Expression data from different levels of anti-CD4 in HIV+ people
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ABSTRACT:
PROVIDER: PRJNA432157 | ENA |
REPOSITORIES: ENA
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Project description:HIV-infected subjects were stratified to two groups high IgG anti-CD4 antibodies and low IgG anti-CD4 antibodies on day 14 (D14) after (“high” ≥ 2-fold increase from baseline; “low” < 2-fold increase)
2019-01-01 | GSE109837 | GEO
Project description:Immune activation in people living with HIV on anti-retroviral therapy is associated with increased risk of morbidity and mortality, but the underlying mechanisms are poorly understood. To identify whether perturbation of immunological pathways persist at systems level, we compared genome-wide whole blood transcriptomes from 26 people living with HIV on long-term anti-retroviral therapy with 12 HIV-negative healthy controls. All participants were Caucasian male adults recruited from London, UK. People living with HIV were on anti-retroviral therapy for a median of 8.5 years (interquartile range 3-16 years). They had undetectable plasma HIV viral load (<40 copies/ml) and median circulating CD4 counts of 703 cells/µl (interquartile range 491-841 cells/µl).
2021-02-26 | E-MTAB-8891 | biostudies-arrayexpress
Project description:Understanding the evolution of broadly neutralizing antibody (bNAb) activity in people living with HIV is crucial for vaccine design and immunization strategies. It has been proposed that antibody cross-reactive activity is associated with lower CD4+ T cell counts during people living with HIV, but the underlying mechanisms remain unclear. To further explore the correlation between antibody reactivity and CD4+ T cell counts, we recruited people living with HIV with varying CD4+ T cell counts: (i) CD4+ T cell <= 50 cells/mL, (ii) 50 cells/mL < CD4+ T cell <= 200 cells/mL, (iii) 200 cells/mL < CD4+ T cell <= 500 cells/mL, (iv) 500 cells/mL < CD4+ T cell. We constructed four SOSIPs.664 trimers and evaluated the antigen-specific antibodies in serum. Immune repertoire sequencing was used to characterize the BCR repertoire of these individuals. The evaluation of antigen-specific antibodies with different SOSIP.664 trimers showed enhanced reactivity in individuals with low CD4+ T cell counts compared to those with high/normal CD4+ T cell counts. Analysis of antibody gene repertoires through BCR high throughput sequencing revealed an increased proportion of IgG with heavy chain complementarity-determining region 3 (CDRH3) loops exceeding 20 amino acids in individuals with CD4+ T cell counts below 50 cells/mL. Notably, the IGHV1-46 and IGHV4-34 germlines, which result in most polyreactive B cells, were preferentially used in individuals with low CD4+ T cell counts. These results suggest that limited engagement of CD4+ T cells could facilitate the survival of aberrant B cell repertoire with long CDRH3 regions.
2025-09-30 | GSE287663 | GEO
Project description:Background: People living with HIV are called immunological non-responders (INR) when their CD4+ T cell count is not restored to immunocompetent levels, despite successful viral suppression. INR have increased risk of progression to AIDS, non-AIDS related morbidity, and death. Impaired mucosal barrier function is a prevailing hypothesis for why INR among people with HIV (PWH) have persistently low CD4+ T cell counts.Objective: To understand the molecular mechanisms behind incomplete immune recovery in INR, we analysed gene regulation and protein expression in gut tissues from INR, immunological responders (IR), and healthy controls (HC).
2025-09-09 | PXD041255 | Pride
Project description:In people with HIV (PWH), the post antiretroviral therapy (ART) window is critical for immune restoration and HIV reservoir stabilization. We employ deep immune profiling, T cell receptor (TCR) sequencing and examine proliferation to assess how ART impacts T cell homeostasis. Hierarchies and frequencies of dominant CD4 TCR clonotypes (0.1-11% of all CD4+ T cells) remain stable post-ART, suggesting that clonal homeostasis can be independent of homeostatic processes regulating CD4+T cell absolute number, phenotypes and function. The slow restoration of host-immunity post-ART also has implications for the design of ART interruption studies.
2023-10-09 | GSE244867 | GEO
Project description:The intestinal environment sustains a state of HIV latency via yet unclear mechanisms. We recently demonstrated that specific cytokines act on intestinal epithelial cells (IEC) to promote viral reservoir (VR) latency or reactivation, with TNF-activated IEC limiting HIV outgrowth in CD4+ T cells of people with HIV (PWH) on antiretroviral therapy (ART). The pro-latency effect of TNF coincided with the induction of IL-32, a pro-inflammatory cytokine overexpressed in ART-treated PWH. Since type I IFNs are strong modulators of IL-32, we investigated IFN-β ability to modulate the crosstalk between IEC and CD4+ T cells via IL-32-dependent mechanisms.
