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Alterations of redox and iron metabolism accompany development of HIV latency

ABSTRACT: Alterations of redox and iron metabolism accompany development of HIV latency

PROVIDER: PRJNA524856 | ENA |

REPOSITORIES: ENA

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Alterations of redox and iron metabolism accompany development of HIV latency

Project description:Metabolic alterations, such as oxidative stress, are hallmarks of HIV-1 infection. However, their influence on the development of viral latency, and thus on HIV-1 persistence during antiretroviral therapy (ART), have just begun to be explored. We analyzed omics profiles of in-vitro and in-vivo models of infection by HIV-1 and its simian homolog SIVmac. We found that cells survive retroviral replication by upregulating antioxidant pathways and intertwined iron import pathways. These changes are associated with remodeling of the redox sensitive promyelocytic leukemia protein nuclear bodies (PML NBs), an important constituent of nuclear architecture and a marker of HIV-1 latency. We found that PML is depleted in productively infected cells and restored by ART. Moreover, we identified intracellular iron as a key link between oxidative stress and PML depletion, thus supporting iron metabolism modulators as pharmacological tools to impair latency establishment.

2020-01-30 | GSE127468 | GEO

Alterations of redox and iron metabolism accompany development of HIV latency

Project description:Metabolic alterations, such as oxidative stress, are hallmarks of HIV-1 infection. However, their influenceon the development of viral latency, and thus on HIV-1 persistence during antiretroviral therapy (ART),have just begun to be explored. We analyzed omics profiles ofin-vitroandin-vivomodels of infection byHIV-1 and its simian homolog SIVmac. We found that cells survive retroviral replication by upregulatingantioxidant pathways and intertwined iron import pathways. These changes are associated withremodeling of the redox sensitive promyelocytic leukemia protein nuclear bodies (PML NBs), an importantconstituent of nuclear architecture and a marker of HIV-1 latency. We found that PML is depleted inproductively infected cells and restored by ART. Moreover, we identified intracellular iron as a key linkbetween oxidative stress and PML depletion, thus supporting iron metabolism modulators aspharmacological tools to impair latency establishment.

2020-03-03 | PXD012907 | Pride

Alterations of redox and iron metabolism accompany development of HIV latency

Project description: Not available

| S-SCDT-EMBOJ-2019-102209R3-95882_4_1582301721_jatsxml_XML | biostudies-other

Alterations of redox and iron metabolism accompany development of HIV latency

Project description: Not available

| S-SCDT-EMBOJ-2019-102209 | biostudies-other

Alterations of redox and iron metabolism accompany the development of HIV latency.

Project description: Not available

| S-EPMC7196916 | biostudies-literature

Astrocyte alterations that accompany neuroinflammation induced anhedonia

Project description:Astrocyte alterations that accompany neuroinflammation induced anhedonia

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Gene expression changes following latency reversal agents screening in a cellular model of HIV-1 latency

Project description:To delineate the mechanism driving JAK2 inhibitors´ induced effects on HIV-1 latency, whole transcriptome profiling was performed in the HIV-1 latency model HL-HIG, treated with the LRA fedratinib, the LPA pacritinib, the pan-JAKi ruxolitinib and PMA as a positive control of latency reactivation and immune activation.

2022-08-24 | GSE195855 | GEO

vzv latency

Project description:vzv latency

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Single-cell RNA-seq in a model for HIV latency reversal

Project description:T cells are the primary target of the virus HIV-1. Upon infection, the expression of the virus may come to a complete shutdown, a phenomenon known as latency. The molecular mechanisms responsible for the latency of HIV-1 are still poorly understood. To shed light on those mechanisms, we used the J-Lat A2 model for latency reversal, that consists of a Jurkat T cell clone containing a mini HIV construct that is transcriptionally silent. We treated J-Lat A2 and Jurkat cells with the latency-reversing drugs SAHA (suberoylanilide hydroxamic acid) and PMA (phorbol 12-myristate 13-acetate), and we performed single-cell RNA-seq to identify transcriptional signatures shared among the cells where HIV is reactivated.

2021-07-15 | GSE180133 | GEO

Intracellular labile iron is a key regulator of hepcidin expression and iron metabolism

Project description:Liver iron overload can induce hepatic expression of hepcidin and regulates iron metabolism. However, the mechanism of iron regulating iron metabolism remains known. Intracellular labile iron represents the nonferritin-bound, redox-active iron which is transitory and serves as a crossroad of cell iron metabolism. The role of intracellular labile iron played in iron metabolism has largely been elucidated. Here we show that intracellular labile iron of hepatocytes has dual function in iron metabolism. It can induce hepatocytes expressing hepcidin via ER stress induced transcription factors on the one hand, on the other hand stimulate BMP2 and BMP6 expression of liver sinusoidal endothelial cells (LSECs) though TNFα secreted by hepatocytes to further regulate iron metabolism. Blockade of TNFα could dysregulate the iron metabolism during iron overload. Our findings reveal the important role of intracellular labile iron in iron metabolism and represent a novel way to modulate iron metabolism during iron overload.

2023-05-03 | GSE186655 | GEO

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