Epigenetic reprogramming of Kaposi’s sarcoma-associated herpesvirus during hypoxic reactivation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA836908 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21091450.fastq.gz | Fastqsanger.gz | |||
| SRR21091451.fastq.gz | Fastqsanger.gz | |||
| SRR21091452.fastq.gz | Fastqsanger.gz | |||
| SRR21091453.fastq.gz | Fastqsanger.gz | |||
| SRR21091454.fastq.gz | Fastqsanger.gz |
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Project description:Chromatin Immuno-precipitaion sequencing was performed using H3-Ac, H3K4Me3, H3K9Me3, H3K27Me3, LANA, RTA and DNA Polymerase 1 alpha antibodies to investigate its enrichment on Kaposi's sarcoma associated herpesvirus (KSHV) genome in BC3 cells under normoxic or hypoxic conditions
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Project description:Herpesviruses are frequently co-present with bacterial infection at multiple sites within the body, including the mouth, gut, and genitourinary tract. The detection of replicating virus in these compartments prompted investigation into the relationship between bacterial infection and Kaposi’s Sarcoma-associated Herpesvirus (KSHV) reactivation. Using a cell line latently infected with KSHV, we examined the ability of crude spent media containing metabolic products from periodontal and gut pathogens to reactivate KSHV. Upon incubation with crude spent media, KSHV was reactivated and we detected the up-regulation of viral early and late genes, linear viral genomes, and virions. Furthermore, KSHV reactivation was associated with global increases in histone H3 and histone H4 acetylation, consistent with viral expression. To explore the transcriptional consequences of spent media, we compared the gene expression changes following reactivation by P. gingivalis spent medium to those of two well-established pharmacological activators of KSHV reactivation, tetradecanolyl phorbol acetate and sodium butyrate. Microarray analyses revealed a unique gene expression signature with P. gingivalis-associated reactivation. Concurrent with KSHV reactivation, P. gingivalis spent medium increased the hypoxia response. Hypoxia was associated with effects on epigenetic regulators, including down-regulation of UHRF1, a modulator of DNA methylation. Our findings demonstrate that products secreted by oral bacteria not only stimulate a hypoxia response, but also result in global changes in epigenetic modifications and modifiers. These findings suggest that epigenetic changes induced by P. gingivalis underlie the KSHV reactivation pathway.
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Project description:Kaposi’s Sarcoma-associated Herpesvirus Viral Protein Kinase Augments Cell Survival
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Project description:Epstein-Barr virus (EBV) Rta is a latent-lytic molecular switch evolutionarily conserved in all gamma-herpesviruses. In previous studies, doxycycline-inducible Rta was shown to potently produce an irreversible G1 arrest followed by cellular senescence in 293 cells. Here, we demonstrate that in this system the inducible Rta not only reactivates resident genome of EBV but also that of Kaposi’s sarcoma-associated herpesvirus (KSHV), to similar efficiency. However, Rta-induced senescence program was terminated by the robust viral lytic cycle replication that eventually caused cell death. Furthermore, prior to the abrupt expression of immediate-early protein (EBV BZLF1 or KSHV RTA), Rta simultaneously down-regulates cell cycle activators (c-Myc, CDK6, CCND2) and up-regulates senescence-related genes (p21, 14-3-3s). Since Rta is a viral immediate-early transcriptional activator, it is envisioned that during the initial stage of viral reactivation, Rta may engage to modulate the host transcriptome, to halt cell cycle progression, and to maintain an ideal environment for manufacturing infectious virions. Refer to individual Series. This SuperSeries is composed of the following subset Series: GSE24585: Expression profiling of host genes modulated by Epstein-Barr virus (EBV) Rta in HEK293 cells GSE24586: Expression profiling of host genes modulated by Epstein-Barr virus Rta in nasopharyngeal carcinoma cells
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Project description:Kaposi’s Sarcoma (KS) is a heterogenous, multifocal vascular malignancy caused by the human herpesvirus 8 (HHV8), also known as Kaposi’s Sarcoma-Associated Herpesvirus (KSHV). Here, we show that KS lesions express iNOS/NOS2 broadly throughout KS lesions, with enrichment in LANA positive spindle cells. The iNOS byproduct 3-nitrotyrosine is also enriched in LANA positive tumor cells and colocalizes with a fraction of LANA-nuclear bodies. We show that iNOS is highly expressed in the L1T3 tumor model of KS. iNOS expression correlated with KSHV lytic cycle gene expression, which was elevated in late-stage tumors (>4 weeks) but to a lesser degree in early stage (1 week) xenografts. Further, we show that L1T3 tumor growth is sensitive to an inhibitor of nitric oxide, L-NMMA. These finding suggest that iNOS is expressed in KSHV infected endothelial-transformed tumor cells in KS, that iNOS expression depends on tumor microenvironment stress conditions, and that iNOS enzymatic activity contributes to KS tumor growth.