2026-06-18 | GSE320067 | GEO
Project description:In this study we performed data-independet mass-spectrometry analysis of blood plasma collected from a cohort consisting of people living with HIV-1, people living with HIV-2, and HIV seronegative individuals. The data was used to infer signs of damage to a wide array of tissues and cell types.
2024-02-16 | PXD045155 | Pride
Project description:The role of aromatic gut-derived bacterial metabolites (GDBMs) in shaping immune cell metabolism and function remains poorly explored. Using ex vivo metabolomic profiling of paired plasma and CD4+ T-cells from people living with HIV-1 (PLWH), we identified a network of aromatic GDBMs whose cell-associated abundance, rather than systemic levels, was linked to broad alterations in CD4+ T-cell metabolic and functional states. Among these metabolites, p-cresol sulfate (PCS) emerged as a mechanistic prototype investigated in depth. Ex vivo flow cytometry and single-cell RNA sequencing of CD4+ T-cells stratified by cell-associated PCS levels revealed dose-dependent enrichment of transcriptional programs associated with impaired differentiation capacity, regulatory-like identity, and cellular senescence. Consistently, in vitro transcriptomic and proteomic analyses of PCS-exposed CD4+ T cells demonstrated induction of cell-cycle arrest, mitochondrial dysfunction, and senescence-associated programs, including upregulation of p16 and p21. Integration of these immunometabolic features with measurements of HIV-1 reservoir size in PLWH revealed that CD4+ T-cell states defined by cell-associated GDBMs track with intact proviral DNA levels in vivo. Together, these findings define a microbiome-derived axis that reshapes CD4+ T-cell metabolism and fate and promotes immune aging-associated states in PLWH. Our data suggest that cell-associated GDBMs may foster immunometabolic CD4+ T-cell states previously linked to long-term HIV-1 reservoir persistence in vivo.
2026-06-25 | PXD077610 | Pride
Project description:Sexually transmitted infections (STIs) are commonly reported among HIV-1 infected patients. The increasing prevalence of the most common STI, Chlamydia trachomatis (CT), among HIV-1 infected people suggests a role in HIV-1 infectivity. However, the mechanisms modulating the enhancement of HIV-1 infectivity during HIV-1/STIs coinfection remain elusive. The stimulation of CD4 T cells during CT infection may modulate the expression of specific genes, which in turn enhance the susceptibility and infectivity of CT-specific CD4 T cells to HIV-1 infection. After three days of CT stimulation of PBMCs followed by 3 days of HIV-1 infection, we observed a significant increase in HIV-1 p24 levels among clinically diagnosed C. trachomatis-infected patients as compared to cells from healthy donors. Similarly, ex vivo CT antigen-stimulated PBMCs from healthy donors showed enhanced susceptibility to HIV-1 as compared to unstimulated PBMCs. CT-specific CD4 T cells also harbour more HIV-1 copy numbers as compared to healthy unstimulated CD4 T cells. RNA-seq data revealed the upregulation of CCR chemokine receptors and cytokines in CD4 T cells from CT-stimulated CD4 T cells infected with HIV-1.
2021-12-31 | GSE164264 | GEO
Project description:The preference of HIV to infect activated CD4 T cells has been proposed to contribute to a numerical reduction of antigen-specific T cells and the loss of T cell-mediated immunity. To date, our understanding of how HIV impact on vaccine-induced cellular immunity is limited. Moreover, the influence of chronic inflammation, that persist in treated HIV infection, is still unclear. Here, we investigated inflammation, immune activation and antigen-specific T cell responses in HIV-uninfected and cART-treated HIV people with prior measles virus and tetanus toxoid immunity. Our findings highlight lower antigen-induced T cell activation and lower cytokine production of antigen-specific CD4 T cells in the HIV group. These lower recall CD4 T cell responses associated with high plasma levels of multiple cytokines and with T cell hyperactivation. Transcriptome analysis of sorted antigen-specific CD4 T cells revealed that upon antigen reencounter, HIV people on cART had a reduced expression of gene sets previously reported to associate with vaccine-induced protective immunity against various pathogens. We further identified a consistent impairment of the IFN and IFN signaling pathways as a mechanism for the functional loss of antigen-specific CD4 T cell responses in cART-treated people with HIV. Together, our findings suggest that vaccine-induced cellular immunity may benefit from strategies to counteract inflammation in HIV infection.pecific
2024-10-16 | GSE273967 | GEO