Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA314765 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3213394_1.fastq.gz | Fastqsanger.gz | |||
| SRR3213394_2.fastq.gz | Fastqsanger.gz | |||
| SRR3213395_1.fastq.gz | Fastqsanger.gz | |||
| SRR3213395_2.fastq.gz | Fastqsanger.gz | |||
| SRR3213396_1.fastq.gz | Fastqsanger.gz |
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Project description:KSHV Infection Mimics the Hypoxic Response Based on Next-Generation Sequencing [miRNA-Seq]
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Project description:Purpose: Kaposi’s sarcoma associated-herpesvirus (KSHV) causes several hyperproliferative disorders, including Kaposi’s sarcoma, primary effusion lymphoma and multicentric Castleman’s disease. KSHV encodes for a number of microRNAs (miRNAs), and KSHV infection can affect the expression of cellular miRNAs. Hypoxia has been shown to induce KSHV reactivation, directly induce several KSHV lytic genes, and also induce the most abundant latent viral protein, LANA. Also, several KSHV proteins can stabilize and increase the cellular levels of hypoxia-inducible factor (HIF-1α). However, the degree to which hypoxic pathways are utilized by KSHV has yet to be determined. Methods: We investigated the interplay between hypoxia and KSHV infection by comparing the 31effects of hypoxia and KSHV infection on miRNA and mRNA expression, and by examining the 32effects of hypoxia on uninfected and KSHV-infected cells. This was accomplished using next-33generation sequencing (NGS), qRT-PCR, Taqman assays, and pathway analysis. Results: NGS analysis of human mRNAs revealed striking similarities (~34%) between the transcriptomic response to hypoxia and the transcriptomic response to KSHV infection. Additionally, hsa-miR-210, a key hypoxia-inducible miRNA with pro-angiogenic and anti-apoptotic properties, was found significantly up-regulated by both KSHV infection and hypoxia using Taqman assays. Finally, KSHV infected cells differed somewhat in their response to hypoxia compared to KSHV-uninfected controls. Conclusions: These results demonstrate that KSHV harnesses a part of the hypoxic cellular response and induces miR-210 up-regulation. The understanding of how these miRNAs, genes and pathways are regulated by HIF-1α and KSHV infection are essential to a better understanding of the biology of KSHV-associated diseases.
2016-12-21 | GSE79029 | GEO
Project description:Purpose: Kaposi’s sarcoma associated-herpesvirus (KSHV) causes several hyperproliferative disorders, including Kaposi’s sarcoma, primary effusion lymphoma and multicentric Castleman’s disease. KSHV encodes for a number of microRNAs (miRNAs), and KSHV infection can affect the expression of cellular miRNAs. Hypoxia has been shown to induce KSHV reactivation, directly induce several KSHV lytic genes, and also induce the most abundant latent viral protein, LANA. Also, several KSHV proteins can stabilize and increase the cellular levels of hypoxia-inducible factor (HIF-1α). However, the degree to which hypoxic pathways are utilized by KSHV has yet to be determined. Methods: We investigated the interplay between hypoxia and KSHV infection by comparing the 31effects of hypoxia and KSHV infection on miRNA and mRNA expression, and by examining the 32effects of hypoxia on uninfected and KSHV-infected cells. This was accomplished using next-33generation sequencing (NGS), qRT-PCR, Taqman assays, and pathway analysis. Results: NGS analysis of human mRNAs revealed striking similarities (~34%) between the transcriptomic response to hypoxia and the transcriptomic response to KSHV infection. Additionally, hsa-miR-210, a key hypoxia-inducible miRNA with pro-angiogenic and anti-apoptotic properties, was found significantly up-regulated by both KSHV infection and hypoxia using Taqman assays. Finally, KSHV infected cells differed somewhat in their response to hypoxia compared to KSHV-uninfected controls. Conclusions: These results demonstrate that KSHV harnesses a part of the hypoxic cellular response and induces miR-210 up-regulation. The understanding of how these miRNAs, genes and pathways are regulated by HIF-1α and KSHV infection are essential to a better understanding of the biology of KSHV-associated diseases.
2016-12-21 | GSE79030 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are using transcriptome profiling (RNA-seq) to evaluate the effects of EBV infection or (and) EBV BART6-3p mimics on the global transcriptome of the BJAB cells. Methods: BJAB cells were transfected with negative control mimics or BART6-3p mimics for 48 h and then infected with EBV virons for 2h. RNAs were extracted by Trizol and sequenced by Solexa high-throughput sequencing service (Oebiotech, Shanghai, China). Data were extracted and normalized according to the manufacturer’s standard protocol. Results: Log-fold changes of up- or down-regulated mRNAs between the control and experiment group were selected with a significance threshold of p<0.05. There are 408 mRNAs were up-regulated and 263 were down-regulated in “EBV infection” group cells comparing to “Mock” group cells. There are 385 mRNAs were up-regulated and 246 were down-regulated in “EBV infection + Bart6-3p mimics” group cells comparing to “EBV infection + negative control mimics” group cells. Conclusions: Our study describes the global transciptome changes of BJAB cells induced by EBV infection or (and) EBV 6-3p mimics.
