Flavivirus

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Flavivirus
YellowFeverVirus.jpg
A TEM micrograph of Yellow fever virus
Zika-chain-colored.png
Zika virus viral envelope model, colored by chains, PDB entry 5ire [1]
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 [2]

See text

Flavivirus, renamed Orthoflavivirus in 2023, [3] 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, [4] as well as insect-specific flaviviruses (ISFs) such as cell fusing agent virus (CFAV), Palm Creek virus (PCV), and Parramatta River virus (PaRV). [5] While dual-host flaviviruses can infect vertebrates as well as arthropods, insect-specific flaviviruses are restricted to their competent arthropods. [6] 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. [7]

Contents

Flaviviruses are named for the yellow fever virus; the word flavus means 'yellow' in Latin, and yellow fever in turn is named from its propensity to cause yellow jaundice in victims. [8]

Flaviviruses share several common aspects: common size (40–65 nm), symmetry (enveloped, icosahedral nucleocapsid), nucleic acid (positive-sense, single-stranded RNA around 10,000–11,000 bases), and appearance under the electron microscope.[ citation needed ]

Most of these viruses are primarily transmitted by the bite from an infected arthropod (mosquito or tick), and hence are classified as arboviruses. Human infections with most of these arboviruses are incidental, as humans are unable to replicate the virus to high enough titers to reinfect the arthropods needed to continue the virus life-cycle – humans are then a dead end host. The exceptions to this are the yellow fever virus, dengue virus and zika virus . These three viruses still require mosquito vectors but are well-enough adapted to humans as to not necessarily depend upon animal hosts (although they continue to have important animal transmission routes, as well).

Other virus transmission routes for arboviruses include handling infected animal carcasses, blood transfusion, sex, childbirth and consumption of unpasteurised milk products. Transmission from nonhuman vertebrates to humans without an intermediate vector arthropod however mostly occurs with low probability. For example, early tests with yellow fever showed that the disease is not contagious.

The known non-arboviruses of the flavivirus family reproduce in either arthropods or vertebrates, but not both, with one odd member of the genus affecting a nematode. [9]

Structure

Zika virus structure and genome Viruses-10-00597-g001.png
Zika virus structure and genome

Flaviviruses are enveloped and spherical and have icosahedral geometries with a pseudo T=3 symmetry. The virus particle diameter is around 50 nm. [10]

Genome

Flaviviruses have positive-sense, single-stranded RNA genomes which are non-segmented and around 10–11 kbp in length. [10] In general, the genome encodes three structural proteins (Capsid, prM, and Envelope) and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5). [11] The genomic RNA is modified at the 5′ end of positive-strand genomic RNA with a cap-1 structure (me7-GpppA-me2). [12]

Life cycle

Replication of Japanese encephalitis virus (JEV) Pathogens-07-00068-g002.webp
Replication of Japanese encephalitis virus (JEV)

Flaviviruses replicate in the cytoplasm of the host cells. The genome mimics the cellular mRNA molecule in all aspects except for the absence of the poly-adenylated (poly-A) tail. This feature allows the virus to exploit cellular apparatuses to synthesize both structural and non-structural proteins, during replication. The cellular ribosome is crucial to the replication of the flavivirus, as it translates the RNA, in a similar fashion to cellular mRNA, resulting in the synthesis of a single polyprotein. [11]

Cellular RNA cap structures are formed via the action of an RNA triphosphatase, with guanylyltransferase, N7-methyltransferase and 2′-O methyltransferase. The virus encodes these activities in its non-structural proteins. The NS3 protein encodes a RNA triphosphatase within its helicase domain. It uses the helicase ATP hydrolysis site to remove the γ-phosphate from the 5′ end of the RNA. The N-terminal domain of the non-structural protein 5 (NS5) has both the N7-methyltransferase and guanylyltransferase activities necessary for forming mature RNA cap structures. RNA binding affinity is reduced by the presence of ATP or GTP and enhanced by S-adenosyl methionine. [12] This protein also encodes a 2′-O methyltransferase.

