Host genetic determinants of HIV infection
Ontology highlight
ABSTRACT:
PROVIDER: EGAS00001005245 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Using microRNA array analyses of in vitro HIV-1-infected CD4+ cells, we find that several host microRNAs are significantly up- or downregulated around the time HIV-1 infection peaks in vitro. While microRNA-223 levels were significantly enriched in HIV-1-infected CD4+CD8? PBMCs, microRNA-29a/b, microRNA-155 and microRNA-21 levels were significantly reduced. Based on the potential for microRNA binding sites in a conserved sequence of the Nef-3?-LTR, several host microRNAs potentially could affect HIV-1 gene expression. Among those microRNAs, the microRNA-29 family has seed complementarity in the HIV-1 3?-UTR, but the potential suppressive effect of microRNA-29 on HIV-1 is severely blocked by the secondary structure of the target region. Our data support a possible regulatory circuit at the peak of HIV-1 replication which involves downregulation of microRNA-29, expression of Nef, the apoptosis of host CD4 cells and upregulation of microRNA-223. Time course of HIV infection on CD4 cells
2012-12-05 | E-GEOD-42737 | biostudies-arrayexpress
Project description:Using microRNA array analyses of in vitro HIV-1-infected CD4+ cells, we find that several host microRNAs are significantly up- or downregulated around the time HIV-1 infection peaks in vitro. While microRNA-223 levels were significantly enriched in HIV-1-infected CD4+CD8− PBMCs, microRNA-29a/b, microRNA-155 and microRNA-21 levels were significantly reduced. Based on the potential for microRNA binding sites in a conserved sequence of the Nef-3′-LTR, several host microRNAs potentially could affect HIV-1 gene expression. Among those microRNAs, the microRNA-29 family has seed complementarity in the HIV-1 3′-UTR, but the potential suppressive effect of microRNA-29 on HIV-1 is severely blocked by the secondary structure of the target region. Our data support a possible regulatory circuit at the peak of HIV-1 replication which involves downregulation of microRNA-29, expression of Nef, the apoptosis of host CD4 cells and upregulation of microRNA-223.
2012-12-05 | GSE42737 | GEO
Project description:Abstract Objectives: HIV infection dysregulates the innate immune system and alters leukocyte gene expression. The objectives were two fold: to characterize the impact of HIV infection on peripheral monocyte gene expression and to identify the predominant factor(s) responsible for altered gene expression. Design and methods: In a cross-sectional study, CD14+ monocytes were isolated from 11 HIV seronegative controls, 22 HIV seropositive subjects with low viral loads (LVL, <= 10,000 RNA copies/ml) and 22 HIV seropositive subjects with high viral loads (HVL, > 10,000 RNA/copies/ml). Total monocyte RNA was hybridized to 55K probes on high-density microarrays to obtained detailed gene expression profiles from control, LVL and HVL subjects. As potential candidates for immune disruption, we evaluated three HIV-related peripheral factors, interferon (IFN)-a, IFN-a and lipopolysaccharide (LPS) by treating HIV seronegative CD14+ monocytes for 48h and then analyzing gene expression. Plasma collected from the HIV subjects were quantified for LPS using a Pyrogene assay and for soluble (s) CD14 by ELISA. Results: In this cross-sectional study of HIV subjects (n=44), viral loads above 10,000 RNA copies/ml were associated with an activated phenotype. Characterization of the gene expression pattern by Gene Ontology reveals an ongoing immune response to viral infection including inflammation and chemotaxis. Gene expression analysis of in vitro treated HIV seronegative monocytes with IFN-a, IFN-g or LPS demonstrated that IFN-a most accurately recapitulated the HIV HVL profile. There was no detectable LPS signature even in those HIV subjects with the highest LPS and sCD14 levels. Conclusions: Monocyte gene expression in subjects with viremia is predominantly due to IFN-a, while subjects with LVL have a non-activated phenotype. In monocytes, there was no discernible expression profile linked to LPS exposure.
