orthoflavivirus in 2023, is a genus of positive-strand RNA viruses in the family Flaviviridae. The genus includes the West Nile virus, dengue virus, tick-borne encephalitis virus, yellow fever virus, Zika virus and several other viruses which may cause encephalitis, as well as insect-specific flaviviruses (ISFs) such as cell fusing agent virus (CFAV), Palm Creek virus (PCV), and Parramatta River virus (PaRV). While dual-host flaviviruses can infect vertebrates as well as arthropods, insect-specific flaviviruses are restricted to their competent arthropods. The means by which flaviviruses establish persistent infection in their competent vectors and cause disease in humans depends upon several virus-host interactions, including the intricate interplay between flavivirus-encoded immune antagonists and the host antiviral innate immune effector molecules.

<span class="mw-page-title-main">Arbovirus</span> Class of viruses which are transmitted by arthropods

Arbovirus is an informal name for any virus that is transmitted by arthropod vectors. The term arbovirus is a portmanteau word. Tibovirus is sometimes used to more specifically describe viruses transmitted by ticks, a superorder within the arthropods. Arboviruses can affect both animals and plants. In humans, symptoms of arbovirus infection generally occur 3–15 days after exposure to the virus and last three or four days. The most common clinical features of infection are fever, headache, and malaise, but encephalitis and viral hemorrhagic fever may also occur.

<i>Dengue virus</i> Species of virus

Dengue virus (DENV) is the cause of dengue fever. It is a mosquito-borne, single positive-stranded RNA virus of the family Flaviviridae; genus Flavivirus. Four serotypes of the virus have been found, and a reported fifth has yet to be confirmed, all of which can cause the full spectrum of disease. Nevertheless, scientists' understanding of dengue virus may be simplistic as, rather than distinct antigenic groups, a continuum appears to exist. This same study identified 47 strains of dengue virus. Additionally, coinfection with and lack of rapid tests for Zika virus and chikungunya complicate matters in real-world infections.

<span class="mw-page-title-main">Japanese encephalitis</span> Infection of the brain caused by the Japanese encephalitis virus

Japanese encephalitis (JE) is an infection of the brain caused by the Japanese encephalitis virus (JEV). While most infections result in little or no symptoms, occasional inflammation of the brain occurs. In these cases, symptoms may include headache, vomiting, fever, confusion and seizures. This occurs about 5 to 15 days after infection.

<i>Tick-borne encephalitis virus</i> Species of virus

Tick-borne encephalitis virus (TBEV) is a positive-strand RNA virus associated with tick-borne encephalitis in the genus Flavivirus.

<i>Alphavirus</i> Genus of viruses

Alphavirus is a genus of RNA viruses, the sole genus in the Togaviridae family. Alphaviruses belong to group IV of the Baltimore classification of viruses, with a positive-sense, single-stranded RNA genome. There are 32 alphaviruses, which infect various vertebrates such as humans, rodents, fish, birds, and larger mammals such as horses, as well as invertebrates. Alphaviruses that could infect both vertebrates and arthropods are referred dual-host alphaviruses, while insect-specific alphaviruses such as Eilat virus and Yada yada virus are restricted to their competent arthropod vector. Transmission between species and individuals occurs mainly via mosquitoes, making the alphaviruses a member of the collection of arboviruses – or arthropod-borne viruses. Alphavirus particles are enveloped, have a 70 nm diameter, tend to be spherical, and have a 40 nm isometric nucleocapsid.

<i>Pestivirus</i> Genus of viruses

Pestivirus is a genus of viruses, in the family Flaviviridae. Viruses in the genus Pestivirus infect mammals, including members of the family Bovidae and the family Suidae. There are 11 species in this genus. Diseases associated with this genus include: hemorrhagic syndromes, abortion, and fatal mucosal disease.

<span class="mw-page-title-main">Astrovirus</span> Family of viruses

Astroviruses (Astroviridae) are a type of virus that was first discovered in 1975 using electron microscopes following an outbreak of diarrhea in humans. In addition to humans, astroviruses have now been isolated from numerous mammalian animal species and from avian species such as ducks, chickens, and turkey poults. Astroviruses are 28–35 nm diameter, icosahedral viruses that have a characteristic five- or six-pointed star-like surface structure when viewed by electron microscopy. Along with the Picornaviridae and the Caliciviridae, the Astroviridae comprise a third family of nonenveloped viruses whose genome is composed of plus-sense, single-stranded RNA. Astrovirus has a non-segmented, single stranded, positive sense RNA genome within a non-enveloped icosahedral capsid. Human astroviruses have been shown in numerous studies to be an important cause of gastroenteritis in young children worldwide. In animals, Astroviruses also cause infection of the gastrointestinal tract but may also result in encephalitis, hepatitis (avian) and nephritis (avian).

<span class="mw-page-title-main">Viral envelope</span> Outermost layer of many types of the infectious agent

A viral envelope is the outermost layer of many types of viruses. It protects the genetic material in their life cycle when traveling between host cells. Not all viruses have envelopes. A viral envelope protein or E protein is a protein in the envelope, which may be acquired by the capsid from an infected host cell.

