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Epstein-Barr virus induces host shutoff extensively via BGLF5-independent mechanisms [RNA-seq]

ABSTRACT: Epstein-Barr virus induces host shutoff extensively via BGLF5-independent mechanisms [RNA-seq]

PROVIDER: PRJNA1132980 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29735605_1.fastq.gz	Fastqsanger.gz
	SRR29735605_2.fastq.gz	Fastqsanger.gz
	SRR29735606_1.fastq.gz	Fastqsanger.gz
	SRR29735606_2.fastq.gz	Fastqsanger.gz
	SRR29735607_1.fastq.gz	Fastqsanger.gz

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Epstein-Barr virus induces host shutoff extensively via BGLF5-independent mechanisms [RNA-seq]

Project description:This study characterizes the effects of Epstein-Barr virus (EBV) reactivation on the host and virus transcriptomes. For this work, a dual-fluorescent lytic reporter (DFLR) EBV was constructed based on the M81 EBV strain and used to transform primary B cells into lymphoblastoid cell lines (LCL). Deposited here is RNA-seq data from these DFLR LCLs that were induced by BCR crosslinking and sorted into latent, early lytic, and late lytic fractions. All samples consist of 40,000 sorted cells and include equal quantities of ERCC spike-in RNAs for normalization. We also performed the same experimental approach on a second DFLR LCL in which the EBV BGLF5 host shutoff nuclease was deleted. This allowed us to define which changes in the transcriptome during EBV replication were due to BGLF5. This approach demonstrated extensive shutoff of host genes during EBV replication and, unexpectedly, revealed that most of those changes were independent of BGLF5.

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Epstein-Barr virus induces host shutoff extensively via BGLF5-independent mechanisms.

Project description:Epstein-Barr virus (EBV) is a ubiquitous oncogenic virus associated with multiple cancers and autoimmune diseases. Unlike most herpesviruses, EBV reactivation from latency occurs asymptomatically, allowing it to spread efficiently to other hosts. However, available models are limited by the inefficient and asynchronous reactivation from latency into lytic replication. To address this problem, we develop a dual-fluorescent lytic reporter (DFLR) EBV that specifically labels cells in the early and late stages of replication. Using lymphoblastoid cell lines transformed by DFLR EBV as a model for EBV reactivation in B cells, we observe extensive reprogramming of the host cell transcriptome during lytic cycle progression. This includes widespread shutoff of host gene expression and disruption of mRNA processing. Unexpectedly, host shutoff remains extensive even in cells infected with DFLR EBV deleted for the BGLF5 nuclease. These findings implicate BGLF5-independent mechanisms as the primary drivers of host transcriptome remodeling during EBV lytic replication.

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Ganciclovir Plus Arginine Butyrate in Treating Patients With Cancer or Lymphoproliferative Disorders Associated With the Epstein Barr Virus

Project description:RATIONALE: The Epstein Barr virus can cause cancer and lymphoproliferative disorders. Ganciclovir is an antiviral drug that acts against the Epstein Barr virus. Arginine butyrate may make virus cells more sensitive to ganciclovir. Combining ganciclovir and arginine butyrate may kill more Epstein Barr virus cells and tumor cells. PURPOSE: Phase I trial to study the effectiveness of arginine butyrate plus ganciclovir in treating patients who have cancer or lymphoproliferative disorders that are associated with the Epstein Barr virus.

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Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression

Project description:Viral infection leads to heterogeneous cellular outcomes ranging from resistance to virion amplification and cell death. In this study, we apply single-cell techniques to analyze diverse fate trajectories during Epstein-Barr virus (EBV) lytic reactivation in three B cell models. We expand upon the previous finding that c-Myc regulates lytic reactivation and determine that MYC downregulation during the lytic phase is correlated with a loss of germinal center (GC) B cell expression signatures. Consistent with prior work, lytic induction yields both abortive and complete reactivation. Abortive lytic cells, which express high STAT3 and initiate but do not complete the lytic cycle, also upregulate NF-kB and IRF3 pathway target genes. Cells that proceeded through the full lytic cycle exhibited unexpected and striking expression of genes associated with cellular reprogramming, developmental progenitor phenotypes, and cytokine upregulation. Distinct subpopulations of lytic cells further displayed variable profiles for transcripts known to escape virus-mediated host shutoff. These data reveal previously unknown and promiscuous outcomes of lytic reactivation with broad implications for viral replication and EBV-associated oncogenesis.

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Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression

Project description:Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression

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Project description:The Epstein-Barr virus nuclear antigen 2 (EBNA2) initiates and maintains the proliferation of infected B cells. In search of additional cellular strategies, that control EBNA2 function, we have performed a label-free mass spectrometry-based quantification of cellular proteins in EBNA2 immuno-precipitates and found polo-like kinase 1 (PLK1) to be bound to EBNA2. EBNA2/PLK1 complex formation is strongly enforced by EBNA2 S379 phosphorylation catalyzed by the mitotic CYCLIN B/CDK1 complex.

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