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KSHV uses viral IL6 to expand infected immunosuppressive macrophages (RNA-seq)

ABSTRACT: KSHV uses viral IL6 to expand infected immunosuppressive macrophages (RNA-seq)

PROVIDER: PRJNA943494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23821577_1.fastq.gz	Fastqsanger.gz
	SRR23821577_2.fastq.gz	Fastqsanger.gz
	SRR23821578_1.fastq.gz	Fastqsanger.gz
	SRR23821578_2.fastq.gz	Fastqsanger.gz
	SRR23821579_1.fastq.gz	Fastqsanger.gz

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KSHV uses viral IL6 to expand infected immunosuppressive macrophages

Project description:KSHV uses viral IL6 to expand infected immunosuppressive macrophages

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KSHV uses viral IL6 to expand infected immunosuppressive macrophages (scRNA-seq)

Project description:KSHV uses viral IL6 to expand infected immunosuppressive macrophages (scRNA-seq)

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KSHV uses viral IL6 to expand infected immunosuppressive macrophages (scRNA-seq)

Project description:Kaposi’s sarcoma-associated herpesvirus (KSHV) is an oncogenic double-stranded DNA virus and the etiologic agent of Kaposi’s sarcoma and hyperinflammatory lymphoproliferative disorders. Understanding the mechanism by which KSHV increases infected cell populations is crucial for curing KSHV-associated diseases. Here, we demonstrate that KSHV preferentially infects CD14+ monocytes and sustains viral replication through the viral interleukin-6 (vIL-6)-mediated activation of STAT1 and 3. Using vIL6-sufficient and vIL6-deficient recombinant KSHV, we demonstrated that vIL6 plays a critical role in promoting the proliferation and differentiation of KSHV-infected monocytes into macrophages. The macrophages derived from vIL6-sufficient (wild type) KSHV infection showed a distinct transcriptional profile of elevated IFN-pathway activation with immune suppression and were compromised in T-cell stimulation function compared to those from vIL6-deficient KSHV infection or uninfected control. These results highlight a clever strategy, in which KSHV utilizes vIL6 to secure its initial viral pool by expanding infected dysfunctional macrophages. This mechanism also facilitates KSHV to escape from host immune surveillance and to establish a lifelong infection.

2023-08-30 | GSE227166 | GEO

KSHV uses viral IL6 to expand infected immunosuppressive macrophages (RNA-seq)

2023-08-30 | GSE227163 | GEO

KSHV uses viral IL6 to expand infected immunosuppressive macrophages

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-30 | GSE227167 | GEO

MDMs Solvent, AA, IL6, AA+IL6

Project description:MDMs Solvent, AA, IL6, AA+IL6

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ac4C-seq of cellular and KSHV transcripts in iSLK-Puro, iSLK-KSHV (i.e. iSLK-RGB), iSLK-KSHV (WT), iSLK-KSHV (ΔNAT10) cells

Project description:We used ac4C-seq to detedc cellular and KSHV transcripts in iSLK-Puro, iSLK-KSHV, iSLK-KSHV (WT), iSLK-KSHV (ΔNAT10) cells after after doxycycline and sodium butyrate treatment.

2023-09-27 | GSE174161 | GEO

Lactylation of NAT10 promotes N4‐acetylcytidine modification on tRNASer-CGA-1-1 to boost oncogenic DNA virus KSHV reactivation

Project description:N4-acetylcytidine (ac4C), a conserved but recently rediscovered RNA modification on tRNAs, rRNAs and mRNAs, is catalyzed by N-acetyltransferase 10 (NAT10). Lysine acylation is a ubiquitous protein modification that controls protein functions. Our latest study demonstrates a NAT10-dependent ac4C modification, which occurs on the polyadenylated nuclear RNA (PAN) encoded by oncogenic DNA virus Kaposi's sarcoma-associated herpesvirus (KSHV), can induce KSHV reactivation from latency and activate inflammasome. However, it remains unclear whether a novel lysine acylation occurs in NAT10 during KSHV reactivation and how this acylation of NAT10 regulates tRNAs ac4C modification. Here, we showed that NAT10 was lactylated by α-tubulin acetyltransferase 1 (ATAT1), as a writer at the critical domain, to exert RNA acetyltransferase function and thus increase the ac4C level of tRNASer-CGA-1-1. Mutagenesis at the ac4C site in tRNASer-CGA-1-1 inhibited its ac4C modifications, translation efficiency of viral lytic genes, and virion production. Mechanistically, KSHV PAN orchestrated NAT10 and ATAT1 to enhance NAT10 lactylation, resulting in tRNASer-CGA-1-1 ac4C modification, eventually boosting KSHV reactivation. Our findings reveal a novel post-translational modification in NAT10, as well as expand the understanding about tRNA-related ac4C modification during KSHV replication, which may be exploited to design therapeutic strategies for KSHV-related diseases.

2024-04-26 | PXD049447 |

KSHV-infected invasive bladder cancer cell: Control vs. KSHV-infected

Project description:Transcriptional profiling of bladder cancer cell lines comparing control uninfected cells with KSHV-infected cells. Transcriptional profiling of bladder cancer cell lines comparing control uninfected cells with KSHV-infected cells.

2015-03-10 | E-GEOD-66682 | biostudies-arrayexpress

Oncolytic reactivation of KSHV as a therapeutic approach for primary effusion lymphoma: high-resolution mapping of BRD4 binding sites in the KSHV genome

Project description:Primary effusion lymphoma (PEL) is an aggressive subtype of non-Hodgkin lymphoma caused by Kaposi's sarcoma-associated herpesvirus (KSHV) infection. Currently, treatment options for patients with PEL are limited. Oncolytic viruses have been engineered as anticancer agents and have recently shown increased therapeutic promise. Similarly, lytic activation of endogenous viruses from latently infected tumor cells can also be applied as a cancer therapy. In theory, such a therapeutic strategy would induce oncolysis by viral replication, while simultaneously stimulating an immune response to viral lytic cycle antigens. We examined the combination of the FDA-approved drug ingenol-3-angelate (PEP005) with epigenetic drugs as a rational therapeutic approach for KSHV-mediated malignancies. JQ1, a bromodomain and extra terminal (BET) protein inhibitor, in combination with PEP005, not only robustly induced KSHV lytic replication, but also inhibited IL6 production from PEL cells. Using the dosages of these agents that was found to be effective in reactivating HIV (as a means to clear latent virus with highly active antiretroviral therapy), we were able to inhibit PEL growth in vitro and delay tumor growth in a PEL xenograft tumor model. KSHV reactivation was mediated by activation of NF-kB pathway by PEP005, which led to increased occupancy of RNA polymerase II onto the KSHV 33 genome. RNA-sequencing analysis further revealed cellular targets of PEP005, JQ1, and the synergistic effects of both. Thus, combination of PEP005 with a BET inhibitor may be considered as a rational therapeutic approach for the treatment of PEL.

2017-10-24 | GSE103395 | GEO

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