Agua-Salud alphavirus, Aedes aegypti cell lines
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA725665 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR14480176.fastq.gz | Fastqsanger.gz |
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Project description:Aedes aegypti mosquitoes infect hundreds of millions of people each year with dangerous viral pathogens including dengue, yellow fever, Zika, and chikungunya. Progress in understanding the biology of this insect, and developing tools to fight it, depends on the availablity of a high-quality genome assembly. Here we use DNA proximity ligaton (Hi-C) and Pacific Biosciences long reads to create AaegL5 - a highly contiguous A. aegypti reference.
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Project description:The ability of many viruses to manipulate the host antiviral immune response often results in complex host-pathogen interactions. In order to study the interaction of dengue virus (DENV) with the Aedes aegypti immune response, we have characterized the DENV infection-responsive transcriptome of the immune-competent A. aegypti cell line Aag2. As in mosquitoes, DENV infection transcriptionally activated the cell line Toll pathway and a variety of cellular physiological systems. Most notably, however, DENV infection down-regulated the expression levels of numerous immune signaling molecules and antimicrobial peptides (AMPs). Functional assays showed that transcriptional induction of AMPs from the Toll and IMD pathways in response to bacterial challenge is impaired in DENV-infected cells. In addition, Escherichia coli, a gram-negative bacteria species, grew better when co-cultured with DENV-infected cells than with uninfected cells, suggesting a decreased production of AMPs from the IMD pathway in virus-infected cells. Pre-stimulation of the cell line with gram-positive bacteria prior to DENV infection had no effect on DENV titers, while pre-stimulation with gram-negative bacteria resulted in an increase in DENV titers. These results indicate that DENV is capable of actively suppressing immune responses in the cells it infects, a phenomenon that may have important consequences for virus transmission and insect physiology.
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2011-10-31 | E-GEOD-33274 | biostudies-arrayexpress
Project description:The midgut of hematophagous insects is the initial site of infection by arthropod-borne viruses (arboviruses) and plays a crucial role in vector competence. To further understand processes that occur in the midgut in response to infection by an arbovirus, DNA microarrays were used to analyze gene expression changes following infection by the alphavirus, Sindbis (MRE16 Malaysian strain). Midgut transcription profiles from mosquitoes fed blood containing 108 pfu/ml of virus were compared with those from mosquitoes ingesting blood meals having no virus. Transcription profiles from both experimental groups were analyzed at 1, 4, and 8 days post feeding. Among the many transcription changes observed by microarray analysis, the most dramatic involved three genes that had twenty-five to forty-fold increases in transcript levels in virus infected mosquitoes at 4 days post infection . These genes were synaptic vesicle protein-2 (SV2), potassium-dependent sodium/calcium exchanger (NCKX), and a homologue of C. elegans Unc-93, a putative component of a two-pore potassium channel. We speculate that these changes represent changes in vesicle transport processes. In addition to these observations, transcript changes were observed in infected mosquitoes that suggested involvement of Toll and JNK immune cascades as a response to viral infection
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Project description:Chikungunya virus (CHIKV) is a single-stranded positive RNA virus that belongs to the genus Alphavirus and is transmitted to humans by infected Aedes aegypti and Aedes albopictus bites. In humans, CHIKV can cause painful symptoms during acute and chronic stages of infection. However, the virus-vector interaction has characteristics that allow a persistent infection, not disturbing the mosquito’s fitness. Here, we aimed to clarify aspects of CHIKV infection in Ae. aegypti Aag-2 cells through label-free quantitative proteomic analysis and transmission electron microscopy (TEM). We used MOI 0.1 to infect Aag-2 cells in biological triplicates over 48 h. TEM images show a high load of intracellular viral cargo at 48 hpi, as well as an elongated unusual mitochondria morphology that might indicate a mitochondrial imbalance. Moreover, a total of 196 Ae. aegypti protein groups were up or downregulated upon infection, related to protein synthesis, energy metabolism, signaling pathways and apoptosis. These regulated Aag-2 proteins might have roles in antiviral and/or in pro-viral mechanisms during CHIKV infection, to support the balance between viral propagation and the survival of host cell, leading to the persistent infection.
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