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Transcriptomic responses and Chromatin accessibility of human monocyte-derived dendritic cells to infection with HIV-1

ABSTRACT: Transcriptomic responses and Chromatin accessibility of human monocyte-derived dendritic cells to infection with HIV-1

PROVIDER: PRJNA517950 | ENA |

REPOSITORIES: ENA

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Chromatin accessibility of human monocyte-derived dendritic cells in response to infection with HIV-1

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Chromatin accessibility of human monocyte-derived dendritic cells in response to infection with HIV-1

Project description:Transcriptional programming of the innate immune response is pivotal for host protection. The transcriptional mechanisms that link pathogen sensing with innate activation remain poorly understood. During infection with HIV-1, human dendritic cells (DCs) can detect the virus through an innate sensing pathway leading to antiviral type I interferon and DC maturation. Here, we have developed an iterative experimental and computational approach to map the innate response circuitry during HIV-1 infection. By integrating genome-wide chromatin accessibility with expression kinetics, we have inferred a gene regulatory network that links 542 transcription factors (TFs) with 21,862 target genes. Through genetic perturbation and drug treatments we identify PRDM1 and RARA as essential regulators of the interferon response and DC maturation, respectively. This work provides a resource for interrogation of regulators of HIV replication and innate immunity, highlighting the complexity and cooperativity in the regulatory circuit controlling the DC response to HIV-1 infection.

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Project description:Myeloid dendritic cells (DCs) have the innate capacity to sense pathogens and orchestrate immune responses. However, DCs do not mount efficient immune responses to HIV-1, due to potent restriction at the level of reverse transcription. Here, we uncover that when reverse transcription is allowed to proceed, DCs detect HIV-1 in distinct phases, before and after integration. Blocking integration suppressed, but did not abolish, activation of the transcription factor, IRF3, interferon responses, and DC maturation. The cytoplasmic DNA sensor, cGAS, and the E3 ligase, TRIM5, were both required for these responses. Consistent with two stages of innate activation, HIV-1 altered host chromatin accessibility before and after integration. Our studies support the hypothesis that HIV-1 replication increases the amount of material available for sensing and that cGAS signaling can be tuned by discrete inflammatory inputs to drive DC maturation.

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HIV-1 infection of human monocyte-derived dendritic cells with and without the integrase inhibitor, Raltegravir (gene expression).

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