MiRNA profiling of peripheral blood mononuclear cells from AIDS patients and healthy control group
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE140650 | GEO | 2021/11/10
REPOSITORIES: GEO
Similar Datasets
Project description:With the purpose of identifying the cascaded miRNA-mRNA regulatory relationships related to infection of HIV in gene level, we extracted mRNA from Peripheral blood mononuclear cells from 50 AIDS patients and 7 uninfected health controls. All AIDS patients in sample were received Antiretroviral Therapy. To further analysis the gene expression pattern in different virus load, we classified high virus loads (HVL, n=14) and low virus loads (LVL, n=16). 2635 and 2826 differentially expressed genes (DEGs) were selected, respectively in LVL and HVL. Functional enrichment analysis indicated DEGs which involved in immune response and apoptosis, played a crucial role in HIV infection. Further, we identified 5 most influential TFs to build miRNA-TF-mRNA regulatory network.
2021-11-10 | GSE140713 | GEO
Project description:The molecular pathogenesis of infection by HIV (human immunodeficiency virus) is extremely complex and is not clearly defined despite intensive research efforts. MiRNA as a class of regulators in cancer development can affect multiple gene pathways by targeting various mRNAs. Thus, studies aimed at transcription and regulation after antiviral treatment combined with beneficial researches related to miRNAs are required. With the purpose of identifying the cascaded miRNA-mRNA regulatory relationships related to infection of HIV in gene level, the parallel miRNA and mRNA expression profiles were analyzed in our study. The differential expressed miRNAs and mRNAs were selected primarily. The differentially regulated miRNA-mRNA interactions were further identified according to the Pearson correlation analysis of gene expression level. In our study, the calculation of the regulatory impact factors (RIF) was also conducted, and it revealed several essential regulators related to antiviral treatment with AIDS. To give a further insight into these TF (transcription factors) regulators, the co-expression gene modules were identified using a threshold-based hierarchical clustering method. Meanwhile, the regulatory network was generated during the computing process. Understanding these regulatory elements may bear significant implications on understanding the pathogenesis of AIDS occurrence.
2023-08-31 | GSE76246 | GEO
Project description:Kaposi's Sarcoma (KS) is a proliferation of aberrant vascular structures lined by spindle cells, and is caused by a gammaherpes virus (HHV8/KSHV). Its course is aggravated by co-infection with HIV-1, where the timing of infection with HIV-1 and HHV8 is important for the clinical outcome. METHODS: In order to better understand the pathogenesis of KS, we have analysed tissue from two AIDS-KS lesions, and from normal skin by serial analysis of gene expression (SAGE). Semi-quantitative RT-PCR was then used to validate the results. RESULTS: The expression profile of AIDS-related KS (AIDS-KS) reflects an active process in the skin. Transcripts of HHV8 were found to be very low, and HIV-1 mRNA was not detected by SAGE, although it could be found using RT-PCR. Comparing the expression profile of AIDS-KS tissue with publicly available SAGE libraries suggested that AIDS-KS mRNA levels are most similar to those in an artificially mixed library of endothelial cells and leukocytes, in line with the description of KS lesions as containing spindle cells with endothelial characteristics, and an inflammatory infiltrate. At least 64 transcripts were found to be significantly elevated, and 28 were statistically downregulated in AIDS-KS compared to normal skin. Five of the upregulated mRNAs, including Tie 1 and sialoadhesin/CD169, were confirmed by semi-quantitative PCR to be elevated in additional AIDS-KS biopsies. Antibodies to sialoadhesin/CD169, a known marker of activated macrophages, were shown to specifically label tumour macrophages. CONCLUSION: The expression profile of AIDS-KS showed 64 genes to be significantly upregulated, and 28 genes downregulated, compared with normal skin. One of the genes with increased expression was sialoadhesin (CD169). Antibodies to sialoadhesin/CD169 specifically labelled tumour-associated macrophages, suggesting that macrophages present in AIDS-KS lesions belong to a subset of human CD169+ macrophages. Keywords: other
2003-07-16 | GSE514 | GEO
Project description:Gene expression profiling (GEP) of ARL patient samples was done to determine whether gene expression signatures derived from HIV- lymphomas retained their ability to molecularly classify HIV+ lymphomas. The GEP-based predictors robustly classified ARL tumors, distinguishing molecular Burkitt lymphoma (BL) and diffuse large B-cell lymphoma (DLBCL), as well as activated B-cell-like (ABC) and germinal center B-cell-like (GCB) molecular subtypes of DLBCL. Gene expression profiles were used to identify coordinately regulated gene sets and pathways that differ between HIV+ and HIV- lymphomas of corresponding molecular subtype. Frozen tumor biopsies were obtained from 20 HIV-positive patients with an AIDS-defining lymphoma. Cases were ascertained at the University of Nebraska Medical Center and through the NCI AIDS and Cancer Specimen Resource tumor bank. Sufficient RNA for hybridization to Affymetrix U133 plus 2 arrays was obtained on 17 ARL cases. Details of all 20 HIV-positive patients can be found in the supplementary file linked below.
