ArticleFrontiers in immunology2025
IFIT3 activation significantly contributes to HIV-1-associated neurodegenerative disorder-mediated neuroinflammation.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Interferon-induced protein IFIT3 as a molecular nexus of neuroinflammation in Alzheimer's disease and HIV-associated neurocognitive disorders.Journal of neuroinflammation · 2026Article
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9 authors.
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Abstract
Introduction: The advent of effective combination antiretroviral therapy (cART) has significantly improved HIV-1 treatment, saving millions of lives. However, HAND remains a concern, particularly among aging individuals with HIV-1. The mechanisms underlying HAND are not well understood. Methods: This study investigated the role of interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) and its upstream regulator, signal transducer, and activator of transcription 1 (STAT1), in HAND pathology. Using the SH-SY5Y neuroblastoma cell line and HIV-infected humanized mice, we examined the effects of the cART drugs, HIV Tat protein, and HIV-1 virus on STAT1 and IFIT3 expression. Results: The results showed that HIV-1 exposure significantly upregulated STAT1 and IFIT3, contributing to neuroinflammation. Discussion: This study identified IFIT3 as a critical molecular marker for HAND, suggesting its potential as a therapeutic target and offering new insights into disease pathology and treatment strategies.
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