2018-07-01 | GSE95634 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are using mRNA and microRNA sequencing analysis to evaluate the effects of EBV-encoded microRNA BART2-5p mimics on the mRNA and microRNA profiles of human nasopharyngeal carcinoma cell line 6-10B. Methods: 6-10B cells were transfected with either EBV microRNA BART2-5p mimics or negative control (NC) mimics for 48 hours. Cellular RNA was then sequenced at the mRNA and microRNA levels using illumina high-throughput sequencing service (Oebiotech, Shanghai, China). Data were extracted and normalized according to the manufacturer's standard protocol. Results: Log-fold changes of up- or down-regulated mRNAs and microRNAs between the control and experiment group were selected with a significance threshold of p<0.05. Conclusions: Our study describes the mRNA and microRNA alterations induced by EBV-miRNA-BART2-5p in 6-10B cells
2023-09-14 | GSE220166 | GEO
Project description:KaposiM-bM-^@M-^Ys sarcoma-associated herpesvirus (KSHV) is an oncogenic gammaherpesvirus which establishes latent infection in endothelial and B cells, as well as in primary effusion lymphoma (PEL). During latency, the viral genome exists as a circular DNA minichromosome (episome) and is packaged into chromatin analogous to human chromosomes. Only a small subset of promoters, those which drive latent RNAs, are active in latent episomes. In general, nucleosome depletion (M-bM-^@M-^\open chromatinM-bM-^@M-^]) is a hallmark of eukaryotic regulatory elements such as promoters and transcriptional enhancers or insulators. We applied formaldehyde-assisted isolation of regulatory elements (FAIRE) followed by next-generation sequencing to identify regulatory elements in the KSHV genome and integrated these data with previously identified locations of histone modifications, RNA polymerase II occupancy, and CTCF binding sites. We found that (i) regions of open chromatin were not restricted to the transcriptionally defined latent loci; (ii) open chromatin was adjacent to regions harboring activating histone modifications, even at transcriptionally inactive loci; and (iii) CTCF binding sites fell within regions of open chromatin with few exceptions, including the constitutive LANA promoter and the vIL6 promoter. FAIRE-identified nucleosome depletion was similar among B and endothelial cell lineages, suggesting a common viral genome architecture in all forms of latency. Ten total samples analyzed by FAIRE-seq from latent KSHV-infected cell lines. Two replicates were performed for BC1, KSHV-BJAB, KSHV-HUVEC, and L1-TIVE cells using the Illumina HiSeq 2000 platform. For BCBL1 cells, 1 FAIRE-seq sample and 1 non-cross-linked control BCBL1 sample was analyzed using the Illumina GAIIx
2013-09-05 | E-GEOD-50581 | biostudies-arrayexpress
Project description:The epitranscriptomic modification m6A is a ubiquitous feature of the mammalian transcriptome. It modulates mRNA fate and dynamics to exert regulatory control over numerous cellular processes and disease pathways, including viral infection. Kaposi’s sarcoma-associated herpesvirus (KSHV) reactivation from the latent phase leads to redistribution of m6A topology upon both viral and cellular mRNAs within infected cells. Here we investigate the role of m6A in cellular transcripts upregulated during KSHV lytic replication. Results show that m6A is crucial for the stability of the GPRC5A mRNA, whose expression is induced by the KSHV latent-lytic switch master regulator, the replication and transcription activator (RTA) protein. Moreover, we demonstrate that GPRC5A is essential for efficient KSHV lytic replication by directly regulating NFκB signalling. Overall, this work highlights the central importance of m6A in modulating cellular gene expression to influence viral infection.
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Project description:Next-Generation Sequencing Analysis Reveals Differential Expression Profiles of miRNA-mRNA Target Pairs in KSHV-Infected Cells [mRNA-Seq]
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Project description:Kaposi’s Sarcoma herpesvirus (KSHV), an oncogenic virus, modulates host cell signaling and metabolism to maintain latent infection. To unravel the underlying cellular mechanisms modulated by KSHV, we identified changes in the host proteome, phosphoproteome and transcriptome landscape upon KSHV infection of endothelial cells. A Steiner Forest algorithm was used to integrate proteomic, phosphoproteomic and transcriptomic data with transcriptome based predicted transcription factor activity to identify cellular networks altered by latent KSHV.
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