2010-03-07 | E-GEOD-17189 | biostudies-arrayexpress
Project description:Immunodeficiency dramatically increases susceptibility to cancer as a result of reduced immune surveillance and enhanced opportunities for virus-mediated oncogenesis. While AIDS-related lymphomas (ARLs) are frequently associated with known oncogenic viruses, many cases contain no known transforming virus. To discover novel transforming viruses, we profiled a set of ARL samples using whole transcriptome sequencing. We determined that Epstein-Barr virus (EBV) was the only virus detected in the tumor samples of this cohort, suggesting that if unidentified pathogens exist in this disease, they are present in fewer than 10% of cases or undetectable by our methods. To evaluate the role of EBV in ARL pathogenesis, we analyzed viral gene expression and found highly heterogeneous patterns of viral transcription across samples. We also found significant heterogeneity of viral antigen expression across a large cohort, with many patient samples presenting with restricted type I viral latency, indicating that EBV latency proteins are under increased immunosurveillance in the post-CART era. Furthermore, EBV infection of lymphoma cells in HIV-positive individuals was associated with a distinct host gene expression program. These findings provide insight into the joint host-virus regulatory network of primary ARL tumor samples and expand our understanding of virus-associated oncogenesis. Our findings may also have therapeutic implications, as treatment may be personalized to target specific viral and virus-associated host processes that are only present in a subset of patients. AIDS-related lymphoma samples were sequenced and analyzed by presnce/absence of EBV. ------------------------------------------------- Raw data not provided - IRB decided that consent form was not consistent with any disclosure of genotyping data, including through dbGaP. This an atypical and highly irregular dataset.
2015-04-11 | E-GEOD-67763 | biostudies-arrayexpress
Project description:This project will help us to have a more accurate and useful explanation at molecular level, of the damage caused by HIV when it infects the central nervous sythem (CNS) in Humans. CNS dysfunction is an important cause of morbidity and mortality in patients with human immunodeficiency virus-I (HIV-1) infection and the acquired immunodeficiency virus syndrome (AIDS). Minor cognitive/motor dysfunction (MCMD) and HIV-1-associated dementia (HAD) develop in the absence of opportunistic infections and lymphoma, cerebrovascular disease and metabolic disorders. Patients with HAD may or may not present an associated HIV encephalitis with viral replication limited to cells of monocyte origin. The inflammatory infiltrates of HIVE include activated microglia and perivascular and parenchymal monocytes, multinucleated giant cells and lymphocytes. In addition, HIVE may be accompanied by significant loss of neurons, presynaptic terminals and abnormal dendrites. To determine if altered expression of neuronal growth factor, chemokine and cell death genes identified possible mechanisms of brain injury in AIDS patients with and without HIVE; Changes of gene expression occurring in brain of AIDS patients with and without HIVE, induce development of brain atrophy, mild gliosis, enhanced vascular permeability, along with alterations in neuronal HIV-1 chemokine coreceptors. In the cases of HIVE more remarkable gene expression changes result in significant loss of neurons, presynaptic terminals and abnormal dendrites. All these changes can be evaluated by microarray gene expression analysis and validated by Q-RT-PCR; The procedure includes 10 steps: 1-Frontal Cortex dissection from fresh frozen autopsy human brain samples (fragments of 0.8-1 cm3 are used) 2-totalRNA extraction using RNeasy Maxi Kit and following hand book protocol; Quiagen Inc., 3-RNA quantity determination using the NanoDrop ND-1000 UV-Vis Spectrophotometer: Nanodrop-Technologies 4-RNA quality analyzed by ribosomal fractions 28s/18s ratio, using by Agilent RNA 6000 Assay Microchips: Agilent Technologies 5-mRNA suitability by RT-PCR test for housekeeping genes and genes of interest. 6-mRNA amplification and labeling in two steps: a-Generation of T7-conatining double stranded cDNA using T7-Poly-T Strategy (Invitrogen) b-mRNA amplification and labeling (aRNA) by in vitro transcription using T7 RNA polymerase, T7-cDNA as template and biotin-labeled ribonucleotides 7-Biotin-labeled aRNA quantity assess, as in step 3 8-Biotin-labeled aRNA determination by amplified RNA electropherogram. Agilent RNA 6000 Assay Microchips: Agilent Technologies 9-Biotin-labeled aRNA fractionation, hybridization onto HG-95aVer2 oligonucleotide array and scanning, using Affymetrix platform: Affymetrix 10-Statistical gene expression analysis: Using GeneSpring Software (Slicon Gnetics) a-Normalization to the 50th percentile and per gene to specific control samples, using 'Disease vs. Normal' as the main parameter. b-Fold of expression filter (2 folds cutoff) using signal data in ratio mode interpretation c-Welch t-test, with p< 0.05 for significance, using log of ratio mode interpretation d-Differentially expressed genes clustering by K-means, experiment and gene trees e-Differentially expressed genes analysis and classes classification by Gene Ontology and GeneMapp pathways
2008-06-13 | E-GEOD-4755 | biostudies-arrayexpress
