ArticleBMC genomics2016
A transcriptome-based model of central memory CD4 T cell death in HIV infection.
Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- CCR5Δ32 polymorphism is associated with increased central memory CD4+ T cells in virologically suppressed people living with HIV on antiretroviral therapy.Medical microbiology and immunology · 2026Article
- Limited restoration of T cell subset distribution and immune function in older people living with HIV-1 receiving HAART.Immunity & ageing : I & A · 2025Article
- Central Memory CD4 T Cells from Persons with HIV Accumulate DNA Content Defects During Proliferative Response.AIDS research and human retroviruses · 2025Article
- TOX2 coordinates with TET2 to positively regulate central memory differentiation in human CAR T cells.Science advances · 2023Article
- HIV Infection Elicits Differential Transcriptomic Remodeling in CD4+ T Cells with Variable Proliferative Responses to the T Cell Receptor Stimulus.Pathogens (Basel, Switzerland) · 2023Article
- Differential Leukocyte Expression ofJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Article
- Article
- Gene Expression: the Key to Understanding HIV-1 Infection?Microbiology and molecular biology reviews : MMBR · 2020Review
- A Disintegrin and Metalloproteinase-Control Elements in Infectious Diseases.Frontiers in cardiovascular medicine · 2020Review
- The Prognostic Landscape of Tumor-Infiltrating Immune Cells and Immune Checkpoints in Glioblastoma.Technology in cancer research & treatment · 2019Article
- HIV Disease Progression: Overexpression of the Ectoenzyme CD38 as a Contributory Factor?BioEssays : news and reviews in molecular, cellular and developmental biology · 2019Review
- Dysregulation of Neuronal Cholesterol Homeostasis upon Exposure to HIV-1 Tat and Cocaine Revealed by RNA-Sequencing.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHuman central memory CD4 T cells are characterized by their capacity of proliferation and differentiation into effector memory CD4 T cells. Homeostasis of central memory CD4 T cells is considered a key factor sustaining the asymptomatic stage of Human Immunodeficiency Virus type 1 (HIV-1) infection, while progression to acquired immunodeficiency syndrome is imputed to central memory CD4 T cells homeostatic failure. We investigated if central memory CD4 T cells from patients with HIV-1 infection have a gene expression profile impeding proliferation and survival, despite their activated state.
methodsUsing gene expression microarrays, we analyzed mRNA expression patterns in naive, central memory, and effector memory CD4 T cells from healthy controls, and naive and central memory CD4 T cells from patients with HIV-1 infection. Differentially expressed genes, defined by Log
resultsCentral memory CD4 T cells from patients and controls showed comparable expression of differentiation-related genes, ruling out an effector-like differentiation of central memory CD4 T cells in HIV infection. However, 210 genes were differentially expressed in central memory CD4 T cells from patients compared with those from controls. Expression of 75 of these genes was validated by semi quantitative RT-PCR, and independently reproduced enrichment results from this gene expression signature. The results of functional enrichment analysis indicated movement to cell cycle phases G1 and S (increased CCNE1, MKI67, IL12RB2, ADAM9, decreased FGF9, etc.), but also arrest in G2/M (increased CHK1, RBBP8, KIF11, etc.). Unexpectedly, the results also suggested decreased apoptosis (increased CSTA, NFKBIA, decreased RNASEL, etc.). Results also suggested increased IL-1β, IFN-γ, TNF, and RANTES (CCR5) activity upstream of the central memory CD4 T cells signature, consistent with the demonstrated milieu in HIV infection.
conclusionsOur findings support a model where progressive loss of central memory CD4 T cells in chronic HIV-1 infection is driven by increased cell cycle entry followed by mitotic arrest, leading to a non-apoptotic death pathway without actual proliferation, possibly contributing to increased turnover.
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