Expression changes in cultured endothelial cells upon infection with HHV-8
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE27136 | GEO | 2011/08/01
SECONDARY ACCESSION(S): PRJNA137717
REPOSITORIES: GEO
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Project description:Tert-immortalized microvascular endothelial (TIME) cells are infected with human herpesvirus (HHV-8) or mocked infected to determine expression changes upon infection. Three samples to TIME cells are infected with HHV-8 and three samples are mock-infected.
2011-07-31 | E-GEOD-27136 | biostudies-arrayexpress
Project description:Roseolovirus, or human herpesvirus 6 (HHV-6) is a ubiquitous human pathogen infecting over 95% of the population by the age of two years. As with other herpesviruses, reactivation of HHV-6 can present with severe complications in immunocompromised individuals. Recent studies have highlighted the importance of herpesvirus-derived micro (mi)RNAs in modulating both cellular and viral gene expression. An initial report, which computed the likelihood of various viruses to encode for miRNAs, did not predict HHV-6 miRNAs. To experimentally screen for small HHV-6 encoded RNAs, we conducted large-scale sequencing of Sup-T-1 cells lytically infected with a laboratory strain of HHV-6B. This revealed an abundant 60-65 nucleotide RNA of unknown function derived from the lytic origin of replication (OriLyt) that gave rise to smaller RNA species of 18-19 nucleotides in length. In addition, we identified four pre-miRNAs, whose mature forms accumulated in Argonaute 2. In contrast to other beta-herpesviruses, HHV-6B miRNAs are expressed from direct repeat regions (DRL and DRR) located at either side of the genome. All miRNAs are conserved in the closely related HHV-6A variant, and one of them is a seed ortholog of the human miR-582-5p. Similar to alpha-herpesvirus miRNAs, they are expressed antisense to immediate early ORFs and thus have the potential to regulate key viral regulators. Small RNA sequencing from total RNA or Ago2 associated small RNAs extracted from HHV-6 infected Sup-T-1 cells
2012-01-01 | E-GEOD-34196 | biostudies-arrayexpress
Project description:Roseolovirus, or human herpesvirus 6 (HHV-6) is a ubiquitous human pathogen infecting over 95% of the population by the age of two years. As with other herpesviruses, reactivation of HHV-6 can present with severe complications in immunocompromised individuals. Recent studies have highlighted the importance of herpesvirus-derived micro (mi)RNAs in modulating both cellular and viral gene expression. An initial report, which computed the likelihood of various viruses to encode for miRNAs, did not predict HHV-6 miRNAs. To experimentally screen for small HHV-6 encoded RNAs, we conducted large-scale sequencing of Sup-T-1 cells lytically infected with a laboratory strain of HHV-6B. This revealed an abundant 60-65 nucleotide RNA of unknown function derived from the lytic origin of replication (OriLyt) that gave rise to smaller RNA species of 18-19 nucleotides in length. In addition, we identified four pre-miRNAs, whose mature forms accumulated in Argonaute 2. In contrast to other beta-herpesviruses, HHV-6B miRNAs are expressed from direct repeat regions (DRL and DRR) located at either side of the genome. All miRNAs are conserved in the closely related HHV-6A variant, and one of them is a seed ortholog of the human miR-582-5p. Similar to alpha-herpesvirus miRNAs, they are expressed antisense to immediate early ORFs and thus have the potential to regulate key viral regulators.
