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

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

PROVIDER: PRJNA1046560 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26991276_1.fastq.gz	Fastqsanger.gz
	SRR26991276_2.fastq.gz	Fastqsanger.gz
	SRR26991277_1.fastq.gz	Fastqsanger.gz
	SRR26991277_2.fastq.gz	Fastqsanger.gz
	SRR26991278_1.fastq.gz	Fastqsanger.gz

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

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 | GSE248996 | GEO

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]

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

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

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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]

| PRJNA1046558 | ENA

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]

| PRJNA1046559 | ENA

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.

2024-05-01 | GSE248999 | GEO

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

EphB2-mediated ephrin-B reverse signaling on microglia drives an antiviral but also inflammatory response in HIV

Project description:HIV Associated Neurocognitive Disorder (HAND) is a condition behaviorally characterized by cognitive and neurological impairments, and pathologically characterized by neuroinflammation and a loss of synaptic integrity and function. Although therapeutics exist to increase the lifespan of people living with HIV, they are not effective at preventing HIV induced neuronal damage and the prevalence of HAND remains virtually unchanged. We observed an increase in expression of ephrin-B/EphB in post-mortem CNS specimen of people who lived with HIV and brain pathology. Given the previously recognized impact of EphB2 on inflammation in the periphery, the functional role of EphB2-mediated ephrin-B reverse signaling on microglia was assessed. A a pro-inflammatory and antiviral mRNA expression profile was observed. The stimulation produced condirioned media, including secreted inflammatory factors, that were sufficient to induce non-cell contact-dependent neurotoxicity. Finally, knockdown of microglial ephrin-B1, EphB2 binding partner, resulted in a partial alleviation of the microglial pro-inflammatory signature and subsequent neurotoxicity. In this study, we show that elevated EphB2, and its reverse signaling through ephrin-B1 in microglia, can drive neuroinflammation and toxicity suggesting this pathway can mediate neurotoxicity in neuroHIV. Furthermore, we propose that this neuroinflammatory mechanism may play a role in promoting other neurodegenerative diseases.

2024-06-01 | GSE260757 | GEO

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