| Orbivirus | |
|---|---|
 | |
| Cryo-EM of the protein structure of abluetongue viruscapsid | |
 | |
| Negatively stainedBluetongue virus–like particle that caused acytopathic effect inBHK-21 cells. Scale bar = 50 nm | |
Virus classification | |
| (unranked): | Virus |
| Realm: | Riboviria |
| Kingdom: | Orthornavirae |
| Phylum: | Duplornaviricota |
| Class: | Resentoviricetes |
| Order: | Reovirales |
| Family: | Sedoreoviridae |
| Genus: | Orbivirus |
Orbivirus is a genus ofdouble-stranded RNA viruses in the orderReovirales and the familySedoreoviridae. Unlike otherreoviruses, orbiviruses arearboviruses. They can infect and replicate within a wide range ofarthropod andvertebrate hosts. Orbiviruses are named after their characteristic doughnut-shapedcapsomers (orbis inLatin means ring).
Many orbiviruses are transmitted byticks orhaematophagus insect vectors (Culicoides,mosquitoes andsand flies) and have a wide host range that includescattle,goats andsheep, wildruminants,equids,camelids,marsupials,sloths,bats,birds, large canine and felinecarnivores, andhumans.
The three economically most important orbiviruses are Bluetongue virus,African horse sickness virus, andepizootic hemorrhagic disease virus, all of which are transmitted byCulicoides species. The genus contains 22 species and at least 130 differentserotypes.[1][2]
In 1719, African horse sickness virus (AHSV) caused the first major recorded orbivirusepidemic, killing 1,500 animals. The most historically significant outbreak of orbivirus occurred in 1854–1855, when AHSV infected 70,000 horses. AHSV was discovered to be a virus in 1900 and bluetongue disease followed shortly thereafter in 1905. Outbreaks have occurred sporadically in the 20th and 21st centuries.[3]
The virons are nonenveloped particles that are 70–80 nm in diameter. Thevirus particles are spherical in appearance and haveicosahedral symmetry.[3] An outer and an innercapsid layer surround thegenome, and have T=13 and T=2 symmetry, respectively.[2] The viron is constructed of two concentric protein shells, the subcore layer which contain 120 copies/particle of the VP3 and the core-surface layer composed of 780 copies/particle of the VP7. VP1, VP4, and VP6 are minor enzymatic proteins that are packaged along with the 10 genome segments within the central space of thevirus core. The orbivirus outer-capsid layer is composed of two additional structural proteins (VP2 and VP5) which mediate cell-attachment and penetration during initiation of infection. The outer-capsid proteins are more variable than the core proteins and most of the non-structural proteins and the specificity of their reactions with neutralising antibodies determines the virus serotype.
These viruses have double-strandedRNA genomes, so are classified as Class III viruses. Their genome is linear and is segmented into 10 segments of various lengths. One copy of each gene segment is packaged per virion. In most cases, each gene segment encodes a singleopen reading frame (ORF). The genome encodes seven major structural proteins (VP1–VP7) and three major nonstructural proteins (NS1–NS3). Exceptions to the one gene–one protein rule are segment 9 (Seg-9) and segment 10 (Seg-10), both of which encode two nearly identical proteins initiated from in-phase AUGcodons close together near the upstream termini (VP6 and VP6a encoded by Seg-9: NS3 and NS3a encoded by Seg-10).
An ORF spans almost the entire length of genome segment 9 and encodes VP6 (the viral helicase). A second ORF (OrfX) is also present on this segment and encodes a fourth nonstructural protein (NS4), which was predicted from sequence analysis of various orbiviruses including segment 9 of Great Island virus which contained a long NS4 ORF (around 21kDa). The existence of NS4 was experimentally confirmed in both insect-borne and tick-borne orbiviruses in 2011.[4]
NS1 is the most abundant protein inbluetongue virus infected cells. It formstubules that may be involved in translocation of progeny virus particles to the cell membrane. NS2 isphosphorylated by cellularkinases and is an important matrix protein of the granular viralinclusion bodies that form within thecytoplasm of infected cells. These viral inclusion bodies act as the centres ofviral replication. Themembraneglycoproteins NS3 and NS3a are expressed in large numbers in insect cells, but not in mammalian cells. They are involved in the release of progeny virus particles from infected cells and may be involved in determination of both vector competence andvirulence.
Many orbiviruses preferentially infectvascularendothelial cells. Orbivirusesenter the host cell byendocytosis and the outer capsid is subsequently removed. The whole cycle ofviral replication takes place within the cytoplasm of thehost cell.Transcription of the viral genome intomRNA occurs within the core particle and mRNA is translated intoproteins using the host cellribosomes. Viral proteins are synthesized 2–14 days after initial infection. New virons self-assemble within the cytoplasm and are then released from the host cell bybudding. During the budding process, they transiently acquire a lipid envelope which can be detected for a short period of time following their release, but this is subsequently lost.
Orbiviruses primarily cause diseases in animals. The differentOrbivirus species have different host specificities. Orbiviruses arevector-borne pathogens transmitted between vertebrate hosts by vectors such asmosquitoes,midges,gnats,sandflies, andticks. Bluetongue virus (BTV) is anOrbivirus that causesbluetongue disease in sheep, cattle, goats, and wildungulates. BTV has been in the forefront of molecular studies for last three decades and now represents one of the best understood viruses at the molecular and structural levels.[5][6] Other species of orbiviruses are responsible for other diseases of animals such asAfrican horse sickness andequine encephalosis virus.[7]
The genusOrbivirus contains the following species, listed by scientific name and followed by the exemplar virus of the species:[1][8]
The genus is divided into several (at least 14)serogroups.[9][10] The serogroups are divided in some cases into subgroups. A number of member viruses have yet to be assigned to a serogroup. The serogroups are differentiated on the basis of a fourfold or greater difference inantibody based tests. These tests includeELISAs andcomplement fixation tests.
Member viruses are transmitted by midges (Culicoides),mosquitoes, andticks. The viruses transmitted by a particular type of vector are generally related both genetically and serologically.
The vector(s) of the St Croix river virus are not known and based on its genome sequence this virus does not appear to group with any other vector group.
The tick group may be ancestral to the other groups.[12]
