Drosophila C virus

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Drosophila C virus
Virus classification
Group IV ((+)ssRNA)
Drosophila C virus

Drosophila C virus belongs to the genus Cripavirus and was previously thought to be a member of the virus family Picornaviridae; it has since been classified as belonging to the Dicistroviridae.[1] It is a single stranded positive sense RNA virus of approximately 9300 nucleotides and it contains two open reading frames.[1] The virus particles are 30 nm in diameter and are made up of approximately 30% of RNA and 70% protein.[2] The virus capsid is composed of three major polypeptides and two minor polypeptides.[2]

Drosophila C virus was first discovered in the early 1970s in a French strain of Drosophila melanogaster,[1] but can also infect other Drosophila species in laboratory settings.[3] The virus is transmitted by feeding and affects survival.[4] However, experimental evidence has shown that when injected into adult flies the virus is pathogenic as it causes the adult flies to die within 3–4 days.[1] Antiviral RNAi has been shown to be an important host defence against DCV, and DCV encodes a viral suppressor of RNAi that sequesters double-stranded RNA to prevent antiviral RNAi targeting the virus.[5] Drosophila that are infected with Drosophila C virus develop more quickly, the females have a greater number of ovarioles than uninfected flies.[1] Whilst based on this evidence it has been suggested DCV is a beneficial virus, this ignores the fact that the virus kills flies in only a few days (so total fitness in infected flies is still reduced),[6] and any changes in development time or ovariole number likely represent a host life history shift (parasite-induced fecundity compensation).[7] Further support for host fecundity compensation following DCV infection comes from work showing that this response varies with fly genetic background, with some fly lines showing increased fecundity following infection, while others show a fecundity reduction.[8] Infection with Drosophila C virus can also increase the mortality rate within a Drosophila population.[9]


  1. ^ a b c d e Genomes
  2. ^ a b Jousset, Francoise-Xaviere; Bergoin, M.; Revet, B. (1 January 1977). "Characterization of the Drosophila C Virus". Journal of General Virology. 34 (2): 269–283. doi:10.1099/0022-1317-34-2-269. PMID 190345.
  3. ^ Kapun, M; Nolte, V; Flatt, T; Schlötterer, C (2010). "Host range and specificity of the Drosophila C virus". PLOS ONE. 5 (8): e12421. doi:10.1371/journal.pone.0012421. PMC 2928731. PMID 20865043.
  4. ^ Roxström-Lindquist, K; Terenius, O; Faye, I (2004). "Parasite-specific immune response in adult Drosophila melanogaster: a genomic study". EMBO Reports. 5 (2): 207–12. doi:10.1038/sj.embor.7400073. PMC 1298984. PMID 14749722.
  5. ^ Van Rij, R. P.; Saleh, M. C.; Berry, B; Foo, C; Houk, A; Antoniewski, C; Andino, R (2006). "The RNA silencing endonuclease Argonaute 2 mediates specific antiviral immunity in Drosophila melanogaster". Genes & Development. 20 (21): 2985–95. doi:10.1101/gad.1482006. PMC 1620017. PMID 17079687.
  6. ^ Longdon, Ben (2015). "Examination of data claiming Drosophila C virus is beneficial do not support this claim" (Data Set). Figshare. doi:10.6084/m9.figshare.1297064.
  7. ^ Chadwick, W; Little, T. J. (2005). "A parasite-mediated life-history shift in Daphnia magna". Proceedings of the Royal Society B: Biological Sciences. 272 (1562): 505–9. doi:10.1098/rspb.2004.2959. PMC 1578704. PMID 15799946.
  8. ^ Gupta, V.; Stewart, C. O.; Rund, S. S. C.; Monteith, K.; Vale, P. F. (2017-07-01). "Costs and benefits of sublethal Drosophila C virus infection". Journal of Evolutionary Biology. 30 (7): 1325–1335. doi:10.1111/jeb.13096. ISSN 1420-9101. PMID 28425174.
  9. ^ Gravot, E; Thomas-Orillard, M; Jeune, B (2000). "Virulence variability of the Drosophila C virus and effects of the microparasite on demographic parameters of the host (Drosophila melanogaster)". Journal of Invertebrate Pathology. 75 (2): 144–51. doi:10.1006/jipa.1999.4913. PMID 10772327.