ArticleJournal of virology2013
Dicer-2- and Piwi-mediated RNA interference in Rift Valley fever virus-infected mosquito cells.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
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Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.
- Pooled it
- Vector competence acrossJournal of virology · 2026Review
- SFTSV NSs protein is a tick antiviral RNAi response suppressor.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- piR-bmo-796514 facilitates the proliferation of exogenous DNA virus (baculovirus) by targeting the host E3 ubiquitin ligase RNF181.PLoS pathogens · 2026Article
- NSs: the multifaceted bunyavirus virulence factor.Npj viruses · 2025Review
- Ultrastructural Insight into Rift Valley Fever Virus Pathogenesis in Different Human Cell Types.International journal of molecular sciences · 2025Article
- Generation of Cas9 Knock-InDNA · 2025Article
- Acute bee paralysis virus regulation of microRNA expression dynamics in the insect host (Frontiers in cellular and infection microbiology · 2025Article
- Article
- An Introduction to Rift Valley Fever Virus.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Interaction between Bombyx mori Cytoplasmic Polyhedrosis Virus NSP8 and BmAgo2 Inhibits RNA Interference and Enhances Virus Proliferation.Microbiology spectrum · 2023Article
- Small RNA sequencing of field Culex mosquitoes identifies patterns of viral infection and the mosquito immune response.Scientific reports · 2023Article
- RNA interference is essential to modulating the pathogenesis of mosquito-borne viruses in the yellow fever mosquitoProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Characterisation of the antiviral RNA interference response to Toscana virus in sand fly cells.PLoS pathogens · 2023Article
- Insect-Specific Chimeric Viruses Potentiated Antiviral Responses and Inhibited Pathogenic Alphavirus Growth in Mosquito Cells.Microbiology spectrum · 2023Article
- Antiviral RNAi Response inViruses · 2023Article
- Article
- Small RNA Response to Infection of the Insect-Specific Lammi Virus and Hanko Virus in anViruses · 2021Article
- NO Synthesis in Immune-Challenged Locust Hemocytes and Potential Signaling to the CNS.Insects · 2021Article
- Interactions of the Insect-Specific Palm Creek Virus with Zika and Chikungunya Viruses inMicroorganisms · 2021Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rift Valley fever virus (RVFV) is a Phlebovirus (Bunyaviridae family) transmitted by mosquitoes. It infects humans and ruminants, causing dramatic epidemics and epizootics in Africa, Yemen, and Saudi Arabia. While recent studies demonstrated the importance of the nonstructural protein NSs as a major component of virulence in vertebrates, little is known about infection of mosquito vectors. Here we studied RVFV infection in three different mosquito cell lines, Aag2 cells from Aedes aegypti and U4.4 and C6/36 cells from Aedes albopictus. In contrast with mammalian cells, where NSs forms nuclear filaments, U4.4 and Aag2 cells downregulated NSs expression such that NSs filaments were never formed in nuclei of U4.4 cells and disappeared at an early time postinfection in the case of Aag2 cells. On the contrary, in C6/36 cells, NSs nuclear filaments were visible during the entire time course of infection. Analysis of virus-derived small interfering RNAs (viRNAs) by deep sequencing indicated that production of viRNAs was very low in C6/36 cells, which are known to be Dicer-2 deficient but expressed some viRNAs presenting a Piwi signature. In contrast, Aag2 and U4.4 cells produced large amounts of viRNAs predominantly matching the S segment and displaying Dicer-2 and Piwi signatures. Whereas 21-nucleotide (nt) Dicer-2 viRNAs were prominent during early infection, the population of 24- to 27-nt Piwi RNAs (piRNAs) increased progressively and became predominant later during the acute infection and during persistence. In Aag2 and U4.4 cells, the combined actions of the Dicer-2 and Piwi pathways triggered an efficient antiviral response permitting, among other actions, suppression of NSs filament formation and allowing establishment of persistence. In C6/36 cells, Piwi-mediated RNA interference (RNAi) appeared to be sufficient to mount an antiviral response against a secondary infection with a superinfecting virus. This study provides new insights into the role of Dicer and Piwi in mosquito antiviral defense and the development of the antiviral response in mosquitoes.
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