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Project description:Modulation of the transcriptome of human umbilical vein endothelial cells (HUVEC) by the anti-apoptotic protein vFLIP/K13 of human herpesvirus type-8 (HHV-8)
2008-11-14 | E-MEXP-1469 | biostudies-arrayexpress
Project description:Human herpesvirus-8 (HHV-8) is the causative agent of Kaposiâs sarcoma and is associated with the angioproliferative disorders primary effusion lymphoma (PEL) and multicentric Castlemanâs disease (MCD). We have previously described evidence of HHV-8 infection within the pulmonary vasculature of patients with idiopathic pulmonary arterial hypertension (IPAH). We speculated that viral infection of the pulmonary microvascular endothelial cells could cause the angioproliferative phenotype characteristic of severe pulmonary arterial hypertension (PAH). We now demonstrate the ability of HHV-8 to infect human pulmonary microvascular endothelial cells (HPMVECs) in vitro, confirming both latent and lytic infection. HHV-8 infection of HPMVECs resulted in significant changes of gene expression including alterations of pathways integral to both cellular apoptosis and angiogenesis. This infection also results in alterations of genes integral to the bone morphogenic protein (BMP) pathway, including down regulation of bone morphogenic protein receptor 1a (BMPR1a) and bone morphogenic protein 4 (BMP4). Other genes previously implicated in the development of PAH are also altered in expression by HHV-8 infection. These include increased expression of Interleukin-6 (IL-6) and the matrix metalloproteinases (MMP)-1, MMP-2 and MMP-10. Lastly, cells infected with HHV-8 apoptosis resistant. Infection of pulmonary microvascular endothelial cells with human herepesvirus-8 results in alteration of the BMP pathway as well as an anti-apoptotic phenotype, consistent with the development of plexiform lesions characteristic of pulmonary arterial hypertension. Experiment Overall Design: ⢠Direct comparison of HHV8-infected and mock-infected human pulmonary microvascular endothelial cells. Experiment Overall Design: ⢠Triplicate infection and mock infection samples were prepared. One hybridization per sample, 6 total hybridizations Experiment Overall Design: ⢠Single channel hybridization (no reference).
2008-06-14 | E-GEOD-6489 | biostudies-arrayexpress
Project description:HHV-6A is a human herpesvirus that integrates into human sub telomeric regions to acquire latency. This latent virus frequently reactivates causing numerous diseases. The project was aimed to understand changes in host cell prteomics upon virus reactivation, which might helpin understanding the pathophysiology of virus reactivation.
2020-04-07 | PXD016211 | Pride
Project description:Limited understanding of the immunopathogenesis of human herpesvirus 6B (HHV-6B) has prevented its acceptance as a pulmonary pathogen after hematopoietic cell transplantation (HCT). We conducted a prospective multicenter study of patients undergoing bronchoalveolar lavage (BAL) for pneumonia after allogeneic HCT. We tested blood and BAL fluid (BALF) for HHV-6B DNA and mRNA transcripts associated with lytic infection and performed RNA-seq on paired blood. Among 116 participants, HHV-6B DNA was detected in 37% of BALs, 49% of which had HHV-6B mRNA detection. We established an HHV-6B DNA threshold (≥2.3 log10copies/ml in BALF) that was highly predictive of HHV-6B mRNA detection and increased risk for death from respiratory failure (adjusted HR, 2.35; 95% CI, 1.08-5.11). Participants with HHV-6B DNA in BALF exhibited distinct host gene expression signatures, notable for enriched interferon signaling pathways in participants clinically diagnosed with idiopathic pneumonia. These data implicate HHV-6B as a pulmonary pathogen after allogeneic HCT.
2023-12-18 | GSE244210 | GEO
Project description:The immune response to viral infection represents complex network of dynamic gene and protein interactions. We present here the dynamic gene network of host immune response during human herpesvirus type 6 (HHV-6) infection in a adult T cell leukemia (ATL) cell line. Using a pathway-focused oligonucleotide DNA microarray, we found a possible association between chemokines genes regulating Th1/Th2 balance and genes regulating T-cell proliferation during HHV-6B infection. Keywords: Time course experiment
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Project description:To determine if HHV-6A infection affects cell metabolism of host cells, we conducted a global RNA sequencing analysis in HHV-6A infected cells
2020-05-05 | GSE149808 | GEO
Project description:In order to understand the effect of HHV-6A reactivation on host cell, U2-OS bone osteosarcoma cells were generated carrying latent HHV-6A genome. These cells were either treated with DMSO (solvent control) or Trichostatin-A (TSA) for viral reactivation. As a control cells carrying no HHV-6A were used and treated similarly. Two biological replicates of each sample were processed for small RNA transcriptomics (small RNAseq). Furthermore, HeLa (cervical epithelial cells) were generated carrying lentiviral insertions of one of the small non-coding RNA from HHV-6A (sncRNA-U14). These cells could be transiently induced for sncRNA-U14 transcription using Doxycycline. HeLa cells having a mock lentiviral backbone was used as a control and was treated similarly. Two biological replicates of each sample were processed for small RNA transcriptomics (small RNAseq).
2022-02-15 | GSE134215 | GEO