Understanding differential expression of genes during EBV lytic cycle reactivation by employing high throughput RNA-sequencing
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ABSTRACT:
PROVIDER: PRJNA995436 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25302171.fastq.gz | Fastqsanger.gz | |||
| SRR25302172.fastq.gz | Fastqsanger.gz | |||
| SRR25302173.fastq.gz | Fastqsanger.gz | |||
| SRR25302174.fastq.gz | Fastqsanger.gz | |||
| SRR25302175.fastq.gz | Fastqsanger.gz |
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Project description:To understand the changes in global transcriptomic landscape during the EBV lytic cycle reactivation from lymphoblastoid cell lines (LCLs), RNA-seq was performed. By examining the transcriptomic changes, we obtained valuable insights into the molecular events and regulatory mechanisms involved in EBV reactivation into lytic cycle replication. The study also enhances our knowledge of the complex interplay between EBV and the host cells during its lytic cycle.
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Project description:Epstein-Barr virus (EBV) uses a biphasic lifecycle of latency and lytic reactivation to infect >95% of adults worldwide. Despite its central role in EBV persistence and oncogenesis, much remains unknown about how EBV latency is maintained. We used a human genome-wide CRISPR/Cas9 screen to identify that the nuclear protein SFPQ was critical for latency. SFPQ supported expression of linker histone H1, which stabilizes nucleosomes and regulates nuclear architecture, but has not been previously implicated in EBV gene regulation. H1 occupied latent EBV genomes, including the immediate early gene BZLF1 promoter. Upon reactivation, SFPQ was sequestered into sub-nuclear puncta, and EBV genomic H1 occupancy diminished. Enforced H1 expression blocked EBV reactivation upon SFPQ knockout, confirming it as necessary downstream of SFPQ. SFPQ knockout triggered reactivation of EBV in B and epithelial cells as well as in Kaposi’s Sarcoma Associated Herpesvirus, suggesting a conserved gamma-herpesvirus role. These findings highlight SFPQ as a major regulator of H1 expression and EBV latency.
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Project description:N6-methyladenosine (m6A) modification is one of the most abundant post-transcriptional modifications that plays an important role in many pathophysiological conditions including host-pathogen interactions. A number of viruses were previously shown to manipulate the cellular m6A machinery usurping its function to their benefit during the course of their life cycle. Previously, we reported that EBV reprograms the host m6A system to regulate the stability of the viral transcripts and drive viral-mediated tumorigenesis by hijacking the functions of methyltransferase METTL14. We now report that during lytic reactivation EBV targets the RNA methylation system of the host to attenuate the innate immune response by suppressing the interferon response to facilitate a successful lytic replication.
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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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Project description:Most humans are infected with Epstein-Barr virus (EBV), a cancer-causing virus. While EBV generally persists silently in B lymphocytes, periodic lytic (re-)activation of latent virus is central to its life cycle and to most EBV-related diseases. However, a substantial fraction of EBV-infected B cells and tumor cells in a population is refractory to lytic activation. This resistance to lytic activation directly and profoundly impacts viral persistence and effectiveness of oncolytic therapy for EBV+ cancers. To identify the mechanisms that underlie susceptibility to EBV-lytic activation, we used host protein-expression profiling of separated-lytic and -refractory cells.
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Project description:Most humans are infected with Epstein-Barr virus (EBV), a cancer-causing virus. While EBV generally persists silently in B lymphocytes, periodic lytic (re-)activation of latent virus is central to its life cycle and to most EBV-related diseases. However, a substantial fraction of EBV-infected B cells and tumor cells in a population is refractory to lytic activation. This resistance to lytic activation directly and profoundly impacts viral persistence and effectiveness of oncolytic therapy for EBV+ cancers. To identify the mechanisms that underlie susceptibility to EBV-lytic activation, we used host protein-expression profiling of separated-lytic and -refractory cells.
