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Unknown,Transcriptomics,Genomics,Proteomics

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Cytokine interactome alterations promote oropharyngeal Epstien-barr virus (EBV) replication and shedding during HIV infection

ABSTRACT: Proteomic analysis of cytokines in unstimulated oropharyngeal secretions. Epstein-barr virus (EBV) is a type 1 carcinogen which causes many cancers in humans. Here we explored the cytokine involvement of the EBV replication process in the oropharynx. Cytokine interactomic profiles were geneerated to understand the involved signalling pathways in HIV infected group and the healthy group. Proteome profilers were used to understand the major cytokine expression levels that are related to infection and immune regulation. We analyzed unstimulated oropharyngeal samples (UOPS) from 42 healthy subjects and 72 HIV positive subjects using the R & D Proteome Profiler array panels. No techinical replicates were performed. 14 samples in HIV group without therapy (NHAART group); 58 HIV patients with highly active antiretroviral therapy (HAART group); 42 samples in healthy group

ORGANISM(S): Homo sapiens

SUBMITTER: R A P Perera

PROVIDER: E-GEOD-21339 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Cytokine interactome alterations promote oropharyngeal Epstien-barr virus (EBV) replication and shedding during HIV infection

Project description:Proteomic analysis of cytokines in unstimulated oropharyngeal secretions. Epstein-barr virus (EBV) is a type 1 carcinogen which causes many cancers in humans. Here we explored the cytokine involvement of the EBV replication process in the oropharynx. Cytokine interactomic profiles were geneerated to understand the involved signalling pathways in HIV infected group and the healthy group. Proteome profilers were used to understand the major cytokine expression levels that are related to infection and immune regulation.

2010-04-15 | GSE21339 | GEO

Salivary cytokine alterations in HIV infection

Project description:This SuperSeries is composed of the following subset Series: GSE24037: Salivary cytokine alterations in HIV infection part 1 GSE24064: Salivary cytokine alterations in HIV infection part 2 Refer to individual Series

2011-09-08 | E-GEOD-24411 | biostudies-arrayexpress

Salivary cytokine alterations in HIV infection part 2

Project description:A 507 protein microarray was employed to provide a broad view of cytokines and chemokines in saliva and plasma in acutely HIV infected subjects as compared to uninfected subjects. A 40 cytokine custom array derived from the initial results was refined to highlight those molecules with significant change relative to control subjects indicating the potential for biological impact. Systemic and local (oral mucosal) immune responses in acutely infected HIV individuals before the initiation of HAART have not been well characterized. Protein microarrays were used to analyze saliva and plasma from HIV infected and HIV uninfected subjects to identify new biomarkers for HIV disease progression and pathogenesis.

2011-09-08 | E-GEOD-24064 | biostudies-arrayexpress

Homo sapiens

Project description:Cytokine interactome alterations promote oropharyngeal Epstien-barr virus (EBV) replication and shedding during HIV infection

| PRJNA126155 | ENA

Integrated Copy Number Analysis of Epstein Barr Virus (EBV)-Positive Diffuse Large B-Cell Lymphoma (DLBCL)

Project description:Copy number analysis was performed on EBV+ DLBCL samples compared with EBV- DLBCL. We analyzed the genomic DNA from 18 cases of EBV+ DLBCL, 21 cases of EBV- DLBCL, and 13 cases of nonneoplastic tonsillar tissues using OncoScan FFPE Express 2.0 (MIP). No technical replication were done.

2014-02-01 | E-MTAB-1971 | biostudies-arrayexpress

Salivary cytokine alterations in HIV infection part 1

Project description:Systemic and local (oral mucosal) immune responses in acutely infected HIV individuals before the initiation of HAART have not been well characterized. Protein microarrays were used to analyze saliva and plasma from HIV infected and HIV uninfected subjects to identify new biomarkers for HIV disease progression and pathogenesis. A 507 protein microarray was employed to provide a broad view of cytokines and chemokines in saliva and plasma in acutely HIV infected subjects as compared to uninfected subjects. A custom array derived from the initial results was refined to highlight those molecules with significant change relative to control subjects indicating the potential for biological impact.

