Drosophila C virus
| Drosophila C virus | |
|---|---|
| Virus classification | |
| Group: | Group IV ((+)ssRNA) |
| Order: | Picornavirales |
| Family: | Dicistroviridae |
| Genus: | Cripavirus |
| Species: | 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] Infection with Drosophila C virus can also increase the mortality rate within a Drosophila population.[8]
References
- 1 2 3 4 5 Genomes
- 1 2 Characterization of the Drosophila C Virus - Jousset et al. 34 (2): 269 - Journal of General Virology
- ↑ 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. PMID 20865043.
- ↑ 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. PMID 14749722.
- ↑ 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.
- ↑ http://dx.doi.org/10.6084/m9.figshare.1297064
- ↑ 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.
- ↑ 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.