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Project description:Kaposi’s Sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi’s sarcoma, which is the most common cancer in acquired immune deficiency syndrome patients. Because KSHV has many viral proteins modulate many response, However, various effects by extracellular vesicles (EVs) during de novo KSHV infection has not been investigated to our best knowledge. We used microarrays to detail of gene expression underlying EV treatment and identified the up-regulated genes during treatment.
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Project description:Kaposi’s sarcoma-associated herpesvirus induces specialized ribosomes to efficiently translate viral lytic mRNAs
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Project description:Historically, ribosomes have been viewed as unchanged homogeneous macromolecular machines with no intrinsic regulatory capacity for mRNA translation. However, an emerging concept is that heterogeneity of ribosomal composition exists, which can exert a regulatory function or specificity in translational control. This is supported by recent discoveries identifying compositionally distinct ‘specialised ribosomes’ that actively regulate mRNA translation. Viruses lack their own translational machinery and impose a high translational demand on the host cell during replication. Here we explore the possibility that Kaposi’s sarcoma-associated herpesvirus (KSHV) can manipulate host ribosome biogenesis during infection to produce specialised ribosomes which preferentially translate viral transcripts. Quantitative proteomic analysis has identified changes in the stoichiometry and composition of precursor ribosomal complexes during the switch from latent to lytic KSHV replication. Intriguingly, we demonstrate the enhanced association of ribosomal biogenesis factors BUD23 and NOC4L, and a previously uncharacterised KSHV lytic protein, ORF11, with small ribosomal subunit precursor complexes during lytic KSHV infection. Notably, BUD23 depletion resulted in significantly reduced viral gene expression and progression through the lytic cascade, culminating in a dramatic reduction of infectious virion production. Importantly, ribosome profiling demonstrated that BUD23 is essential for the reduced association of ribosomes with KSHV uORFs in late lytic genes, required for the efficient translation of the main open reading frame. Together our results provide new mechanistic insights into KSHV-mediated manipulation of cellular ribosome composition inducing a population of specialised ribosomes to facilitate efficient translation of viral mRNAs.
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Project description:Epstein-Barr virus (EBV) Rta is a latent-lytic molecular switch evolutionarily conserved in all gamma-herpesviruses. In previous studies, doxycycline-inducible Rta was shown to potently produce an irreversible G1 arrest followed by cellular senescence in 293 cells. Here, we demonstrate that in this system the inducible Rta not only reactivates resident genome of EBV but also that of Kaposi’s sarcoma-associated herpesvirus (KSHV), to similar efficiency. However, Rta-induced senescence program was terminated by the robust viral lytic cycle replication that eventually caused cell death. Furthermore, prior to the abrupt expression of immediate-early protein (EBV BZLF1 or KSHV RTA), Rta simultaneously down-regulates cell cycle activators (c-Myc, CDK6, CCND2) and up-regulates senescence-related genes (p21, 14-3-3s). Since Rta is a viral immediate-early transcriptional activator, it is envisioned that during the initial stage of viral reactivation, Rta may engage to modulate the host transcriptome, to halt cell cycle progression, and to maintain an ideal environment for manufacturing infectious virions. This SuperSeries is composed of the SubSeries listed below.
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