[1][2] The name "orthoreovirus" comes from the Greek word ortho, meaning "straight" and the reovirus, which comes from taking the letters: R, E, and O from "respiratory enteric orphan virus".
[3] It was discovered in the early 1950s when it was isolated from the respiratory as well as gastrointestinal tracts of both sick and healthy individuals [4] Orthoreovirus is part of the family Reoviridae.
The Orthoreovirus genus has 10 segments that have been isolated from a large range of hosts including mammals, birds, and reptiles.
[3] The following ten species are assigned to the genus:[2] Mammalian orthoreovirus virions are non-enveloped with icosahedral symmetry created by a double-layered capsid reaching about 80 nm wide.
[6] One hundred and twenty copies of the λ1 protein arranged in 12 decameric units make up the shell of the inner capsid structure.
At the 12 five-fold axes of symmetry, pentamers of the λ2 protein form turret-like structures that protrudes from the surface of the shell.
Guanylyltransferase enzymatic activity in the λ2 turret adds a 5' guanosine cap to the extruded mRNA.
[7] It has been proposed that λ2 is involved in replication due to its placement at the fivefold axes and its ability to interact with λ3 in solution.
[8] σ1, a filamentous trimer extruding from the outer capsid, is responsible for cell attachment by interacting with sialic acid and other entry receptors.
[9][10] This orthoreovirus has been extracted from the heart blood of a fruit bat (Pteropus policephalus) in Australia with different viruses being isolated from different species, such as the flying fox (Pteropus hypomelanus) which have been found to cause respiratory infections in humans in Southeast Asia.
Avian orthoreovirus induces apoptosis by what has been proposed as an upregulation of p53 and Bax, a mitochondria-mediated pathway.
Species that are known to become infected with the virus include: humans, birds, cattle, monkeys, sheep, swine, baboons, and bats[21] Replication occurs in the cytoplasm of the host cell.
After the attachment to the receptors, entry to the host cell occurs via receptor-mediated endocytosis through the aid of clathrin coated pits.
After uncoating is completed, the active virus is released in the cytoplasm where replication of the genome and virion takes place.
It has been determined that this protein has some enzymatic functions such as NTPase activity, capping the mRNA transcript, even serving as RNA helicase to separate the dsRNA strands.
Mammalian orthoreovirus mRNA transcripts have a short 5’ un translated region (UTR), do not have 3’ poly A tails, and may even lack 5’ caps during late post-infection.
[23] Thus is it not known how exactly how these uncapped versions of viral mRNA are able to use host cell ribosome to aid in translation.
[25] Positive and negative strands of RNA produced during the transcription state must base pair correctly in order to serve as the genome in the newly formed virus particle.
Even though the virus is fairly common, the infection produced is either asymptomatic or causes a mild disease which is self-limiting in the gastrointestinal tract and respiratory region for children and infants.
[27] Members of the Orthoreovirus genus have been known to cause apoptosis in host cells, and have thus been studied fairly extensively for this very purpose.
[7] The avian orthoreovirus has also been proven to promote autophagy of the host which could contribute to disease in a similar manner as apoptosis.
[31] These viruses are particularly ideal for these sort of therapies because they are self-limiting while simultaneously harnessing the ability to induce apoptosis in tumor cells exclusively.