ArticleJournal of neuroinflammation2025
Antiretroviral drug therapy does not reduce neuroinflammation in an HIV-1 infection brain organoid model.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Implications of HIV persistence and pathogenesis in microglia.Current opinion in HIV and AIDS · 2026Review
- Neuroinflammation and NeuroHIV: understanding the role of HIV-1 related factors in microglial activation.Translational psychiatry · 2026Review
- HIV gp120 induces TREM1 expression through TLR-PGE₂ signalling in human monocyte-derived microglia.Journal of neuroinflammation · 2026Article
- Review
- Vascularized human brain organoids as a model of the brain-peripheral axis in HIV-1 neuropathogenesis.Scientific reports · 2026Article
- Integrating brain organoids, meningeal immunity, and glymphatic dynamics: toward modeling neuroimmune clearance and crosstalk in disease.Frontiers in immunology · 2026Review
- Targeting HIV myeloid and central nervous system reservoirs for HIV cure.Current opinion in HIV and AIDS · 2025Review
- Neuroinflammation associated with proviral DNA persists in the brain of virally suppressed people with HIV.Frontiers in immunology · 2025Article
- Beyond the amyloid hypothesis: leveraging human-centered complexFrontiers in toxicology · 2025Review
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Abstract
backgroundHIV-1-associated neurocognitive impairment (HIV-1-NCI) is marked by ongoing and chronic neuroinflammation with loss and decline in neuronal function even when antiretroviral drug therapy (ART) successfully suppresses viral replication. Microglia, the primary reservoirs of HIV-1 in the central nervous system (CNS), play a significant role in maintaining this neuroinflammatory state. However, understanding how chronic neuroinflammation is generated and sustained by HIV-1, or impacted by ART, is difficult due to limited access to human CNS tissue.
methodsWe generated an in vitro model of admixed hematopoietic progenitor cell (HPC) derived microglia embedded into embryonic stem cell (ESC) derived Brain Organoids (BO). Microglia were infected with HIV-1 prior to co-culture. Infected microglia were co-cultured with brain organoids BOs to infiltrate the BOs and establish a model for HIV-1 infection, "HIV-1 M-BO". HIV-1 M-BOs were treated with ART for variable directions. HIV-1 infection was monitored with p24 ELISA and by digital droplet PCR (ddPCR). Inflammation was measured by cytokine or p-NF-kB levels using multiplex ELISA, flow cytometry and confocal microscopy.
resultsHIV-1 infected microglia could be co-cultured with BOs to create a model for "brain" HIV-1 infection. Although HIV-1 infected microglia were the initial source of pro-inflammatory cytokines, astrocytes, neurons and neural stem cells also had increased p-NF-kB levels, along with elevated CCL2 levels in the supernatant of HIV-1 M-BOs compared to Uninfected M-BOs. ART suppressed the virus to levels below the limit of detection but did not decrease neuroinflammation.
conclusionsThese findings indicate that HIV-1 infected microglia are pro-inflammatory. Although ART significantly suppressed HIV-1 levels, neuronal inflammation persisted in ART-treated HIV-1 M-BOs. Together, these findings indicate that HIV-1 infection of microglia infiltrated into BOs provides a robust in vitro model to understand the impact of HIV-1 and ART on neuroinflammation.
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