Replication complex formed on the cytoplasmic side of the ER membrane Viruses-07-02837-g002.png
Replication complex formed on the cytoplasmic side of the ER membrane

Once translated, the polyprotein is cleaved by a combination of viral and host proteases to release mature polypeptide products. [13] Nevertheless, cellular post-translational modification is dependent on the presence of a poly-A tail; therefore this process is not host-dependent. Instead, the poly-protein contains an autocatalytic feature which automatically releases the first peptide, a virus specific enzyme. This enzyme is then able to cleave the remaining poly-protein into the individual products. One of the products cleaved is a RNA-dependent RNA polymerase, responsible for the synthesis of a negative-sense RNA molecule. Consequently, this molecule acts as the template for the synthesis of the genomic progeny RNA.[ citation needed ]

Flavivirus genomic RNA replication occurs on rough endoplasmic reticulum membranes in membranous compartments. New viral particles are subsequently assembled. This occurs during the budding process which is also responsible for the accumulation of the envelope and cell lysis.[ citation needed ]

A G protein-coupled receptor kinase 2 (also known as ADRBK1) appears to be important in entry and replication for several viruses in Flaviviridae. [14]

Humans, mammals, mosquitoes, and ticks serve as the natural host. Transmission routes are zoonosis and bite. [10]

RNA secondary structure elements

Flavivirus RNA genome showing the 3' and 5' UTRs and cyclisation Fgene-09-00595-g001.jpg
Flavivirus RNA genome showing the 3' and 5' UTRs and cyclisation

The positive sense RNA genome of Flavivirus contains 5' and 3' untranslated regions (UTRs).

5'UTR

The 5'UTRs are 95–101 nucleotides long in Dengue virus . [15] There are two conserved structural elements in the Flavivirus 5'UTR, a large stem loop (SLA) and a short stem loop (SLB). SLA folds into a Y-shaped structure with a side stem loop and a small top loop. [15] [16] SLA is likely to act as a promoter, and is essential for viral RNA synthesis. [17] [18] SLB is involved in interactions between the 5'UTR and 3'UTR which result in the cyclisation of the viral RNA, which is essential for viral replication. [19]

3'UTR

RNA secondary structure elements of different flavivirus 3'UTRs Viruses-11-00298-g002.webp
RNA secondary structure elements of different flavivirus 3′UTRs

The 3'UTRs are typically 0.3–0.5 kb in length and contain a number of highly conserved secondary structures which are conserved and restricted to the flavivirus family. The majority of analysis has been carried out using West Nile virus (WNV) to study the function the 3'UTR.[ citation needed ]

Currently 8 secondary structures have been identified within the 3'UTR of WNV and are (in the order in which they are found with the 3'UTR) SL-I, SL-II, SL-III, SL-IV, DB1, DB2 and CRE. [20] [21] Some of these secondary structures have been characterised and are important in facilitating viral replication and protecting the 3'UTR from 5' endonuclease digestion. Nuclease resistance protects the downstream 3' UTR RNA fragment from degradation and is essential for virus-induced cytopathicity and pathogenicity.[ citation needed ]

SL-II has been suggested to contribute to nuclease resistance. [21] It may be related to another hairpin loop identified in the 5'UTR of the Japanese encephalitis virus (JEV) genome. [22] The JEV hairpin is significantly over-represented upon host cell infection and it has been suggested that the hairpin structure may play a role in regulating RNA synthesis.[ citation needed ]

This secondary structure is located within the 3'UTR of the genome of Flavivirus upstream of the DB elements. The function of this conserved structure is unknown but is thought to contribute to ribonuclease resistance.[ citation needed ]

Secondary structure of the Flavivirus DB element RF00525.png
Secondary structure of the Flavivirus DB element

