Wikipedia

Flavivirus

Flavivirus,renamedOrthoflavivirusin 2023,[3]is a genus ofpositive-strand RNA virusesin the familyFlaviviridae.The genus includes theWest Nile virus,dengue virus,tick-borne encephalitis virus,yellow fever virus,Zika virusand several otherviruseswhich may causeencephalitis,[4]as well as insect-specific flaviviruses (ISFs) such as cell fusing agent virus (CFAV),Palm Creek virus(PCV), andParramatta River virus(PaRV).[5]While dual-host flaviviruses can infectvertebratesas 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]

Flavivirus
A TEM micrograph of the "Yellow fever virus"
ATEMmicrographofYellow fever virus
"Zika virus" capsid model, colored by chains, PDB entry 5ire
Zika virusviral envelopemodel, colored by chains,PDBentry5ire[2]
Virus classificationEdit this classification
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Kitrinoviricota
Class: Flasuviricetes
Order: Amarillovirales
Family: Flaviviridae
Genus: Flavivirus
Species[1]

See text

Flaviviruses are named for the yellow fever virus; the wordflavusmeans 'yellow' inLatin,and yellow fever in turn is named from its propensity to cause yellowjaundicein victims.[8]

Flaviviruses share several common aspects: common size (40–65 nm), symmetry (enveloped,icosahedralnucleocapsid),nucleic acid(positive-sense,single-strandedRNAaround 10,000–11,000 bases), and appearance under theelectron microscope.[citation needed]

Most of these viruses are primarily transmitted by the bite from an infectedarthropod(mosquito or tick), and hence are classified asarboviruses.Human infections with most of these arboviruses are incidental, as humans are unable to replicate the virus to high enoughtitersto reinfect the arthropods needed to continue the virus life-cycle – humans are then adead end host.The exceptions to this are theyellow fever virus,dengue virusandzika 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 ofunpasteurisedmilk 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 notcontagious.

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

Structure

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Zika virusstructure and genome

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

Genome

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Flaviviruses havepositive-sense,single-stranded RNAgenomeswhich are non-segmented and around 10–11 kbp in length.[10]In general, the genome encodes three structural proteins (Capsid, prM, and Envelope) and sevennon-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

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Replication ofJapanese encephalitis virus(JEV)

Flaviviruses replicate in thecytoplasmof the host cells. The genome mimics the cellularmRNAmolecule 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, duringreplication.The cellularribosomeis 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 singlepolyprotein.[11]

Cellular RNA cap structures are formed via the action of anRNA triphosphatase,withguanylyltransferase,N7-methyltransferaseand 2′-O methyltransferase. The virus encodes these activities in its non-structural proteins. The NS3 protein encodes aRNA triphosphatasewithin itshelicasedomain. 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 ofATPorGTPand enhanced byS-adenosyl methionine.[12]This protein also encodes a 2′-O methyltransferase.

Replication complex formed on the cytoplasmic side of theER membrane

Oncetranslated,the polyprotein is cleaved by a combination of viral and hostproteasesto release maturepolypeptideproducts.[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 anautocatalyticfeature which automatically releases the first peptide, a virus specific enzyme. This enzyme is then able tocleavethe remaining poly-protein into the individual products. One of the products cleaved is aRNA-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 genomicprogenyRNA.[citation needed]

Flavivirusgenomic RNA replication occurs onrough endoplasmic reticulummembranes in membranous compartments. New viral particles are subsequently assembled. This occurs during thebuddingprocess which is also responsible for the accumulation of the envelope and celllysis.[citation needed]

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

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

RNA secondary structure elements

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FlavivirusRNA genome showing the 3' and 5' UTRs and cyclisation

The positive sense RNA genome ofFlaviviruscontains 5' and 3'untranslated regions(UTRs).

5'UTR

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Main article:Flavivirus 5' UTR

The 5'UTRs are 95–101 nucleotides long inDengue virus.[15]There are two conserved structural elements in theFlavivirus5'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

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Main article:Flavivirus 3' UTR
RNA secondary structure elements of differentflavivirus3′UTRs

The 3'UTRs are typically 0.3–0.5 kb in length and contain a number of highly conservedsecondary structureswhich are conserved and restricted to theflavivirusfamily. The majority of analysis has been carried out usingWest 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 facilitatingviral replicationand protecting the 3'UTR from 5'endonucleasedigestion. Nuclease resistance protects the downstream 3' UTR RNA fragment from degradation and is essential for virus-induced cytopathicity and pathogenicity.[citation needed]

  • SL-II

SL-II has been suggested to contribute to nuclease resistance.[21]It may be related to anotherhairpin loopidentified in the 5'UTR of theJapanese 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]

  • SL-IV

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

  • DB1/DB2
Secondary structure of theFlavivirusDB element

These two conserved secondary structures are also known as pseudo-repeat elements. They were originally identified within the genome ofDengue virusand 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 reducedtranslationefficiency of the viral genome to 25%.[20]

  • CRE

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 apseudoknotstructure 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

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Aconserved hairpin (cHP)structure was later found in severalFlavivirusgenomesand is thought to direct translation of capsid proteins. It is located just downstream of the AUGstart codon.[25]

The role of RNA secondary structures in sfRNA production

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Different fates of viral RNA of flaviviruses and formation of sfRNA

SubgenomicflavivirusRNA (sfRNA) is an extension of the 3' UTR and has been demonstrated to play a role inflavivirusreplication and pathogenesis.[26]sfRNA is produced by incomplete degradation of genomic viral RNA by the host cells5'-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 theflavivirusin 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

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Phylogenetic treeofFlaviviruswith 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 byCulexspecies and to have bird reservoirs. The second branch is the non-neurotropic viruses associated with human haemorrhagic disease. These tend to haveAedesspecies as vectors andprimatehosts.[citation needed]

The tick-borne viruses also form two distinct groups: one is associated withseabirdsand the other – the tick-borne encephalitis complex viruses – is associated primarily withrodents.[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 withbats;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 thesea spiderEndeis 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

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 virusdiverged fromWest Nile virusapproximately 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.

Phylogeneticstudies of theWest Nile virushas 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 Africazoonosis.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 1West Nile viruswas detected in South Africa in 2010 in amareand her abortedfetus;previously, only lineage 2West Nile virushad been detected in horses and humans in South Africa.[42]A 2007 fatal case in akiller whaleinTexasbroadened the knownhost rangeofWest Nile virusto includecetaceans.[43]

Omsk haemorrhagic fever virusappears 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 muskratOndatra zibethicus,which is highly susceptible to this virus, was introduced into this area in the 1930s.

Taxonomy

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Species

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In the genusFlavivirusthere are 53 defined species:[45]

Sorted by vector

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List of species and strains of flavivirus by vector


Phylogenetic tree ofFlaviviruswith 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 oftick-borne encephalitis virus(TBEV),Kyasanur forest disease virus(KFDV),Omsk hemorrhagic fever virus(OHFV),Powassan virus(POWV), andLouping-ill virus(LIV)

Mammaliantick-borne virus group

Seabirdtick-borne virus group

Mosquito-borne viruses

Viruses with no known arthropod vector

Non vertebrate viruses

Viruses known only from sequencing

Vaccines

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Time-line of historical highlights offlavivirusresearch

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

Effective inactivatedJapanese encephalitisandTick-borne encephalitisvaccines were introduced in the middle of the 20th century. Unacceptable adverse events have prompted change from a mouse-brain inactivatedJapanese encephalitis vaccineto 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, severaldengue vaccinesare 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-specificalphavirusEilat virusas avaccine 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]

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