Homo sapiens
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PROVIDER: PRJNA314765 | ENA |
REPOSITORIES: ENA
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Project description:KSHV Infection Mimics the Hypoxic Response Based on Next-Generation Sequencing [miRNA-Seq]
| PRJNA314773 | ENA
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: 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: 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: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.
2023-07-20 | PXD039669 | Pride
Project description:Next-Generation Sequencing Analysis Reveals Differential Expression Profiles of miRNA-mRNA Target Pairs in KSHV-Infected Cells [mRNA-Seq]
| PRJNA265452 | ENA
Project description:Primary effusion lymphomas (PELs) are specifically associated with KSHV/HHV-8 infection, and most frequently occur in HIV-positive individuals as lymphomatous effusions in the serous cavities without a detectable solid tumor mass. Most PELs have concomitant EBV infection, suggesting that EBV is an important pathogenetic co-factor, although other as yet unidentified cofactors, such as cellular genetic alterations, are also likely to play a role. Lymphomatous effusions that lack KSHV also occur; these are frequently EBV-associated in the setting of HIV infection. Here we used gene expression profile analysis to determine the viral impact on cellular gene expression and the pathogenesis of these lymphomatous effusions. We used the Affymetrix HG-U133A microarray to analyze the gene expression profile of these effusion lymphomas (three virologic groups: KSHV-positive EBV-positive PELs, KSHV-positive EBV-negative PELs and KSHV-negative EBV-positive lymphomatous effusions). Nine cell lines derived from patients with lymphomatous effusions (three from each virologic group and each cell line was done in duplicates.) and three PEL patient samples were used in the study. Our results suggest that KSHV-positive PELs are very different from KSHV-negative lymphomatous effusions, and the genes that are differentially expressed include apoptosis regulators, cell cycle regulators, transcriptional factors and signal transduction regulators. KSHV clearly plays a dominant role in the phenotype of PEL. Within the KSHV-positive PELs, two subgroups can be identified, which were correlated with their EBV viral status. Among these genes (45 gene probes), four were regulators of the MAP kinase pathway that were up-regulated in the KSHV-positive, EBV-negative PELs, suggesting that in the absence of EBV, events that lead to the activation of the MAP kinase pathway may act as a cofactor for the development of PEL. Next we determined whether we could predict the viral status of the three primary patient cases of PEL based on the 45 gene probes that were differentially expressed in KSHV-positive cell lines according to EBV status (pt. 1: KSHV-positive, EBV-positive; Pt. 2: KSHV-positive, low proportion of EBV-positive; pt. 3: KSHV-positive EBV-negative), and we could.<br><br>Samples:<br>KSHV-positive EBV-positive cell lines: BC-1, BC-2, BC-5 <br>KSHV-positive EBV-negative cell lines: BC-3, BCBL-1, PEL-5 <br>KSHV-negative EBV-positive cell lines: IBL4, SM1, BCKN-1 <br>Patient 1: KSHV-positive, EBV-positive <br>Patient 2: KSHV-positive, EBV-positive (low number of positive cells) <br>Patient 3: KSHV-positive, EBV-negative.
2007-08-25 | E-GEOD-2149 | biostudies-arrayexpress
Project description:Transcriptional profiling of HUVECs transfected with KSHV miRNA mimics (vMix) or a negative control mimic (neg). To identify host RNA targets of KSHV miRNAs, we took advantage of the observation that RNAs targeted by miRNAs can display small reductions in their steady-state levels. Cells transfected with negative control miRNA compared to cells transfected with KSHV miRNAs. Experimental treatment versus control treatment
2014-09-01 | E-GEOD-43640 | biostudies-arrayexpress
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.
2017-02-08 | GSE84237 | GEO