These two conserved secondary structures are also known as pseudo-repeat elements. They were originally identified within the genome of Dengue virus and are found adjacent to each other within the 3'UTR. They appear to be widely conserved across the Flaviviradae. These DB elements have a secondary structure consisting of three helices and they play a role in ensuring efficient translation. Deletion of DB1 has a small but significant reduction in translation but deletion of DB2 has little effect. Deleting both DB1 and DB2 reduced translation efficiency of the viral genome to 25%. [20]

CRE is the Cis-acting replication element, also known as the 3'SL RNA elements, and is thought to be essential in viral replication by facilitating the formation of a "replication complex". [23] Although evidence has been presented for an existence of a pseudoknot structure in this RNA, it does not appear to be well conserved across flaviviruses. [24] Deletions of the 3' UTR of flaviviruses have been shown to be lethal for infectious clones.

Conserved hairpin cHP

A conserved hairpin (cHP) structure was later found in several Flavivirus genomes and is thought to direct translation of capsid proteins. It is located just downstream of the AUG start codon. [25]

The role of RNA secondary structures in sfRNA production

Different fates of viral RNA of flaviviruses and formation of sfRNA Fgene-09-00595-g002.jpg
Different fates of viral RNA of flaviviruses and formation of sfRNA

Subgenomic flavivirus RNA (sfRNA) is an extension of the 3' UTR and has been demonstrated to play a role in flavivirus replication and pathogenesis. [26] sfRNA is produced by incomplete degradation of genomic viral RNA by the host cells 5'-3' exoribonuclease 1 (XRN1). [27] As the XRN1 degrades viral RNA, it stalls at stemloops formed by the secondary structure of the 5' and 3' UTR. [28] This pause results in an undigested fragment of genome RNA known as sfRNA. sfRNA influences the life cycle of the flavivirus in a concentration dependent manner. Accumulation of sfRNA causes (1) antagonization of the cell's innate immune response, thus decreasing host defense against the virus [29] (2) inhibition of XRN1 and Dicer activity to modify RNAi pathways that destroy viral RNA [30] (3) modification of the viral replication complex to increase viral reproduction. [31] Overall, sfRNA is implied in multiple pathways that compromise host defenses and promote infection by flaviviruses.[ citation needed ]

Evolution

Phylogenetic tree of Flavivirus with corresponding vectors and groups Fimmu-11-00334-g001.jpg
Phylogenetic tree of Flavivirus with corresponding vectors and groups

The flaviviruses can be divided into two clades: one with vector-borne viruses and the other with no known vector. [32] The vector clade, in turn, can be subdivided into a mosquito-borne clade and a tick-borne clade. These groups can be divided again. [33]

The mosquito group can be divided into two branches: one branch contains neurotropic viruses, often associated with encephalitic disease in humans or livestock. This branch tends to be spread by Culex species and to have bird reservoirs. The second branch is the non-neurotropic viruses associated with human haemorrhagic disease. These tend to have Aedes species as vectors and primate hosts.[ citation needed ]

The tick-borne viruses also form two distinct groups: one is associated with seabirds and the other – the tick-borne encephalitis complex viruses – is associated primarily with rodents.[ citation needed ]

The viruses that lack a known vector can be divided into three groups: one closely related to the mosquito-borne viruses, which is associated with bats; a second, genetically more distant, is also associated with bats; and a third group is associated with rodents.[ citation needed ]

Evolutionary relationships between endogenised viral elements of Flaviviruses and contemporary flaviviruses using maximum likelihood approaches have identified that arthropod-vectored flaviviruses likely emerged from an arachnid source. [34] This contradicts earlier work with a smaller number of extant viruses showing that the tick-borne viruses emerged from a mosquito-borne group. [35]

Several partial and complete genomes of flaviviruses have been found in aquatic invertebrates such as the sea spider Endeis spinosa [36] and several crustaceans and cephalopods. [37] These sequences appear to be related to those in the insect-specific flaviviruses and also the Tamana bat virus groupings. While it is not presently clear how aquatic flaviviruses fit into the evolution of this group of viruses, there is some evidence that one of these viruses, Wenzhou shark flavivirus, infects both a crustacean (Portunus trituberculatus) Pacific spadenose shark (Scoliodon macrorhynchos) shark host, [38] [37] indicating an aquatic arbovirus life cycle.

