Nodamura virus | |
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Structure of Nodamura virus [1] | |
Virus classification | |
(unranked): | Virus |
Realm: | Riboviria |
Kingdom: | Orthornavirae |
Phylum: | Kitrinoviricota |
Class: | Magsaviricetes |
Order: | Nodamuvirales |
Family: | Nodaviridae |
Genus: | Alphanodavirus |
Species: | Nodamura virus |
Nodamura virus (NoV) is a member of the family Nodaviridae, which was originally isolated from mosquitoes ( Culex tritaeniorhynchus ) in Japan near the village of Nodamura in 1956. [2] Other members of Nodaviridae are flock house virus (FHV) and black beetle virus (BBV). [3] NoV has been found to multiply in several insect and tick species; however, these infected individuals seem to be asymptomatic. Nodamura virus is the only member of the genus Alphanodavirus that can infect insects, fish, and mammals. [4]
Nodamura virus is a +ssRNA virus. It is a member of the virus family Nodaviridae. Nodaviridae is made up of two genera, Alphanodavirus and Betanodavirus. NoV is a member of the Alphanodavirus. Other viruses in this genus are Flock House virus and Black beetle virus . [5]
The structure of nodamura virus is consistent with the structure of other viruses in the family Nodaviridae. These viruses contain a non-enveloped virion that has a diameter of approximately 30 nm. The virion is made up of 180 copies of a single viral capsid protein. [2] The virion is organized in T=3 icosahedral symmetry, which means there are 60 triangular subunits each made up of 3 viral capsid proteins. The virion contains both RNA1 and RNA2, but RNA3 is not included into the virion and is transcribed after infection of a host cell. RNA1 and RNA2 are required for successful infectivity of nodamura virus. [5]
Nodamura virus capsid contains a segmented RNA genome made up of RNA1 and RNA2. RNA1 is responsible for encoding protein A, which is the RNA dependent RNA polymerase. RNA dependent RNA polymerase is necessary for replication of the nodamura virus genome. RNA1 is approximately 3.2 kb in length. [6] RNA2 encodes the viral capsid protein, alpha. RNA2 is approximately 1.3 kb in length. [7] RNA1's Protein A is also responsible for the synthesis of RNA3, which is synthesized from RNA1. In NoV, RNA3 is responsible for the translation of proteins B2-137, B2-134, and B1. Studies have shown that B2 proteins help to repress an antiviral response in nodamura infected cells. [8]
Virus penetrates into the host cell. Uncoating, and release of the viral genomic RNA into the cytoplasm. Specific mechanisms of viral attachment to host cell and entry into the host cell are currently unknown. No specific receptor has been identified.[ citation needed ]
Replication of Nodamura virus, a +ssRNA virus, occurs in the cytoplasm of cells. Once the virus has entered the host cell, the virus is uncoated and the viral RNA is released into the cytoplasm. The viral RNA-1 is then translated to produce the RdRp protein. Replication then begins in cytoplasmic viral factories. A dsRNA genome is synthesized from the genomic ssRNA(+) and further transcribed providing viral mRNAs/new ssRNA(+) genomes. The subgenomic RNA-3 is then transcribed along with the RNA-2, which encodes capsid protein alpha.[ citation needed ]
Virus assembly in the cytoplasm around genomic RNA1 and RNA2. Assembled capsid protein alpha is cleaved into capsid protein beta and gamma. Release of infectious particles. [5]
The nodamura virus protein B2 (encoded by RNA3) has been shown to modulate the host process of antiviral response. B2 has been found to repress the host's antiviral response to allow the virus to successfully replicate. [8]
Since nodamura virus infects insects, fish, and mammals, there are different diseases caused in different species. [5] In wax moth larvae and honey bees, nodamura virus has been found to cause paralysis. Suckling mice and hamsters that have been inoculated with nodamura virus showed paralysis in their limbs, followed by death. In Aedes albopictus and Toxorhynchites amboinensis mosquitoes, nodamura virus induced a loss of balance and an inability to fly. This was then followed by paralysis and death. [3]
Nodavirus has been found to successfully replicate in muscle cells and impair muscle fibrils causing paralysis.[ citation needed ]
Rhabdoviridae is a family of negative-strand RNA viruses in the order Mononegavirales. Vertebrates, invertebrates, plants, fungi and protozoans serve as natural hosts. Diseases associated with member viruses include rabies encephalitis caused by the rabies virus, and flu-like symptoms in humans caused by vesiculoviruses. The name is derived from Ancient Greek rhabdos, meaning rod, referring to the shape of the viral particles. The family has 40 genera, most assigned to three subfamilies.
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Pseudoviridae is a family of viruses, which includes three genera.
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Baltimore classification is a system used to classify viruses based on their manner of messenger RNA (mRNA) synthesis. By organizing viruses based on their manner of mRNA production, it is possible to study viruses that behave similarly as a distinct group. Seven Baltimore groups are described that take into consideration whether the viral genome is made of deoxyribonucleic acid (DNA) or ribonucleic acid (RNA), whether the genome is single- or double-stranded, and whether the sense of a single-stranded RNA genome is positive or negative.
Batai orthobunyavirus (BATV) is a RNA virus belonging to order Bunyavirales, genus Orthobunyavirus.
Alphanodavirus is a genus of non-enveloped positive-strand RNA viruses in the family Nodaviridae. Insects, mammals, and fishes serve as natural hosts. Diseases associated with this genus include: Nodamura virus paralysis in infected wax moth larvae. Member viruses can also provoke paralysis and death to suckling mice and suckling hamsters. There are five species in this genus.
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Flock House virus (FHV) is in the alphanodavirus genus of the Nodaviridae family of viruses. Flock House virus was isolated from a grass grub at the Flock House research station in Bulls, New Zealand. FHV is an extensively studied virus and is considered a model system for the study of other non-enveloped RNA viruses owing to its small size and genetic tractability, particularly to study the role of the transiently exposed hydrophobic gamma peptide and the metastability of the viral capsid. FHV can be engineered in insect cell culture allowing for the tailored production of native or mutant authentic virions or virus-like-particles. FHV is a platform for nanotechnology and nanomedicine, for example, for epitope display and vaccine development. Viral entry into host cells occurs via receptor-mediated endocytosis. Receptor binding initiates a sequence of events during which the virus exploits the host environment in order to deliver the viral cargo in to the host cytosol. Receptor binding prompts the meta-stability of the capsid–proteins, the coordinated rearrangements of which are crucial for subsequent steps in the infection pathway. In addition, the transient exposure of a covalently-independent hydrophobic γ-peptide is responsible for breaching cellular membranes and is thus essential for the viral entry of FHV into host cells.
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Black beetle virus (BBV) is a virus that was initially discovered in the North Island of New Zealand in Helensville in dead New Zealand black beetles in 1975.
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