Ontology highlight
ABSTRACT:
PROVIDER: PRJNA907782 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22502500.fastq.gz | Fastqsanger.gz | |||
| SRR22502501.fastq.gz | Fastqsanger.gz | |||
| SRR22502502.fastq.gz | Fastqsanger.gz | |||
| SRR22502503.fastq.gz | Fastqsanger.gz | |||
| SRR22502504.fastq.gz | Fastqsanger.gz |
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Project description:Aedes mosquitoes transmit pathogenic arthropod-borne (arbo) viruses, putting nearly half the world’s population at risk. Blocking virus replication in mosquitoes rather than in humans serves as a promising approach to prevent arbovirus transmission, which requires in-depth knowledge of mosquito immunity. By integrating multi-omics data, we identified that heat shock factor 1 (Hsf1) regulates eight small heat shock protein (sHsp) genes within one topological associated domain. This Hsf1-sHsp cascade acts as an early response against chikungunya virus (CHIKV) infection and shows pan-antiviral activity in three vector mosquitoes, Aedes aegypti, Aedes albopictus, and Anopheles gambiae. We then assessed the baseline expression of sHsp genes in different tissues of female Ae. aegypti using RNA-seq, and we observed a highly dynamic expression pattern of sHsp genes that varied dramatically across different tissues. Interestingly, sHsp genes were expressed at low levels in two main barrier tissues, the midgut and salivary glands, compared to other tissues such as the crop. Importantly, activation of Hsf1 led to a reduced CHIKV infection rate in adult Ae. aegypti mosquitoes, demonstrating Hsf1 as a promising target for the development of novel intervention strategies to limit arbovirus transmission by mosquitoes.
2024-01-01 | GSE225070 | GEO
Project description:The impact of global climate change on the transmission dynamics of infectious diseases is the subject of extensive debate. The transmission of mosquito-borne viral diseases is particularly complex, with climatic variables directly affecting many parameters associated with the prevalence of disease vectors. While evidence shows that warmer temperatures often decrease the extrinsic incubation period of an arthropod-borne virus (arbovirus), exposure to cooler temperatures often predisposes disease vector mosquitoes to higher infection rates. RNA interference pathways are essential to antiviral immunity in the mosquito; however, few experiments have explored the effects of temperature on the RNAi machinery. Total small RNAs (miRNAs, siRNAs, piRNAs, etc.) were isolated and sequenced from the heads of sensor strain Aedes aegypti mosquitoes, or from the whole bodies of CHIKV-infected Aedes albopictus mosquitoes 8 hours post infection. Mosquitoes were grown at 18C or 28C in replicates of 1 (Ae. aegypti) or 3 (Ae. albopictus).
2013-08-13 | E-GEOD-46204 | biostudies-arrayexpress
Project description:Arthropod-borne viruses (arboviruses) such as dengue virus (DENV) and Zika virus (ZIKV) pose a significant threat to global health. Novel approaches to control arbovirus spread are focused on harnessing the antiviral immune system of their main vector, the Aedes aegypti mosquito. In arthropods, genes of the Vago family are often presented as analogs of mammalian cytokines with potential antiviral functions, but the role of Vago genes upon virus infection in Ae. aegypti is largely unknown. We performed a phylogenetic analysis of the Vago gene family in Diptera that prompted us to focus on a Vago-like gene that we named VLG-1. Using CRISPR/Cas9-mediated gene editing, we generated a VLG-1 mutant line of Ae. aegypti that revealed a proviral effect of this gene upon DENV and ZIKV infection. In the absence of VLG-1, virus dissemination throughout the mosquito’s body was impaired, albeit not altering virus transmission rates. A tissue-specific transcriptome analysis revealed that the loss of VLG-1 impacted numerous biological processes potentially linked to viral replication, such as the oxidative stress response. Our results challenge the conventional understanding of Vago-like genes as antiviral factors and underscores the need for further research to elucidate the molecular mechanisms underlying mosquito-arbovirus interactions.
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Project description:Aedes aegypti (L.) is the primary vector of many emerging arboviruses. Insecticide resistance among mosquito populations is a consequence of the application of insecticides for mosquito control. We used RNA-sequencing to compare transcriptomes between permethrin resistant and susceptible strains of Florida Ae. aegypti in response to Zika virus infection. A total of 2,459 transcripts were expressed at significantly different levels between resistant and susceptible Ae. aegypti. Gene ontology analysis placed these genes into 7 categories of biological processes. The 863 transcripts were expressed at significantly different levels between two strains (up/down regulated) more than 2-fold. Quantitative real-time PCR analysis validated Zika-infected response, and suggested a highly overexpressed P450, with AAEL014617 and AAEL006798 as potential candidates for the molecular mechanism of permethrin resistance in Ae. aegypti. Our findings indicated that most detoxification enzymes and immune system enzymes altered their gene expression between the two strains of Ae. aegypti in response to Zika virus infection. Understanding the interactions of arboviruses with resistant mosquito vectors at the molecular level allows for the possible development of new approaches in mitigating arbovirus transmission. This information sheds light on Zika-induced changes in the insecticide resistance of Ae. aegypti with implications for mosquito control strategies.
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2021-03-21 | PXD020565 | Pride
Project description:Zika virus, an arbovirus, relies on mosquitoes as vectors for its spread and transmission. During blood feeding mosquitoes inoculate saliva containing various proteins. Recently, AgBR1, an Aedes aegypti salivary gland protein, has garnered attention for its immunomodulatory viral activity, along with another protein, NeSt1. We have solved the crystal structure of AgBR1, whose chitinase fold has been repurposed, likely to help blood feeding. We show that AgBR1 and NeSt1, when present in murine macrophages, alter functional cellular pathways related to virus entry by endocytosis, immune response, and cell proliferation. AgBR1 (and NeSt1) do not directly bind to the Zika virus or modulate its replication. In this light, we suggest that their immunomodulatory activity on Zika transmission is through the modulation of host-cell response, likely a consequence of evolutionary crosstalk and virus opportunism. Our structural and functional insights are prerequisites for developing strategies to halt the spread of mosquito-borne disease.
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