Distribution of major flaviviruses Viruses-09-00097-g001.png
Distribution of major flaviviruses

Estimates of divergence times have been made for several of these viruses. [39] The origin of these viruses appears to be at least 9400 to 14,000 years ago. The Old World and New World dengue strains diverged between 150 and 450 years ago. The European and Far Eastern tick-borne encephalitis strains diverged about 1087 (1610–649) years ago. European tick-borne encephalitis and louping ill viruses diverged about 572 (844–328) years ago. This latter estimate is consistent with historical records. Kunjin virus diverged from West Nile virus approximately 277 (475–137) years ago. This time corresponds to the settlement of Australia from Europe. The Japanese encephalitis group appears to have evolved in Africa 2000–3000 years ago and then spread initially to South East Asia before migrating to the rest of Asia.

Phylogenetic studies of the West Nile virus has shown that it emerged as a distinct virus around 1000 years ago. [40] 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 Africa 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 in 2008. [41] 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. [42] A 2007 fatal case in a killer whale in Texas broadened the known host range of West Nile virus to include cetaceans. [43]

Omsk haemorrhagic fever virus appears to have evolved within the last 1000 years. [44] The viral genomes can be divided into 2 clades — A and B. Clade A has five genotypes, and clade B has one. These clades separated about 700 years ago. This separation appears to have occurred in the Kurgan province. Clade A subsequently underwent division into clade C, D and E 230 years ago. Clade C and E appear to have originated in the Novosibirsk and Omsk Provinces, respectively. The muskrat Ondatra zibethicus , which is highly susceptible to this virus, was introduced into this area in the 1930s.

Taxonomy

Species

In the genus Flavivirus there are 53 defined species: [45]

Sorted by vector

List of species and strains of flavivirus by vector


Phylogenetic tree of Flavivirus with vectors; tick-borne (black), mosquito-borne (purple), with no known vector (red), invertebrate viruses (blue/green) Viruses-09-00154-g001.webp
Phylogenetic tree of Flavivirus with vectors; tick-borne (black), mosquito-borne (purple), with no known vector (red), invertebrate viruses (blue/green)

Species and strains sorted by vectors:

Tick-borne viruses

Distribution of tick-borne encephalitis virus (TBEV), Kyasanur forest disease virus (KFDV), Omsk hemorrhagic fever virus (OHFV), Powassan virus (POWV), and Louping-ill virus (LIV) Viruses-10-00340-g001.png
Distribution of tick-borne encephalitis virus (TBEV), Kyasanur forest disease virus (KFDV), Omsk hemorrhagic fever virus (OHFV), Powassan virus (POWV), and Louping-ill virus (LIV)

Mammalian tick-borne virus group

Seabird tick-borne virus group

Mosquito-borne viruses

Viruses with no known arthropod vector

Non vertebrate viruses

Viruses known only from sequencing

Vaccines

Time-line of historical highlights of flavivirus research Viruses-09-00097-g002.png
Time-line of historical highlights of flavivirus research

The very successful yellow fever 17D vaccine, introduced in 1937, produced dramatic reductions in epidemic activity.[ citation needed ]

Effective inactivated Japanese encephalitis and Tick-borne encephalitis vaccines were introduced in the middle of the 20th century. Unacceptable adverse events have prompted change from a mouse-brain inactivated Japanese encephalitis vaccine to safer and more effective second generation Japanese encephalitis vaccines. These may come into wide use to effectively prevent this severe disease in the huge populations of Asia—North, South and Southeast.[ citation needed ]

The dengue viruses produce many millions of infections annually due to transmission by a successful global mosquito vector. As mosquito control has failed, several dengue vaccines are in varying stages of development. CYD-TDV, sold under the trade name Dengvaxia, is a tetravalent chimeric vaccine that splices structural genes of the four dengue viruses onto a 17D yellow fever backbone. [50] [51] Dengvaxia is approved in five countries. [52]

