Mammalian orthoreovirus
Mammalian orthoreovirus | |
---|---|
Virus classification | |
(unranked): | Virus |
Realm: | Riboviria |
Kingdom: | Orthornavirae |
Phylum: | Duplornaviricota |
Class: | Resentoviricetes |
Order: | Reovirales
|
Family: | Sedoreoviridae |
Genus: | Orthoreovirus |
Species: | Mammalian orthoreovirus |
Serotypes[2] | |
Mammalian orthoreovirus (MRV) is a
There are four serotypes, or distinct variations within the viral species, of Mammalian orthoreovirus. This means that there are four separate strains of Mammalian orthoreovirus: Type 1 Lang, Type 2 Jones, Type 3 Dearing, Type 4 Ndelle. An example of these strains is Mammalian orthoreovirus type 3, or Mammalian orthoreovirus 3-Dearing (MRV-3; Strain Dearing). It induces cell death preferentially in transformed cells and therefore displays inherent oncolytic properties.[4][5]
It is believed that Mammalian orthoreovirus causes subclinical infection in humans more so than in other mammals. Meaning, that a human infected with Mammalian orthoreovirus, regardless of the serotype, is nearly or completely asymptomatic, and therefore, don't exhibit signs or symptoms of the virus. This theory is based upon evidence that the majority of people have antibodies for all of the serotypes, meaning they were exposed to the virus at some point and the body's immune system built an immunity to it after being infected.[3]
Viral classification
Based upon the
Within the
History
The etymology of the Mammalian orthoreovirus is based upon “ortho-“ translated from Greek as “straight” and “reovirus“ from respiratory enteric orphan virus.[7] The Mammalian orthoreovirus was labeled an orphan virus in the 1950s when it was discovered. It was described as a “ubiquitous presence” in mammals meaning it was found virtually everywhere. Serum surveys conducted in the 1950s found neutralizing antibodies to mammalian orthoreovirus in humans, monkeys, rabbits and guinea pigs. More recent studies suggest that MRV is still a ubiquitous presence in humans. The Mammalian orthoreovirus is well researched and understood on the biochemical and structural levels, additionally their pathogenesis in mice serves as a model system for studying the pathogenesis of the reoviruses in general. The Orthoreovirus genus is subdivided into fusogenic and non-fusogenic. The division is based upon fusogenic orthoreoviruses having the ability to cause fusion of infected cells, resulting in multinucleated cellular syncytia. These fusogenic orthoreoviruses encode a fusion-associated small transmembrane (FAST) protein that is plays a role in this ability. Prototypical Mammailian orthoreovirsus are non-fusogenic, and do not produce syncytia because of the lack of the fusion-associated transmembrane protein.[4][7]
The Mammalian orthoreovirus serotypes have been studied significantly at the antigenetic and sequence levels. Serotypes 1 (Lang), 2 (Jones), and 3 (Dearing) were originally recognized based upon virus neutralization and hemaglutination-inhibition profiles. Serotype 4 (Ndelle) have been studied at the antigenetic and molecular levels.[4][6][8]
Structure and genome
Just as the rest of the reoviruses are structured, the Mammalian orthoreovirus contains a segmented genome with a linear genomic arrangement, which is enclosed in a 70-80 nm double layered protein
Generally, these
The internal structure of MRV has been fully reconstructed. λ3 is the RNA replicase, whereas µ2 is a transcription factor.[9]
Replication cycle
As stated in the beginning of the article, the natural hosts of the Mammalian orthoreovirus are mammals, ranging from pigs to humans, and the majority of all mammalian species. This is why the Mammalian orthoreovirus is described as a ubiquitous presence, because antibodies for one (or more) serotypes have been found in virtually every mammalian species. This is at least partially due to because the Mammalian orthoreovirus does not rely on arthropods for transmission as many viruses do. Instead the Mammalian orthoreovirus is transmitted via the oral-fecal route, meaning in some way an infected host's feces are ingested by another person, or the aerosol route, meaning the viral particles travel through the air and are breathed in by a person.[6][7][10]
Entry into cell
Once inside the person the Mammalian orthoreovirus attaches to target cells via the σ1 protein, a filamentous trimer that protrudes from the outer capsid layer. Junctional adhesion molecule-A is a receptor for the Mammalian orthoreovirus regardless of the serotype. Sialic acid, resident within the respiratory system of most mammals is a co-receptor for Mammalian orthoreovirus Type 3 (Dearing). After binding to the receptors on the surface of the to-be host cell, the virus is brought into the cell via receptor-mediated endocytosis. Following the internalization of the virus, the viral outer capsid is disassembled within the endocytic compartment (the vesicle). This disassembly of the outer capsid of the virus is performed by endocytic proteases, during acidic pH conditions. This leads to the removal of the σ3 protein, resulting in the exposure of micro1, a membrane-penetration mediator, as well as a conformational change in the σ1 attachment protein.[7][10][11][12]
Replication and transcription
After the uncoated virus particles penetrate the endosomes, early transcription of the double stranded RNA genome by viral polymerase occurs inside the uncoated (naked) viral core. This process occurs in this manner so the viral double stranded RNA is not exposed to the cytoplasm, as this would cause the cell to attack the viral particle. The viral core is then released into the cytoplasm of the host cell, where replication occurs. Replication is completed with the aid of protein λ3, which acts as RNA-dependent RNA polymerase. Positive-strand transcripts from each of the double stranded RNA segments are synthesized, these transcripts are then used as templates for the translation of proteins, in addition to make the negative-strand RNA. Viral protein μ2, is a transcriptase cofactor that is a part of transcription, it also has enzymatic functions such as capping the mRNA, and acts as RNA helicase, which separates double stranded RNA strands.[7][11][13][14]
Assembly and release
Mammalian orthoreovirus messenger RNA transcripts have a short 5’ untranslated region, and do not have 3’ poly A tails, some lack 5’ caps during post-infection. It is unknown as to how uncapped versions of MRV's
Interaction with hosts
The Mammalian orthoreovirus as stated previously is ubiquitous among mammals, infecting a large variety of species all over the world. Examples include, pigs, cattle, horses, primates, dogs, cats, rabbits, mice, marsupials, and humans. Experimental infection of Mammalian orthoreovirus Type 3 resulted in 100% mortality in neonatal pigs, the pigs developed acute gastroenteritis and severe diarrhea within 72 hours of infection. Additionally, it has been reported that MRV-3 causes enteritis, pneumonia, encephalitis and reproductive failure in swine. Experimental infection of Mammalian orthoreovirus Type 1 resulted in pneumonia, enteritis, fever, and diarrhea.[15][16]
References
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- ^ "ICTV 9th Report (2011) Reoviridae". International Committee on Taxonomy of Viruses (ICTV). Retrieved 29 December 2018.
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- ^ a b "disease.html". web.stanford.edu. Retrieved 2017-11-04.
- ^ ISBN 9780080920368.
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- ^ a b c d e f g h "Orthoreovirus". viralzone.expasy.org. Retrieved 2017-11-04.
- ^ a b Center for Food Security and Public Health, College of Veterinary Medicine, Iowa State University (July 2016). "Orthoreovirus" (PDF). swinehealth.org.
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- ^ a b Attachment and Cell Entry of Mammalian Orthoreovirus (PDF Download Available). Vol. 309. February 2006. Retrieved 2017-11-04.
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