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Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1

ABSTRACT: Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1

PROVIDER: PRJNA1046554 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26990700_1.fastq.gz	Fastqsanger.gz
	SRR26990700_2.fastq.gz	Fastqsanger.gz
	SRR26990701_1.fastq.gz	Fastqsanger.gz
	SRR26990701_2.fastq.gz	Fastqsanger.gz
	SRR26990702_1.fastq.gz	Fastqsanger.gz

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Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1 [iPSCMG_TFS]

Project description:HIV-associated neurocognitive disorders (HAND) persist as a notable cause of illness among individuals with HIV. Despite significant progress in antiretroviral therapy (ART), HAND continues to be a major concern, impacting approximately one-third of those infected with HIV. Recent research underscores the pivotal role of microglia, the primary immune cells in the central nervous system (CNS), in the development and progression of HAND. The infection and activation of microglia by HIV leads to the release of pro-inflammatory markers, cytokines, chemokines, secondary messengers, and reactive oxygen species (ROS). These factors collectively initiate signalling pathways that contribute to neuroinflammation, a central process in the development of HAND. In order to validate stem cell-derived microglia (iMGL) as a viable model system for HAND investigation, we infected iMGLs and human monocyte-derived macrophages (MDMs) with the primary HIV-1 isolate Ba-L at an MOI of 0.25. Total RNA was extracted from cell populations on days 1, 2, 4, 6, and 8 following infection. Subsequently, we conducted bulk RNA sequencing to examine the longitudinal transcriptomic alterations induced by the virus over this time frame

2024-05-01 | GSE248998 | GEO

Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1 [iPSCMG]

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Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1 [MDM]

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Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1 [iPSCMG_TFS]

Project description:Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1 [iPSCMG_TFS]

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Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1 [iPSCMG]

Project description:Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1 [iPSCMG]

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Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1 [MDM]

Project description:Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1 [MDM]

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Stem Cell-derived Microglia Exhibit HAND Gene Expression Signature Early Upon Infection with HIV-1

Project description:This SuperSeries is composed of the SubSeries listed below.

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Deciphering HAND Pathogenesis Using Single-Nucleotide Omics Approaches

Project description:Although antiretroviral therapy (ART) effectively suppresses HIV-1 replication to undetectable levels and restores many immune parameters in people living with HIV (PLWH), these individuals remain at elevated risk for HIV-associated comorbidities. Among the most prevalent is neurocognitive impairment—a mild form of HIV-associated neurocognitive disorders (HAND)—which affects up to 50% of PLWH. Despite extensive investigation, the precise mechanisms underlying HAND pathogenesis remain unclear, in part due to its multifactorial nature. To address this, we conducted a comparative single-nucleus multi-omics analysis—integrating RNA sequencing (RNA-seq) and chromatin accessibility profiling (ATAC-seq)—of post-mortem brain tissues from HIV-infected individuals with and without HAND, as well as uninfected controls. Our results reveal substantial dysregulation in genes involved in inflammation, innate immunity, glycosylation, and cholesterol metabolism in HIV-infected brains (HAND+ and HAND−) relative to uninfected controls. Notably, these changes were further accentuated in HAND+ samples compared to HAND−, with microglia and oligodendrocytes emerging as the most affected cell populations—highlighting their potential central role in sustaining neuroinflammation. Interestingly, we observed a disconnect between transcriptomic and epigenomic signals: many inflammation-related genes located in accessible chromatin regions in HAND+ brains were not transcriptionally upregulated. This epigenetic priming—particularly in microglia and astrocytes—is consistent with the concept of trained immunity (TRIM), wherein prior exposures epigenetically “train” innate immune cells to respond differently to subsequent stimuli. Our findings suggest that maladaptive TRIM may be a key contributor to persistent neuroinflammation and the pathogenesis of HAND in the ART era.

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HIV-1 integration in microglia

Project description:HIV-1 integration in microglia

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Single-cell RNA sequencing study of brain-derived cells from two individuals with HIV-associated neurocognitive dysfunction

Project description:The high prevalence of cognitive alterations in persons with HIV (PWH) despite effective antiretroviral therapy (ART) is associated with sustained neuroinflammation. Here, we uncover the signaling pathways that are essential for persistent immune activation and might underly development of HIV associated Neurocognitive Disorder (HAND). We analyze the brain proteome from PWH on ART during HAND progression. We observe that 73.3% of the significantly upregulated proteins in brains from PWH and HAND (compared to PWH with normal cognition) belong to immune pathways. Among them, 36.4% of upregulated innate immune-related proteins are within the type I interferon (IFN-I) signaling, suggesting that persistent IFN-I activation is central to HAND-associated brain immune activation. Single cell (sc)RNA-seq analysis confirmed that FN-I occurs mainly in astrocytes during acute HIV infection in the microglia-containing organoid (MCO) model of HIV infection and persistent in microglia in the brain of PLWH on ART. Of note, IFN-I persistence is independent of HIV status but associated with the induction of human endogenous retroviruses-W (HERV-W) Env during HAND progression after initial HIV infection and its associated immune activation. When induced, HERV-W Env directly activates IFN-I signaling in astrocytes, but not in microglia. Together, IFN-I signaling may be initiated directly in the astrocytes after acute HIV infection then sustained in the microglia during ART. IFN-I persists due to expression of HERV-W Env, thereby contributing to the persistent immune activation in the HAND brain on ART, independent of HIV and insensitive to ART. Our data link the neuroinflammation of persistent IFN-I signaling to the HAND brain on ART.

2024-05-25 | GSE233717 | GEO

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