<span class="mw-page-title-main">Mosquito-borne disease</span> Diseases caused by bacteria, viruses or parasites transmitted by mosquitoes

Mosquito-borne diseases or mosquito-borne illnesses are diseases caused by bacteria, viruses or parasites transmitted by mosquitoes. Nearly 700 million people get a mosquito-borne illness each year, resulting in over 725,000 deaths.

<i>Zika virus</i> Species of flavivirus

Zika virus is a member of the virus family Flaviviridae. It is spread by daytime-active Aedes mosquitoes, such as A. aegypti and A. albopictus. Its name comes from the Ziika Forest of Uganda, where the virus was first isolated in 1947. Zika virus shares a genus with the dengue, yellow fever, Japanese encephalitis, and West Nile viruses. Since the 1950s, it has been known to occur within a narrow equatorial belt from Africa to Asia. From 2007 to 2016, the virus spread eastward, across the Pacific Ocean to the Americas, leading to the 2015–2016 Zika virus epidemic.

Spondweni virus is an arbovirus, or arthropod-borne virus, which is a member of the family Flaviviridae and the genus Flavivirus. It is part of the Spondweni serogroup which consists of the Sponweni virus and the Zika virus (ZIKV). The Spondweni virus was first isolated in Nigeria in 1952, and ever since, SPONV transmission and activity have been reported throughout Africa. Its primary vector of transmission is the sylvatic mosquito Aedes circumluteolus, though it has been isolated from several different types of mosquito. Transmission of the virus into humans can lead to a viral infection known as Spondweni fever, with symptoms ranging from headache and nausea to myalgia and arthralgia. However, as SPONV is phylogenetically close to the ZIKV, it is commonly misdiagnosed as ZIKV along with other viral illnesses.

<span class="mw-page-title-main">Palm Creek virus</span> Species of virus

Palm Creek virus (PCV) is an insect virus belonging to the genus Flavivirus, of the family Flaviviridae. It was discovered in 2013 from the mosquito Coquillettidia xanthogaster. The female mosquitoes were originally collected in 2010 from Darwin, Katherine, Alice Springs, Alyangula, Groote Eylandt, Jabiru and the McArthur River Mine, and had since been preserved. The discovery was made by biologists at the University of Queensland. The virus is named after Palm Creek, near Darwin, from where it was originally isolated.

<i>Middelburg virus</i> Species of virus

Middelburg virus (MIDV) is an alphavirus of the Old World Group that has likely endemic and zoonotic potential. It is of the viral family Togaviridae. It was isolated from mosquitos in 1957 in South Africa, MDIV antigens have now been found in livestock, horses, and humans.

Yokose virus (YOKV) is in the genus Flavivirus of the family Flaviviridae. Flaviviridae are often found in arthropods, such as mosquitoes and ticks, and may also infect humans. The genus Flavivirus includes over 50 known viruses, including Yellow Fever, West Nile Virus, Zika Virus, and Japanese Encephalitis. Yokose virus is a new member of the Flavivirus family that has only been identified in a few bat species. Bats have been associated with several emerging zoonotic diseases such as Ebola and SARS.

<i>Sepik virus</i> Mosquito transmitted virus endemic to Papua New Guinea

Sepik virus (SEPV) is an arthropod-borne virus (arbovirus) of the genus Flavivirus and family Flaviviridae. Flaviviridae is one of the most well characterized viral families, as it contains many well-known viruses that cause diseases that have become very prevalent in the world, like Dengue virus. The genus Flavivirus is one of the largest viral genera and encompasses over 50 viral species, including tick and mosquito borne viruses like Yellow fever virus and West Nile virus. Sepik virus is much less well known and has not been as well-classified as other viruses because it has not been known of for very long. Sepik virus was first isolated in 1966 from the mosquito Mansoniaseptempunctata, and it derives its name from the Sepik River area in Papua New Guinea, where it was first found. The geographic range of Sepik virus is limited to Papua New Guinea, due to its isolation.

<i>Modoc virus</i> Species of virus

Modoc virus (MODV) is a rodent-associated flavivirus. Small and enveloped, MODV contains positive single-stranded RNA. Taxonomically, MODV is part of the Flavivirus genus and Flaviviridae family. The Flavivirus genus includes nearly 80 viruses, both vector-borne and no known vector (NKV) species. Known flavivirus vector-borne viruses include Dengue virus, Yellow Fever virus, tick-borne encephalitis virus, and West Nile virus.

Rio Negro virus is an alphavirus that was first isolated in Argentina in 1980. The virus was first called Ag80-663 but was renamed to Rio Negro virus in 2005. It is a former member of the Venezuelan equine encephalitis complex (VEEC), which are a group of alphaviruses in the Americas that have the potential to emerge and cause disease. Río Negro virus was recently reclassified as a distinct species. Closely related viruses include Mucambo virus and Everglades virus.

References

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