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Effect of Flavivirus infections on host cell gene and protein expression

ABSTRACT: As obligate intracellular parasites, viruses rely heavily on their host cells for their replication, and therefore dysregulate several cellular processes for their benefit. In return, host cells activate multiple signaling pathways to limit viral replication and eradicate viruses. The present study explores the complex interplay between viruses and their host cells through next generation RNA sequencing as well as mass spectrometry (SILAC).

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Carolin Brand

LAB HEAD: Martin Bisaillon

PROVIDER: PXD042208 | Pride | 2023-10-24

REPOSITORIES: Pride

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	M1-YF2-1.raw	Raw
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Publications

Kunjin Virus, Zika Virus, and Yellow Fever Virus Infections Have Distinct Effects on the Coding Transcriptome and Proteome of Brain-Derived U87 Cells.

Brand Carolin C Deschamps-Francoeur Gabrielle G Bullard-Feibelman Kristen M KM Scott Michelle S MS Geiss Brian J BJ Bisaillon Martin M

Viruses 20230623 7

As obligate intracellular parasites, viruses rely heavily on host cells for replication, and therefore dysregulate several cellular processes for their benefit. In return, host cells activate multiple signaling pathways to limit viral replication and eradicate viruses. The present study explores the complex interplay between viruses and host cells through next generation RNA sequencing as well as mass spectrometry (SILAC). Both the coding transcriptome and the proteome of human brain-derived U87 ...[more]

PMID: 37515107

Similar Datasets

Effect of Flavivirus infections (Kunjin, Zika, Yellow Fever) on gene expression and alternative splicing in U87 cells.

Project description:As obligate intracellular parasites, viruses rely heavily on their host cells for their replication, and therefore dysregulate several cellular processes for their benefit. In return, host cells activate multiple signaling pathways to limit viral replication and eradicate viruses. The present study explores the complex interplay between viruses and their host cells through next generation RNA sequencing. The coding transcriptome of human brain-derived U87 cells infected with Kunjin virus, Zika virus, or Yellow Fever virus were compared to the transcriptome of mock-infected cells. Changes in the abundance of several hundred mRNAs were found in each infection. Moreover, the alternative splicing of hundreds of mRNAs was found to be modulated upon viral infection.

2023-06-28 | GSE232504 | GEO

TMEM41B is a pan-flavivirus host factor

Project description:Flaviviruses pose a constant threat to human health. These RNA viruses are transmitted by the bite of infected mosquitoes and ticks and regularly cause outbreaks. To identify host factors required for flavivirus infection we performed full-genome loss of function CRISPR-Cas9 screens. Based on these results we focused our efforts on characterizing the roles that TMEM41B and VMP1 play in the virus replication cycle. Our mechanistic studies on TMEM41B revealed that all members of the Flaviviridae family that we tested require TMEM41B. We tested 12 additional virus families and found that SARS-CoV-2 of the Coronaviridae also required TMEM41B for infection. Remarkably, single nucleotide polymorphisms (SNPs) present at nearly twenty percent in East Asian populations reduce flavivirus infection. Based on our mechanistic studies we propose that TMEM41B is recruited to flavivirus RNA replication complexes to facilitate membrane curvature, which creates a protected environment for viral genome replication.

2020-11-24 | GSE162040 | GEO

Understanding the role of microRNAs in the interaction of Aedes aegypti mosquitoes with an insect-specific flavivirus

Project description:The Flavivirus genus contains some of the most prevalent vector-borne viruses such as dengue, Zika and yellow fever viruses that cause devastating diseases in humans. However, the insect-specific clade of flaviviruses is restricted to mosquito hosts; albeit they have retained the general features of the genus such as genome structure and replication. The interaction between insect-specific flaviviruses (ISFs) and their mosquito hosts are largely unknown. Pathogenic flaviviruses are known to modulate host-derived microRNAs (miRNAs), a class of non-coding RNAs that are important in controlling gene expression. Alteration in miRNAs may represent changes in host gene expression and provide understanding of virus-host interactions. The role of miRNAs in ISF-mosquito interactions is largely unknown. A recently discovered Australian ISF, Palm Creek virus (PCV), has the ability to suppress medically relevant flaviviruses. Here, we investigated the potential involvement of miRNAs in PCV infection using the model mosquito Aedes aegypti. By combining small RNA sequencing and bioinformatics analysis, differentially expressed miRNAs were determined. Our results indicated that PCV infection hardly affects host miRNAs. Out of 101 reported miRNAs of Ae. aegypti, only aae-miR-2940-5p had significant altered expression over the course of infection. However, further analysis of aae-miR-2940-5p revealed that this miRNA does not have any direct impact on PCV replication in vitro. Thus, the results overall suggest that PCV infection has a limited effect on the mosquito miRNA profile and therefore, they may not play a significant role the PCV- Ae. aegypti interaction.

