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Updated: Jul 2, 2025
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Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models
Published on: December 3, 2019
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Accelerated Neuroimmune Dysfunction in Aged HIV-1-Infected Humanized Mice
Chen Zhang1, Hang Su1, Emiko Waight1
1Department of Pharmacology and Experimental Neuroscience, College of Medicine, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Pharmaceuticals (Basel, Switzerland)
|February 24, 2024
Summary
This study reveals that human immunodeficiency virus type one (HIV-1) infection accelerates aging in mice, impacting immune cells and brain function. Key biomarkers identified offer insights into potential interventions for aging individuals with HIV.
Area of Science:
- Immunology
- Virology
- Gerontology
Background:
- Disordered immunity, aging, and human immunodeficiency virus type one (HIV-1) infection are interconnected but poorly understood.
- Accelerated aging, advanced HIV-1, inflammation, and genetics are linked to cellular, mitochondrial, and metabolic changes, with elusive mechanisms.
Purpose of the Study:
- To model aging in HIV-1 infection using CD34-NSG humanized mice.
- To uncover associations between HIV-1 infection and aging, identifying immune disease-based biomarkers.
Main Methods:
- Chronically HIV-1-infected CD34-NSG humanized mice were used.
- Brain tissues were analyzed using transcriptomics, qPCR, and immunofluorescence assays.
- Age-associated genes and pathways linked to HIV-1 infection were identified.
Main Results:
- CD4+ T cell decline correlated with viral load and age.
- Upregulated genes (C1QA, CD163, CXCL16) and downregulated genes (LMNA, CLU) were identified as age-associated in HIV-1 infection.
- Pathways linked to innate immunity, pyroptosis, neuroinflammation, mitochondrial dysfunction, and senescence were affirmed.
Conclusions:
- CD34-NSG humanized mice serve as a valuable model for HIV-1-associated aging research.
- Biomarkers of immune senescence and neuronal signaling are associated with both age and HIV-1 infection.
- Understanding these mechanisms can lead to interventions for HIV-1 patients.
