Aedes aegypti (Aag2 cells) & Aedes albopictus (C6/36 cells)
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ABSTRACT:
PROVIDER: PRJNA1201772 | ENA |
REPOSITORIES: ENA
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Project description:To determine codon optimality in Aedes Albopictus C6/36 cells, we blocked transcription using three independent transcription inhibitors (5,6-Dichlorobenzimidazole 1-β-D-ribofuranoside (DRB), Flavopiridol and Triptolide) and measured the RNA level at 6 hours post treatment using RNA-seq.
2024-07-23 | GSE234878 | GEO
Project description:The dengue virus (DENV) cause frequent epidemics infecting ~390 million people annually in over 100 countries. There are no approved vaccines or antiviral drugs for treatment of infected patients. However, there is a novel approach to control transmission of DENV by the mosquito vectors, Aedes aegypti and Ae. albopictus, using Wolbachia symbiont. The wMelPop strain of Wolbachia suppresses DENV transmission and shortens the mosquito life span. However, the underlying mechanism is poorly understood. To clarify this mechanism, either naïve Ae. albopictus (C6/36) or wMelPop-C6/36 cells were infected with DENV2. Analysis of host transcript profiles by RNAseq revealed that the presence of wMelPop had profound effects on mosquito host cell transcription in response to DENV2 infection. The viral RNA evolved from wMelPop-C6/36 contained low frequency mutations (~25%) within the coding region of transmembrane domain-1 (TMD1) of E protein. Mutations with >97 % frequencies were distributed within other regions of E, NS5 RNA-dependent RNA polymerase (NS5POL) domain, the TMDs of NS2A, NS2B, and NS4B. Moreover, while DENV2-infected naïve C6/36 cells showed syncytia formation, DENV2-infected wMelPop-C6/36 cells did not. The Wolbachia-induced mutant DENV2 can readily infect and replicate in naïve C6/36 cells; whereas, in the mutant DENV2- infected BHK-21 or Vero cells, the virus replication was delayed. In LLC-MK2 cells, the mutant failed to produce plaques. Additionally, in BHK-21 cells, many mutations in the viral genome reverted to WT and compensatory mutations in NS3 gene appeared. Our results suggest that wMelPop impacts significantly the interactions of DENV2 with mosquito and mammalian host cells.
2019-02-25 | GSE125580 | GEO
Project description:Transcription inhibition in Aedes Albopictus C6/36 cells
| PRJNA983406 | ENA
Project description:Aedes albopictus strain:HT | isolate:Larva Mosquito Asian Tiger | cultivar:C6/36 Transcriptome or Gene expression
| PRJNA371623 | ENA
Project description:The dengue virus NS1protein interacts with DIDO1 to promote flavivirus replication in mosquito cells.
| PRJNA823398 | ENA
Project description:Mosquitoes rely on RNA interference (RNAi) as their primary defense against viral infections. To this end, the combination of RNAi and invertebrate cell culture systems has become an invaluable tool in studying virus-vector interactions. Nevertheless, a recent study failed to detect an active RNAi response to West Nile virus (WNV) infection in C6/36 (Aedes albopictus) cells, a mosquito cell line frequently used to study arthropod-borne viruses (arboviruses). Therefore, we sought to determine if WNV actively evades the host's RNAi response or if C6/36 cells have a dysfunctional RNAi pathway. C6/36 and Drosophila melanogaster S2 cells were infected with WNV (Flaviviridae), Sindbis virus (SINV, Togaviridae) and La Crosse virus (LACV, Bunyaviridae) and total RNA recovered from cell lysates. Small RNA (sRNA) libraries were constructed and subjected to high-throughput sequencing. In S2 cells, virus-derived small interfering RNAs (viRNAs) from all three viruses were predominantly 21 nt in length, a hallmark of the RNAi pathway. However, in C6/36 cells, viRNAs were primarily 17 nt in length from WNV infected cells and 26-27 nt in length in SINV and LACV infected cells. Furthermore, the origin (positive or negative viral strand) and distribution (position along viral genome) of S2 cell generated viRNA populations was consistent with previously published studies, but the profile of sRNAs isolated from C6/36 cells was altered. In total, these results suggest that C6/36 cells lack a functional antiviral RNAi response. These findings are analogous to the type-I interferon deficiency described in Vero (African green monkey kidney) cells and suggest that C6/36 cells may fail to accurately model mosquito-arbovirus interactions at the molecular level.
| S-EPMC2964293 | biostudies-literature
Project description:An iTRAQ-based quantitative proteomic analysis of ZIKV infected Aedes albopictus C6/36 cells was performed to investigate host proteins involved in ZIKV infection process. A total of 3,544 host proteins were quantified, with 200 being differentially regulated. Bioinformatics analysis on regulated host proteins highlights several ZIKV infection regulated biological processes.
2017-04-21 | PXD004727 | Pride
Project description:Aag2, Aag2.wAlbB, and Aag2.tet Raw sequence reads
| PRJNA901205 | ENA
Project description:Dengue virus (DENV), a member of the Flavivirus genus of the Flaviviridae family, can cause dengue fever (DF) and more serious diseases and thus imposes a heavy burden worldwide. As the main vector of DENV, mosquitoes are a serious hazard. After infection, they induce a complex host-pathogen interaction mechanism. Our goal is to further study the interaction mechanism of viruses in homologous, sensitive, and repeatable C6/36 cell vectors. Transcriptome sequencing (RNA-Seq) technology was applied to the host transcript profiles of C6/36 cells infected with DENV2. Then, bioinformatics analysis was used to identify significant differentially expressed genes and the associated biological processes. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to verify the sequencing data. A total of 1239 DEGs were found by transcriptional analysis of Aedes albopictus C6/36 cells that were infected and uninfected with dengue virus, among which 1133 were upregulated and 106 were downregulated. Further bioinformatics analysis showed that the upregulated DEGs were significantly enriched in signaling pathways such as the MAPK, Hippo, FoxO, Wnt, mTOR, and Notch; metabolic pathways and cellular physiological processes such as autophagy, endocytosis, and apoptosis. Downregulated DEGs were mainly enriched in DNA replication, pyrimidine metabolism, and repair pathways, including BER, NER, and MMR. The qRT-PCR results showed that the concordance between the RNA-Seq and RT-qPCR data was very high (92.3%). The results of this study provide more information about DENV2 infection of C6/36 cells at the transcriptome level, laying a foundation for further research on mosquito vector-virus interactions. These data provide candidate antiviral genes that can be used for further functional verification in the future.
| S-EPMC7926344 | biostudies-literature
Project description:ObjectiveThe mosquito transmitted RNA virus dengue virus (DENV) shows significant variation as a consequence of the lack of proofreading activity of the RNA-dependent RNA polymerase that synthesizes new virus genomes. How this variation affects DENV replication, and how this in turn impacts drug development remains largely unknown. Given the technical limitations in working with large numbers of isolates few studies have sought to investigate this area. This study used a panel of 14 DENV isolates of different serotypes and origins to determine how much virus replication in Aedes albopictus C6/36 cells was affected by DENV variability.ResultsThe results showed that there was considerable variation, with peak titers ranging from 6Log10 to 8Log10, and maximum titer being reached from day 3 to day 9 post infection. While strains from DENV 1 and 4 serotypes showed considerable uniformity, DENV 2 and 3 strains showed much greater variation. Overall, these results show that serotype specific strain variation can have a significant impact on DENV replication, suggesting that studies either investigating DENV pathogenesis or developing drug therapeutics should consider the contribution of DENV variability.
| S-EPMC7552352 | biostudies-literature