Project description:Gene expression profiling (GEP) of ARL patient samples was done to determine whether gene expression signatures derived from HIV- lymphomas retained their ability to molecularly classify HIV+ lymphomas. The GEP-based predictors robustly classified ARL tumors, distinguishing molecular Burkitt lymphoma (BL) and diffuse large B-cell lymphoma (DLBCL), as well as activated B-cell-like (ABC) and germinal center B-cell-like (GCB) molecular subtypes of DLBCL. Gene expression profiles were used to identify coordinately regulated gene sets and pathways that differ between HIV+ and HIV- lymphomas of corresponding molecular subtype. Frozen tumor biopsies were obtained from 20 HIV-positive patients with an AIDS-defining lymphoma. Cases were ascertained at the University of Nebraska Medical Center and through the NCI AIDS and Cancer Specimen Resource tumor bank. Sufficient RNA for hybridization to Affymetrix U133 plus 2 arrays was obtained on 17 ARL cases. Details of all 20 HIV-positive patients can be found in the supplementary file below. Third party array data from HIV- lymphomas of corresponding molecular subtype were used for the comparison and molecular classification of the HIV+ cases in this study. The third party HIV- lymphoma samples include the following. [1] HIV- lymphoma, BL cases: 84 samples profiled on the Affymetrix HG U133 Plus 2 array. The data are publicly available on the website companion to Dave et al. NEJM 2006; Volume 354:13-24 (http://llmpp.nih.gov/BL/) and were used 'as is' (ie, not reanalyzed). [2] HIV- lymphoma, DLBCL cases: 200 of the 414 cases in Series GSE10846 (listed in the supplementary file below). These included all R-CHOP treated cases of either ABC or GCB subtype. These data were also used as is. These data were published in Lenz et al. NEJM 2008; Volume 359: 2313-2323.
2012-07-17 | E-GEOD-17372 | biostudies-arrayexpress
Project description:HIV â??controllersâ?? are individuals infected with the human immunodeficiency virus, type I (HIV) who maintain long-term control of viremia without antiviral therapy and who usually do not develop the acquired immune deficiency syndrome (AIDS). In this study, we have used oligonucleotide expression arrays to characterize the mucosal immune responses of these subjects in relation to untreated HIV+ individuals with high viral loads and progressive disease (â??non-controllersâ??). Recto-sigmoid biopsies were analyzed from 9 controllers and 11 non-controllers. All of the genes identified to be significantly different were more highly expressed in the non-controllers. Many of these genes are involved in immunity and defence. These results underscore the importance of the sustained inflammatory response that attends progressive HIV disease. Keywords: Recto-sigmoid biopsy profiles from HIV infected individuals We analyzed a series of 20 HEEBO arrays on which were hybed RNA amplified from the recto-sigmoid biopsies of HIV infected individuals that either have progressive disease or can maintain long term control of viremia.
2010-10-08 | E-GEOD-20075 | biostudies-arrayexpress
Project description:HIV “controllers” are individuals infected with the human immunodeficiency virus, type I (HIV) who maintain long-term control of viremia without antiviral therapy and who usually do not develop the acquired immune deficiency syndrome (AIDS). In this study, we have used oligonucleotide expression arrays to characterize the mucosal immune responses of these subjects in relation to untreated HIV+ individuals with high viral loads and progressive disease (“non-controllers”). Recto-sigmoid biopsies were analyzed from 9 controllers and 11 non-controllers. All of the genes identified to be significantly different were more highly expressed in the non-controllers. Many of these genes are involved in immunity and defence. These results underscore the importance of the sustained inflammatory response that attends progressive HIV disease. Keywords: Recto-sigmoid biopsy profiles from HIV infected individuals
2010-02-02 | GSE20075 | GEO
Project description:Immunodeficiency dramatically increases susceptibility to cancer as a result of reduced immune surveillance and enhanced opportunities for virus-mediated oncogenesis. While AIDS-related lymphomas (ARLs) are frequently associated with known oncogenic viruses, many cases contain no known transforming virus. To discover novel transforming viruses, we profiled a set of ARL samples using whole transcriptome sequencing. We determined that Epstein-Barr virus (EBV) was the only virus detected in the tumor samples of this cohort, suggesting that if unidentified pathogens exist in this disease, they are present in fewer than 10% of cases or undetectable by our methods. To evaluate the role of EBV in ARL pathogenesis, we analyzed viral gene expression and found highly heterogeneous patterns of viral transcription across samples. We also found significant heterogeneity of viral antigen expression across a large cohort, with many patient samples presenting with restricted type I viral latency, indicating that EBV latency proteins are under increased immunosurveillance in the post-CART era. Furthermore, EBV infection of lymphoma cells in HIV-positive individuals was associated with a distinct host gene expression program. These findings provide insight into the joint host-virus regulatory network of primary ARL tumor samples and expand our understanding of virus-associated oncogenesis. Our findings may also have therapeutic implications, as treatment may be personalized to target specific viral and virus-associated host processes that are only present in a subset of patients.
2015-04-11 | GSE67763 | GEO