2017-07-08 | GSE100917 | GEO

Single cell transcriptional dynamics of flavivirus infection

Project description:Dengue and Zika viral infections affect millions of people annually and can be complicated by hemorrhage or neurological manifestations, respectively. However, a thorough understanding of the host response to these viruses is lacking, partly because conventional approaches ignore heterogeneity in virus abundance across cells. We present viscRNA-Seq (virus-inclusive single cell RNA-Seq), an approach to probe the host transcriptome together with intracellular viral RNA at the single cell level. We applied viscRNA-Seq to monitor dengue and Zika virus infection in cultured cells and discovered extreme heterogeneity in virus abundance. We exploited this variation to identify host factors that show complex dynamics and a high degree of specificity for either virus, including proteins involved in the endoplasmic reticulum translocon, signal peptide processing, and membrane trafficking. We validated the viscRNA-Seq hits and discovered novel proviral and antiviral factors. viscRNA-Seq is a powerful approach to assess the genome-wide virus-host dynamics at single cell level.

2018-02-27 | GSE110496 | GEO

An RNA-centric dissection of host complexes controlling flavivirus infection [GeCKO]

Project description:Flaviviruses including dengue virus (DENV) and Zika virus (ZIKV) cause significant human disease. Co-opting cellular factors for viral protein translation and viral genome replication at the endoplasmic reticulum (ER) is a shared replication strategy, despite different clinical outcomes. While the protein products of these viruses have been studied in depth, how the RNA genomes operate inside human cells is poorly understood. Using comprehensive identification of RNA binding proteins by mass spectrometry (ChIRP-MS), we took an RNA-centric viewpoint of flaviviral infection and identified several hundred proteins associated with both DENV and ZIKV genomic RNA inside human cells. Intersection with genome-scale knockout screens assigned putative functional relevance to the RNA-protein interactions. ER RNA binding proteins such vigilin and RRBP1 directly bound viral RNA and each operated at distinct points in the life cycle of flaviviruses. Thus, this versatile strategy can elucidate features of human biology that control pathogenesis of clinically relevant viruses.

2019-04-16 | GSE109192 | GEO

An RNA-centric dissection of host complexes controlling flavivirus infection [irCLIP]

2019-04-16 | GSE109191 | GEO

An RNA-centric dissection of host complexes controlling flavivirus infection [RNA-Seq]

2019-04-16 | GSE109190 | GEO

An RNA-centric dissection of host complexes controlling flavivirus infection [LAM-PCR]

2019-04-16 | GSE109193 | GEO

RNA-Seq of U2OS cells with and without IFNα2 pretreatment

Project description:RNA viruses are among the most prevalent pathogens and represent a major burden on society. While RNA viruses have been studied extensively, little is known about the processes that occur during the first several hours of infection due to a lack of sensitive assays. Here, we develop a single-molecule imaging assay, virus infection real-time imaging (VIRIM), to study translation and replication of individual RNA viruses in live cells. VIRIM uncovered a striking heterogeneity in replication dynamics between cells and revealed extensive coordination between translation and replication of single viral RNAs. Furthermore, using VIRIM we identify the replication step of the incoming viral RNA as a major bottleneck of successful infection, and identify host genes that are responsible for inhibition of early virus replication. Single-molecule imaging of virus infection represents a powerful tool to study virus replication and virus-host interactions that may be broadly applicable to RNA viruses.

2020-11-18 | GSE159280 | GEO

p97/VCP as a therapy target for developing drugs against human coronavirus

Project description:Understanding how human coronavirus dysregulate host proteome during infection in human cells will identify general pathways that are common to coronavirus infection. NMS-873 is an allosteric p97/VCP ATPase inhibitor and was show to have antiviral effect in multiple viruses including SARS-CoV2. We first demonstrated that genetic knock down of p97 reduced HCoV-229E, HCoV-OC43 infection and secretion. To investigate how p97/VCP assists virus infection, we used unbiased quantitative proteomics to compare dysregulated proteomes caused by HCoV-229E, HCoV-OC43 and SARS-CoV2 infection. We then compared dysregulated proteomes after HCoV-229E and HCoV-OC43 infection with and without p97 knockdown. Moreover, we elucidated the impact of p97 on different stages of viral life cycle using two potent p97 inhibitors, CB-5083 and NMS-873 and demonstrate their can block HCoV replication. Together, our data provide insights to repurpose potential cancer drugs that target the essential host protein p97/VCP.

2021-11-03 | PXD026216 | Pride

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