Null
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB89854 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR15075903_1.fastq.gz | Fastqsanger.gz | |||
| ERR15075903_2.fastq.gz | Fastqsanger.gz | |||
| ERR15075904_1.fastq.gz | Fastqsanger.gz | |||
| ERR15075904_2.fastq.gz | Fastqsanger.gz | |||
| ERR15075905_1.fastq.gz | Fastqsanger.gz |
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Project description:In recent years, arboviral infections have surged dramatically due to the geographic expansion of Aedes and Culex mosquitoes, their main vector mosquitoes. Despite significant efforts to uncover arbovirus–host interactions and viral protein effector functions in mammals, systematic studies aiming to characterize virus–vector interactions in arthropods are largely missing, and the functions and cellular targets of many arboviral proteins in mosquitoes remain elusive. Here, we applied a multi-omic approach to systematically evaluate the ability of arboviral capsids to interact with the Ae. aegypti proteome. This extensive multi-modal atlas across 12 pathogenic arboviral species spanning three viral genera revealed shared and distinct host factor specificities, uncovering species-, genus- and vector preference-specific patterns of host usage in mosquitoes. Functional phenotypic screening of 110 newly discovered host proteins across three prototypic arboviruses (La Crosse virus, dengue virus and West Nile virus) identified several novel host dependency factors, including a new role for the chromatin-remodeling Brahma complex in orthoflavivirus replication. Using a combination of biochemical and sequencing approaches, we characterized the cellular determinants of these interactions and profiled their functional consequences on the chromatin landscape. Altogether, this study provides a multi-layered repository to categorize and characterize arboviral capsid effector functions in invertebrates, providing important cues on novel mechanisms of transcriptional regulation via capsid-mediated modulation of chromatin accessibility in insects.
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Project description:In recent years, arbovirus cases have surged dramatically due to the expanding distribution of the main arbovirus-vectors Aedes and Culex mosquitoes. Despite significant efforts to uncover Orthoflavivirus-specific host adaptation mechanisms of humans, systematic studies aiming to characterize virus–host interactions in arthropods are largely missing. The capsid protein is highly versatile, with multiple functions and subcellular localizations, making it an attractive target for studying host susceptibility, vector competence, and virus–vector adaptation. Here, we employed affinity purification coupled to mass spectrometry to systematically evaluate the ability of capsid proteins of 12 different pathogenic arboviruses spanning three genera to interact with the Ae. aegypti proteome. This extensive protein-protein interaction atlas uncovered novel host targets, implicated in diverse cellular pathways i.e. translation, apoptosis and RNA processing. To functionally characterize prioritized interacting host proteins, we systematically silenced 110 host genes in Ae. aegypti-derived cells and characterized their impact on the replication of three representative arboviruses: La Crosse virus, dengue virus and West Nile virus. This approach identified several novel host-dependency factors, including a new role for two components of the chromatin-remodeling Brahma complex. Interestingly, systematic silencing of individual Brahma BAP subunits revealed a conserved pan-orthoflavivirus role for both BAP and PBAP subcomplexes, when compared to prototypic alphaviruses. Furthermore, using a combination of biochemical and sequencing approaches, we characterized the cellular determinants of these interactions and profiled their functional consequences on the chromatin landscape. Altogether, this study provides an evidence-based repository to categorize and characterize novel arboviral capsid targets and explore arbovirus-vector interactions.
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Project description:Efficient virus replication in its vector, Aedes mosquitoes, is essential for the transmission of arboviral diseases like dengue virus (DENV) in populations. In order to identify RNA-independent host factors involved in DENV replication in mosquitoes, we established a system expressing all non-structural proteins within the context of the macro protein complex as observed during viral infections. Mosquito host factors interacting with 3xFLAGED-tagged DENV non-structural proteins NS1 or NS5 proteins were identified by label-free mass spectrometry.