2011-09-08 | E-GEOD-24037 | biostudies-arrayexpress

CCR-5 using HIV-1 induces an anti-inflammatory profile in primary macrophages

Project description:Macrophages are important effector cells of the immune system and play an important role in mounting inflammatory responses. Macrophages can be activated by different stimuli in the tissue, either by cytokines produced by T helper cells (M1 or M2 polarization) or by the pathogens they encounter. Macrophages are also important target cells of HIV-1 and are preferentially infected by CCR5-using viruses. In this study, we investigated the ability of HIV-1 to induce changes in gene expression in unpolarized macrophages as well as in M1 or M2 polarized cells. We observed that CCR5-using HIV-1 regulates the expression of genes that are also regulated by IL-4 in macrophages. Genes regulated by HIV-1 infection and IL-4 polarization are involved in dampening pro-inflammatory responses in macrophages, which may facilitate HIV-1 to escape from detection by other immune cells. We also observed that changes in macrophage gene expression triggered by CCR5-using HIV-1 differed from those regulated by a CXCR4-using virus. This indicates that CCR5-using HIV-1 may be able to modulate macrophage gene expression to achieve successful replication. Our results provide insight in the complex interplay between HIV-1 and cells of the immune system. Polarized macrophages were obtained by stimulation of primary human monocytes with IFN-gamma (250 U/ml) in combination with TNF-alpha (12.5 ng/ml) (M1), IL-4 (50 ng/ml) (M2a), IL-10 (50 ng/ml) (M2c) for 5 days. Cells were inoculated for 24 hours with one of two HIV-1 strains (CCR5 or CXCR4 using HIV1) or their non replicating counterparts (heat inactivated virus). Macrophages that were not stimulated wiht cyokines or inoculates with HIV-1 were used as control. A total of 16 treatment conditions were tested in triplicate, for a total of 48 samples analysed.

2015-08-01 | E-GEOD-55029 | biostudies-arrayexpress

IL-27 Inhibits HIV-1 Infection in Human Macrophages by Down-regulating Host Factor SPTBN1 during Monocyte to Macrophage Differentiation

Project description:The susceptibility of macrophages to HIV-1 infection is modulated during monocyte differentiation. IL-27 is an anti-HIV cytokine that also modulates monocyte activation. Here, we present new evidence that IL-27 promotes monocyte differentiation into macrophages that are non-permissive for HIV-1 infection. While IL-27 treatment does not affect expression of macrophage differentiation markers or macrophage biological functions, it confers HIV resistance by down-regulating spectrin beta non-erythrocyte 1 (SPTBN1), a required host factor for HIV-1 infection. IL-27 down-regulates SPTBN1 through a TAK-1-mediated MAPK signaling pathway. Knockdown of SPTBN1 strongly inhibits HIV-1 infection of macrophages; conversely, overexpression of SPTBN1 markedly increases HIV susceptibility of IL-27 treated macrophages. Moreover, we demonstrate that SPTBN1 associates with HIV-1 gag proteins. Collectively, our results underscore the ability of IL-27 to protect macrophages from HIV-1 infection by down-regulating SPTBN1, thus indicating that SPTBN1 is an important host target to reduce HIV-1 replication in one major element of the viral reservoir. 2 samples with different treatments were analyzed. Genes with absolute fold change >= 5 were selected.

2013-01-18 | E-GEOD-43595 | biostudies-arrayexpress

Interaction between HIV-1 Tat and EBV Zta favours immune escape of B cells by downregulating HLA-ABC expression

Project description:Both Human immunodeficiency virus (HIV) and Epstein-Barr virus (EBV) are associated with an increased risk of malignancies. People living with HIV frequently have EBV reactivation and develop EBV-associated B-cell malignancies. In this study, we aimed to uncover the involvement of HIV-1 and EBV co-existence in the development of B-cell malignancies. We studied two viral transcriptional activators (HIV-1 Tat and EBV Zta) and their possible interaction since they both have cell-penetration domains and can be found simultaneously in the blood or cells of people with HIV. We found that Tat and Zta directly bound each other in human B cells, T cells, and blood serum. Using RNA-sequencing, we found that combined Tat and Zta action in B cells differed from a simple combination of two proteins. A subset of genes, activated by Tat or Zta alone, that trigger an immune response and antigen presentation in B cells, remained unchanged when two proteins were combined. B cells, treated or transfected with Tat and Zta, exhibited a substantial decrease in HLA-ABC (MHC class I) expression, a critical component of the antigen processing and presentation pathway. HLA-ABC downregulation induced by Tat and Zta interaction conferred protection against cytotoxic T cell recognition of EBV-infected B cells. Tat and Zta interaction was also observed in serum from an HIV-positive individual. To conclude, we demonstrated for the first time the direct interaction between HIV-1 Tat and EBV Zta; this interaction can bring about immune evasion of EBV-infected or transformed B cells.

2024-04-01 | GSE255092 | GEO

Treatment of CML CD34+ cells with EZH2 inhibitor GSK343

Project description:Transcriptional profiling by array of CML CD34+ cells to understand the response of chronic myeloid leukaemia stem cells to an EZH2 inhibitor, GSK343.

2016-11-01 | E-MTAB-2893 | biostudies-arrayexpress

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