An alternate approach to the development of flavivirus vaccine vectors is based on the use of viruses that infect insects. Insect-specific flaviviruses, such as Binjari virus, are unable to replicate in vertebrate cells. Nevertheless, recombinant viruses in which structural protein genes (prME) of Binjari virus are exchanged with those of dengue virus, Zika virus, West Nile virus, yellow fever virus, or Japanese encephalitis virus replicate efficiently in insect cells where high titers of infectious virus particles are produced. Immunization of mice with a Binjari vaccine bearing the Zika virus structural proteins protected mice from disease after challenge. A similar approach employs the insect-specific alphavirus Eilat virus as a vaccine platform. ... These new vaccine platforms generated from insect-specific flaviviruses and alphaviruses represent affordable, efficient, and safe approaches to rapid development of infectious, attenuated vaccines against pathogens from these two virus families. [53]

Related Research Articles

<i>Flaviviridae</i> Family of viruses

Flaviviridae is a family of enveloped positive-strand RNA viruses which mainly infect mammals and birds. They are primarily spread through arthropod vectors. The family gets its name from the yellow fever virus; flavus is Latin for "yellow", and yellow fever in turn was named because of its propensity to cause jaundice in victims. There are 89 species in the family divided among four genera. Diseases associated with the group include: hepatitis (hepaciviruses), hemorrhagic syndromes, fatal mucosal disease (pestiviruses), hemorrhagic fever, encephalitis, and the birth defect microcephaly (flaviviruses).

<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.

<i>Bunyavirales</i> Order of RNA viruses

Bunyavirales is an order of segmented negative-strand RNA viruses with mainly tripartite genomes. Member viruses infect arthropods, plants, protozoans, and vertebrates. It is the only order in the class Ellioviricetes. The name Bunyavirales derives from Bunyamwera, where the original type species Bunyamwera orthobunyavirus was first discovered. Ellioviricetes is named in honor of late virologist Richard M. Elliott for his early work on bunyaviruses.

<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.

Powassan virus (POWV) is a Flavivirus transmitted by ticks, found in North America and in the Russian Far East. It is named after the town of Powassan, Ontario, where it was identified in a young boy who eventually died from it. It can cause encephalitis, inflammation of the brain. No approved vaccine or antiviral drug exists. Prevention of tick bites is the best precaution.

<span class="mw-page-title-main">Veterinary virology</span> Study of viruses affecting animals

Veterinary virology is the study of viruses in non-human animals. It is an important branch of veterinary medicine.

<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.

Royal Farm virus, previously known as Karshi virus, was not viewed as pathogenic or harmful to humans. Although infected people suffer with fever-like symptoms, some people in Uzbekistan have reported with severe disease such as encephalitis and other large outbreaks of fever illness connected infection with the virus.

<i>West Nile virus</i> Species of flavivirus causing West Nile fever

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. 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.

Parramatta River virus (PaRV) is an insect virus belonging to Flaviviridae and endemic to Australia. It was discovered in 2015. The virus was identified from the mosquito Aedes vigilax collected from Sydney under the joint research project by scientists at the University of Queensland and the University of Sydney. In experimental infections, the virus is unable to grow in vertebrate cells, but only in Aedes-derived mosquito cell lines. This suggests that the virus does not infect vertebrates. The name is given because it was discovered from Silverwater, a suburb of Sydney on the southern bank of the Parramatta River. The mosquitoes from which the virus was isolated were actually collected in 2007, and had been preserved since then. The study commenced only after the development of the technique of viral detection in mosquitoes in the University of Queensland.

<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.

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.

<span class="mw-page-title-main">Flavivirus 5' UTR</span> Untranslated regions in the genome of viruses in the genus Flavivirus

Flavivirus 5' UTR are untranslated regions in the genome of viruses in the genus Flavivirus.

Flavivirus 3' UTR are untranslated regions in the genome of viruses in the genus Flavivirus.

References

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