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Project description:We report a global survey of viral small RNAs (vsmRNAs) from >200 Aedes aegypti samples to identify many mosquito viruses that actively infect this prominent arboviral vector. Ae. aegypti viruses in the Americas were abundant, with some displaying geographical boundaries. Viruses infecting Asian Ae. aegypti were similar to those in the Americas and revealed the first wild example of dengue vsmRNAs. African Ae. aegypti displayed vsmRNAs from viruses unique to these African strains. Academic lab colonies generally lacked viruses, yet two commercial strains were deeply infected by a tombus-like virus that is related to plant viruses. Comparing matched viral long RNAs to vsmRNAs revealed viral transcripts evading the mosquito RNA interference (RNAi) pathway. By infecting mosquito cells with Ae. aegypti homogenates, we generated stably infected cell lines which produced vsmRNAs that were comparable to native mosquito vsmRNA patterns. Lastly, we demonstrate that these stably infected mosquito cells producing vsmRNAs can exert gene silencing of reporters bearing viral sequence segments, providing a potential explanation for how Ae. aegypti can tolerate the persistence of viral infections. This vsmRNA genomics approach in Ae. aegypti can add to existing vector surveillance approaches by discovering new viruses that persist in mosquito populations.
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Project description:In this study, we describe a viral suppressor of RNA silencing encoded by the prototype flavivirus, yellow fever virus (YFV). We show that the YFV capsid protein inhibits RNA silencing in the mosquito Aedes aegypti by interfering with Dicer. These results suggest a molecular arms race between vector and pathogen underlies the continued existence of flaviviruses in nature.
2017-01-04 | GSE80691 | GEO
Project description:The emergence of mosquito-borne diseases because of climate change emphasizes the need to study arbovirus-vector protein-protein interactions (PPI) to better understand viral replication and transmission. One such human pathogenic arbovirus is Zika virus (ZIKV; Flaviviridae), transmitted by Aedes aegypti mosquitoes. With the lack of molecular tools to study mosquito cells, we developed an Ae. aegypti AF5 cell line stably expressing ZIKV capsid to investigate PPI through label-free quantification proteomics. We identified 157 interactors with 8 potentially pro-viral during ZIKV infection and showed that the transitional endoplasmic reticulum 94 (TER94) protein of the ubiquitin-proteasome pathway (UPP) was important during ZIKV infection in mosquito cells. Silencing TER94 in AF5 cells prevented ZIKV capsid degradation and significantly reduced the establishment of replication at the early stages of infection. Human TER94 ortholog, valosin containing protein (VCP), identified through ortholog mapping, was found to have a similar function during ZIKV infection in A549 cells. ZIKV had reduced ability to replicate when ubiquitination and VCP function were blocked by chemical inhibitors. Furthermore, ubiquitin protein ligase E3 component n-recognin 5 (UBR5) was identified as a TER94/VCP co-factor for capsid interaction. Our study demonstrates a conserved function for TER94/VCP-UPP during early ZIKV infection in mosquito and human cells.
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Project description:Mosquito Cell Atlas: A single-nucleus transcriptomic atlas of the adult Aedes aegypti mosquito
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Project description:The recent outbreaks of Zika virus (ZIKV) and its association with birth defects known as Congenital Zika Syndrome warrant investigation on the molecular processes related to its infection and pathogenesis. Among the flavivirus family, only ZIKV is linked to microcephaly as announced by World Health Organization, suggesting uniqueness of ZIKV infection compared to other members. By analyzing the ZIKV-host interactome, we found that the key microRNA (miRNA) processing enzyme Dicer was a leading target of ZIKV capsid protein in neural stem cells (NSCs), and its deficiency facilitated ZIKV infection. Mechanistically, ZIKV capsid can directly interact with Dicer and block its ribonuclease activity, dampening the production of host miRNAs that are essential for neurogenesis. Interestingly, this capsid-mediated immune evasion is specific to ZIKV because capsid proteins from other close flaviviruses, e.g., dengue, yellow fever and West Nile viruses, cannot bind to Dicer or inhibit its function. By molecular mapping, we defined a ZIKV capsid H41R mutant with loss of interaction to Dicer and no longer affecting its activity. More importantly, ZIKV H41R mutant exerted almost no impact on neurogenesis in vitro when expressed in NSCs compared to wild type capsid, and in utero infection of recombinant ZIKV-H41R mutant virus resulted in less inhibition on corticogenesis than wild-type ZIKV in mouse embryos. Interestingly, the epidemic ZIKV strain reinforces the capsid-Dicer interaction by two amino acid substitution compared to ancient Africa strain. Thus, our study demonstrated that capsid-dependent suppression of Dicer function is a unique determinant of ZIKV immune evasion and pathogenesis, which may unveil a new mechanism for ZIKV-mediated microcephaly.
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