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Project description:As a human tumor virus, EBV is present as a latent infection in its associated malignancies where genetic and epigenetic changes have been shown to impede cellular differentiation and viral reactivation. One such change is increased levels of the Wnt signaling effector, lymphoid enhancer binding factor 1 (LEF1) following EBV epithelial infection. In silico analysis of EBV type 1 and 2 genomes identified over 20 Wnt-response elements suggesting that LEF1 may directly bind the EBV genome and regulate the viral life cycle. Using CUT&RUN-seq, LEF1 was shown to bind the latent EBV genome at various sites encoding viral lytic products that included the immediate early transactivator BZLF1 and viral primase BSLF1 genes. SiRNA depletion of specific LEF1 isoforms revealed that the alternative-promoter derived isoform with an N-terminal truncation (∆N LEF1) transcriptionally repressed lytic genes associated with LEF1 binding. Furthermore, forced expression of the ∆N LEF1 isoform antagonized EBV reactivation from latency. The LEF1 mediated repression requires histone deacetylase activity through either recruitment or a direct intrinsic histone deacetylase activity. SiRNA depletion of LEF1 resulted in increased histone 3 lysine 9 and lysine 27 acetylation at LEF1 binding sites and across the EBV genome. These results support a novel role for LEF1 in maintaining EBV latency and restriction viral reactivation via repressive chromatin remodeling of critical lytic cycle factors
2023-12-05 | GSE245534 | GEO
Project description:Epstein-Barr virus (EBV) has a lifelong latency period after initial infection. Rarely, however, when the EBV immediate early gene BZLF1 is expressed by a specific stimulus, the virus switches to the lytic cycle to produce progeny viruses. We found that EBV infection reduced levels of various ceramide species in gastric cancer cells. As ceramide is a bioactive lipid implicated in the infection of various viruses, we assessed the effect of ceramide on the EBV lytic cycle. Treatment with C6-ceramide (C6-Cer) induced an increase in the endogenous ceramide pool and increased production of the viral product as well as BZLF1 expression. Treatment with the ceramidase inhibitor ceranib-2 induced EBV lytic replication with an increase in the endogenous ceramide pool. The glucosylceramide synthase inhibitor Genz-123346 inhibited C6-Cer-induced lytic replication. C6-Cer induced ERK1/2 and CREB phosphorylation, c-JUN expression, and accumulation of the autophagosome marker LC3B. Treatment with MEK1/2 inhibitor U0126 or autophagy initiation inhibitor 3-MA suppressed C6-Cer-induced EBV lytic replication. In contrast, the autophagosome-lysosome fusion inhibitor chloroquine induced BZLF1 expression. Transfection with siCREB reduced ERK1/2 phosphorylation and C6-Cer-induced BZLF1 expression. On the other hand, siJUN transfection did not affect BZLF1 expression. Our results show that increased endogenous ceramide and glycosyl ceramide (GlyCer) following C6-Cer treatment induce EBV lytic replication in gastric cancer cells via ERK1/2 and CREB phosphorylation and autophagosome accumulation.
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Project description:The Nucleic Acid Binding Protein SFPQ Represses EBV Lytic Reactivation by Promoting Histone H1 Expression
| PRJNA985633 | ENA
Project description:We proposed that the frequency of EBV reactivation may be crucial for its pathogenic role and highly recurrent EBV reactivations exert a profound influence on genome instability. Recurrent reactivations were induced in the EBV-latently infected NPC cells (NA cells) by treating with 12-o-tetradecanoylphorbol-13-acetate (TPA) and sodium n-butyrate (SB) once per passage periodically. Genome-wild oligoarray-based comparative genomic hybridization (CGH) technology was applied to investigate the copy-number aberrations in response for different frequencies of EBV reactivation. The results showed that the NR15 cells, NA cells with the highest frequency (15 times) of reactivation, exhibit extensive genomic copy-number alterations (CNAs) mostly involving chromosome 3p, 3q, 8p, 8q, 9p and 9q, whereas limited number of CNAs were observed both in NR1 cells where only the initial reactivation take place and NP15 cells which were culture in parallel with NR15 cells without EBV-reactivation. We concluded that it is the highly recurrent reactivations of EBV, but neither just a primary reactivation nor EBV-latent infection, may intimately involve in carcinogenesis of nasopharyngeal epithelial cells with the progressive genome instabilities and the accumulation of genetic mutations. Keywords: array-based comparative genomic hybridization, reactivation of EBV, incidence, frequency, recurrent, genome instability, copy-number alterations, carcinogenesis, and nasopharyngeal carcinoma (NPC).
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