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Sigmavirus

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Sigmavirus
Virus classification Edit this classification
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Negarnaviricota
Class: Monjiviricetes
Order: Mononegavirales
Family: Rhabdoviridae
Genus: Sigmavirus

Sigmavirus is a genus of viruses in the family Rhabdoviridae, order Mononegavirales. Sigmaviruses naturally infect dipterans.[1][2] It is not to be confused with the Mega Man character of the same name.

Taxonomy

The genus contains the following species:[2]

Discovery

Drosophila melanogaster sigmavirus (DMelSV) was discovered by a group of French researchers in 1937 [3] after they observed certain fly lines became paralysed and died on exposure to carbon dioxide (which is commonly used as an anesthetic for Drosophila). They found the carbon dioxide sensitivity was caused by an infectious agent which they named sigma, and was later found to be a rhabdovirus.[4] More recently new sigmaviruses have been discovered in diptera of six species ; five in species of Drosophila and one in the family Muscidae.[5][6]

Transmission

DMelSV, DAffSV and DObsSV are transmitted vertically by both drosophila parents (i.e. through both eggs and sperm) suggesting sigmaviruses may be a clade of vertically transmitted viruses.[7][8] This unusual mode of biparental vertical transmission allows the virus to spread through host populations even if it reduces the fitness of infected hosts.[9]

Host resistance

In Drosophila melanogaster resistance alleles in the genes ref(2)p and CHKov 1 and 2 and have been identified that explain a large amount of the genetic variation in susceptibility to DMelSV infection.[10][11][12]

Structure

Sigmavirions are enveloped, with bullet shaped geometries. Sigmavirus genomes are linear, around 12.6 kb in length. The genome codes for 6 proteins (3' to 5': N-P-X-M-G-L).[5][7]

Genus Structure Symmetry Capsid Genomic arrangement Genomic segmentation
Sigmavirus Bullet-shaped Enveloped Linear

Life cycle

Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment of the viral G glycoproteins to host receptors, which mediates clathrin-mediated endocytosis. Replication follows the negative stranded RNA virus replication model. Negative stranded RNA virus transcription, using polymerase stuttering is the method of transcription. The virus exits the host cell by budding, and tubule-guided viral movement. Drosophilae serve as the natural host.[1]

Genus Host details Tissue tropism Entry details Release details Replication site Assembly site Transmission
Sigmavirus Drosophila None Clathrin-mediated endocytosis Budding Cytoplasm Cytoplasm Unknown

References

  1. ^ a b "Viral Zone". ExPASy. Retrieved 13 August 2015.
  2. ^ a b "Virus Taxonomy: 2020 Release". International Committee on Taxonomy of Viruses (ICTV). March 2021. Retrieved 18 May 2021.
  3. ^ L'Heritier, P. H.; Teissier, G. (1937). "Une anomalie physiologique héréditaire chez la Drosophile". C. R. Acad. Sci. Paris. 231: 192–194.
  4. ^ L'Heritier, P (1957). "The hereditary virus of Drosophila". Advances in Virus Research Volume 5. Vol. 5. pp. 195–245. doi:10.1016/S0065-3527(08)60674-0. ISBN 9780120398058. PMID 13508405. {{cite book}}: |journal= ignored (help)
  5. ^ a b Longdon, B; Obbard, DJ; Jiggins, FM (2010). "Sigma viruses from three species of Drosophila form a major new clade in the rhabdovirus phylogeny". Proceedings of the Royal Society B. 277 (1698): 35–44. doi:10.1098/rspb.2009.1472. PMC 2842628. PMID 19812076.
  6. ^ Longdon, B; Wilfert, L; Osei-Poku, J; Cagney, H; Obbard, DJ; Jiggins, FM (2011). "Host-switching by a vertically transmitted rhabdovirus in Drosophila". Biology Letters. 7 (5): 747–750. doi:10.1098/rsbl.2011.0160. PMC 3169049. PMID 21450721.
  7. ^ a b Brun, G. and N. Plus (1980). The viruses of Drosophila. The genetics and biology of Drosophila. M. Ashburner and T. R. F. Wright. New York, Academic Press: 625-702.
  8. ^ Longdon, B; Wilfert, L; Obbard, DJ; Jiggins, FM (2011). "Rhabdoviruses in two species of Drosophila: vertical transmission and a recent sweep". Genetics. 188 (1): 141–150. doi:10.1534/genetics.111.127696. PMC 3120147. PMID 21339477.
  9. ^ L'Heritier, PH (1970). "Drosophila viruses and their role as evolutionary factors". Evolutionary Biology. Vol. 4. Appleton-Century-Crofts. pp. 185–209. ISBN 978-0-390-27033-7.
  10. ^ Wayne, M L; Contamine, D; Kreitman, M (1996). "Molecular population genetics of ref(2)P, a locus which confers viral resistance in Drosophila". Mol Biol Evol. 13 (1): 191–199. doi:10.1093/oxfordjournals.molbev.a025555. PMID 8583891.
  11. ^ Bangham, J; Obbard, DJ; Kim, KW; Haddrill, PR; Jiggins, FM (2007). "The age and evolution of an antiviral resistance mutation in Drosophila melanogaster". Proceedings of the Royal Society B. 274 (1621): 2027–2034. doi:10.1098/rspb.2007.0611. PMC 1914336. PMID 17550883.
  12. ^ Magwire, MM; Bayer, F; Webster, CL; Cao, C; Jiggins, FM (2011). "Successive Increases in the Resistance of Drosophila to Viral Infection through a Transposon Insertion Followed by a Duplication". PLOS Genet. 7 (10): e1002337. doi:10.1371/journal.pgen.1002337. PMC 3197678. PMID 22028673.
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