2009-10-09 | GSE18464 | GEO
Project description:Throughout HIV-1 replication cycle, a complex interplay of host-pathogen interactions takes place in the infected cell, leading to production of new virions. The virus modulates the host cellular machinery in order to support its life cycle, while controlling intracellular defense. We have investigated the dynamic host response to HIV-1 infection by systematically measuring transcriptome, proteome and phosphoproteome expression changes in infected and uninfected SupT1 CD4+ T cells at 5 time-points throughout the HIV-1 replication cycle. Genome-wide transcript levels were assessed by RNA-Seq, while protein and phosphoprotein relative abundances were obtained using SILAC mass spectrometry. By the means of a Gaussian mixed-effects model, we stratified host genes based on their gene expression temporal patterns at the three levels, showing how HIV may affect regulation of certain host genes. The results of the implemented integrative analysis of time-series omics data offers a catalogue of dynamic host response to HIV infection allowing a more comprehensive understanding of host-virus interactions. Furthermore, it facilitates identifying novel host factors potentially promoting or restricting HIV replication.
2018-12-31 | GSE100587 | GEO
Project description:Hepatic complications of HCV infection, including fibrosis and cirrhosis are accelerated in HIV-infected individuals. Although liver biopsy remains the gold standard for staging HCV-associated liver disease, this test can result in serious complications and is subject to sampling error. These challenges have prompted a search for non-invasive methods for liver fibrosis staging. To this end, we compared serum proteome profiles at different stages of fibrosis in HIV/HCV co- and HCV mono-infected patients using SELDI-TOF MS.
2018-04-09 | PXD009007 | Pride
Project description:NAD besides its key role in cellular metabolism can serve as an alternative 5’ cap at several short non-coding RNAs. However, the function of the NAD cap remains elusive. Here, we investigate NAD capping of RNAs upon HIV-1 infection, which is associated with intracellular pellagra – depletion of NAD/NADH cellular pool. We applied NAD captureSeq on HIV-1 infected/noninfected cells and we revealed that four snRNAs (U1, U4ATAC, U5E and U7) and four snoRNAs (snord3G, snord102, snorA50A and snord3B) lost NAD cap upon HIV-1 infection. Interestingly, U1 snRNA was previously shown to be essential for HIV-1 replication. We provide evidence that the NAD cap reduces the stability of the U1 - HIV-1 pre-mRNA duplex. The importance of NAD RNA cap in HIV-1 infection was further supported by NAD decapping enzyme DXO overexpression, which led to increase in HIV-1 infectivity. This is the first example of NAD cap function in mammalian cells and suggests a general role of non-canonical RNA caps in antiviral innate immunity response.
2024-05-16 | GSE191019 | GEO
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.
2011-09-09 | GSE24037 | GEO
Project description:This phase I trial studies the side effects and best dose of ibrutinib in treating B-cell non-Hodgkin lymphoma that has returned or does not respond to treatment in patients with human immunodeficiency virus (HIV) infection. Ibrutinib may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth. It is not yet known whether it is safe for patients with HIV infection to receive ibrutinib while also taking anti-HIV drugs.
| 2164362 | ecrin-mdr-crc
Project description:Opioid use is associated with worse outcome in HIV-infected patients. The exacerbated disease progression by opioids is mainly driven by increased epithelial damage and less regenerative response. The present study investigates how opioids potentiate HIV disease progression by impairing intestinal epithelial self-repair. Abnormal intestinal morphology and reduced epithelial proliferation were observed in HIV-infected humanized mice, which were exposed to opioids. For this study, we had 4 groups of BLT humanized mice- (A) Untreated, (B) Morphine treated, (C) HIV infected and (D) HIV infected + Morphine treated. HIV infection was done for 4 weeks and Morphine treatment was done for 7 days. Morphine treatment was done via subcutaneous implantation of slow-release morphine pellet in individual mouse in the appropriate groups. In other groups, a matching Placebo pellet was implanted.
2020-01-11 | E-MTAB-7883 | biostudies-arrayexpress
Project description:To explore if specific host responses are linked to HIV disease severity, we here investigated blood gene expression profiles comparing different progressor groups, including those with HIV-1, HIV-2 or HIV-1/HIV-2 dual infection and HIV seronegative individuals. We found interferon alpha-inducible protein 27 (IFI27) to be the most strongly, and significantly, upregulated gene in HIV infected, compared with HIV seronegative, individuals. The expression of IFI27 was higher in HIV-1, compared with HIV-2, infected individuals and correlated with both plasma viral load (pVL) and CD4% levels.
2022-05-31 | GSE200606 | GEO