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The nuclear RNA exosome is co-opted to enhance host:viral RNA hybrids that propel influenza virus ribogenesis and infectivity

ABSTRACT: The nuclear RNA exosome is co-opted to enhance host:viral RNA hybrids that propel influenza virus ribogenesis and infectivity

PROVIDER: PRJNA379330 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5346870.fastq.gz	Fastqsanger.gz
	SRR5346880.fastq.gz	Fastqsanger.gz
	SRR5346890.fastq.gz	Fastqsanger.gz
	SRR5346871.fastq.gz	Fastqsanger.gz
	SRR5346881.fastq.gz	Fastqsanger.gz

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The nuclear RNA exosome is co-opted to enhance host:viral RNA hybrids that propel influenza virus ribogenesis and infectivity

Project description:The nuclear RNA exosome is an essential multi-subunit complex that controls RNA homeostasis. Congenital mutations in exosome genes are associated with neurodegenerative diseases. Here, we show that transient depletion of nuclear RNA exosome subunits in epithelial cells inhibits influenza virus replication. Similarly, viral biogenesis was suppressed in cells derived from mice with conditional ablation of the RNA exosome subunit Exosc3. Furthermore, patient-derived cells with a congenital EXOSC3 mutation were less susceptible to influenza virus infection. Using proteomics and next generation sequencing during infection, we show that the viral polymerase complex (PA, PB2, PB1) co-opts the nuclear RNA exosome complex and cellular RNAs en route to 3’ end degradation. Mechanistically, the nuclear RNA exosome coordinates the initial steps of viral transcription with RNAPII at host promoters. Exosome deficiency uncouples chromatin targeting of the viral polymerase complex and the formation of cellular:viral RNA hybrids, which are essential RNA intermediates that license transcription of antisense genomic viral RNAs. Overall, we discovered a critical nexus between an essential component of the influenza virus (polymerase) and an essential component of the cell (exosome), alteration of which leads to breakage of host-pathogen symmetry and a lose-lose scenario (viral impairment and neurodegeneration).

2017-05-08 | GSE96677 | GEO

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Murine MSCs: MSC-exosome-hypoxia vs MSC-exosome-normoxia

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Lipid Droplet Biogenesis by Phase-Separated pORF3 Facilitates HEV Infectivity

Project description:Lipid droplets (LDs) are dynamic organelles mediating lipid metabolism and diverse cellular processes. However, the interplay between hepatocyte LDs and hepatitis E remains poorly understood. Using targeted lipidomics and lipid profiling, we reveal in cellular and rodent models that hepatitis E virus (HEV) infection substantially increases hepatocyte LD biogenesis. Mechanistically, HEV pORF3 is a key LD biogenesis inducer and an essential factor for viral infectivity in vivo. pORF3 formed a unique LD organelle through its liquid-liquid phase-separation (LLPS) property, associating with enhancing cholesterol anabolic pathways, thereby facilitating the synthesis of triglycerides and cholesterol esters. Accordingly, deleting ORF3 or inhibiting LD biogenesis with LD-lowering agent atorvastatin substantially suppressed HEV infection in vivo. These findings position LDs as critical hubs for HEV infection, reveal lipid biogenesis as a crucial function of HEV infectivity, and suggest alternative strategies for HEV intervention.

2025-06-09 | GSE299317 | GEO

Murine cells: MSC+LLC-serum-exosome vs LLC-serum-exosome

Project description:Murine cells: MSC+LLC-serum-exosome vs LLC-serum-exosome

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The role of glycans and glycosylation in cell-type specific effects on viral infectivity

Project description:Our lab has previously used the Glyco v3 gene-chip to analyze RNA from human macrophages and T-cells, as part of a project examining the effect of cellular origin on the viral infectivity of HIV/SIV. Our experiments have led us to hypothesize that the different glycosylation pathways present in macrophages and T-cells result in the production of virions with differently glycosylated viral proteins and different glycans present on the virion surface. Furthermore, studies with glycosidases using the Glyco v3 gene-chip have indicated that these differences in the glycosylation profiles of virions derived from different cell types may influence viral infectivity.

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Reassessment of Exosome Composition

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Infectivity, pathogenicity, and immune protection of the pangolin-origin SARS-CoV-2 related coronavirus

Project description:The natural host of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains elusive. A panel of SARS-CoV-2-related coronaviruses have been identified in pangolins, while the infectivity and pathogenicity of these pangolin-origin coronaviruses (pCoV) to human remains largely unknown. Herein, we comprehensively characterized the infectivity and pathogenicity of pCoV-GD01, the most closest pCoV to SARS-CoV-2, in human cells, human tracheal epithelium organoids, and established animal models in comparision with. The results show that pCoV-GD01 showed similar infectivity to SARS-CoV-2 in human cells and organoids. Remarkably, intranasal inoculation of pCoV-GD01 caused severe lung pathological damage in hACE2 mice, and could establish efficient transmission among co-caged hamsters. Interestingly, in-depth antigenic analysis and animal heterologous challenge experiments demonstrate that pre-existing immunity induced by SARS-CoV-2 infection or vaccination was sufficient to provide cross-protection against pCoV-GD01 challenge. These collective results highlight the potential risk of persistent spillover from animal hosts like the pangolin, and the COVID-19 pandemic and massive vaccination have reduced the possibility of pCoVs circulation in mankind.

2023-05-25 | GSE217796 | GEO

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