ArticleScientific reports2016
Proliferation of Perivascular Macrophages Contributes to the Development of Encephalitic Lesions in HIV-Infected Humans and in SIV-Infected Macaques.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- The cognitive remediation of attention in HIV-associated neurocognitive disorders (HAND): A meta-analysis and systematic review.F1000Research · 2023Pooled it
- Resolving inflammation: The impact of antiretroviral therapy on macrophage traffic in and out of the CNS.PLoS pathogens · 2025Article
- Liver biopsies obtained throughout SIV infection reveal evolving interferon stimulated protein expression within distinct monocyte/macrophage subsets.PLoS pathogens · 2025Article
- M1-type polarized macrophage contributes to brain damage through CXCR3.2/CXCL11 pathways after RGNNV infection in grouper.Virulence · 2024Article
- CSF1R inhibition depletes brain macrophages and reduces brain virus burden in SIV-infected macaques.Brain : a journal of neurology · 2024Article
- Brain perivascular macrophages: current understanding and future prospects.Brain : a journal of neurology · 2024Review
- Infections in the Etiology of Parkinson's Disease and Synucleinopathies: A Renewed Perspective, Mechanistic Insights, and Therapeutic Implications.Journal of Parkinson's disease · 2024Review
- Infectious Diseases.Advances in neurobiology · 2024Review
- Proliferation of monocytes and macrophages in homeostasis, infection, injury, and disease.Journal of leukocyte biology · 2023Review
- Downregulation of CCR5 on brain perivascular macrophages in simian immunodeficiency virus-infected rhesus macaques.Brain and behavior · 2023Article
- CNS-associated macrophages shape the inflammatory response in a mouse model of Parkinson's disease.Nature communications · 2023Article
- Simian immunodeficiency virus-infected rhesus macaques with AIDS co-develop cardiovascular pathology and encephalitis.Frontiers in immunology · 2023Article
- Independent actions by HIV-1 Tat and morphine to increase recruitment of monocyte-derived macrophages into the brain in a region-specific manner.Neuroscience letters · 2022Article
- Review
- Neuropathogenesis of HIV and emerging therapeutic targets.Expert opinion on therapeutic targets · 2022Review
- Advances in SIV/SHIV Non-Human Primate Models of NeuroAIDS.Pathogens (Basel, Switzerland) · 2021Review
- The far-reaching HAND of cART: cART effects on astrocytes.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Review
- Role of P2X7 Receptors in Immune Responses During Neurodegeneration.Frontiers in cellular neuroscience · 2021Review
- Perivascular macrophages in the neonatal macaque brain undergo massive necroptosis after simian immunodeficiency virus infection.Brain pathology (Zurich, Switzerland) · 2020Article
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The aim of the present study was to investigate if macrophage proliferation occurs in the brain during simian immunodeficiency virus (SIV) infection of adult macaques. We examined the expression of the Ki-67 proliferation marker in the brains of uninfected and SIV-infected macaques with or without encephalitis. Double-label immunohistochemistry using antibodies against the pan-macrophage marker CD68 and Ki-67 showed that there was a significant increase in CD68+Ki-67+ cells in macaques with SIV encephalitis (SIVE) compared to uninfected and SIV-infected animals without encephalitis, a trend that was also confirmed in brain samples from patients with HIV encephalitis. Multi-label immunofluorescence for CD163 and Ki-67 confirmed that the vast majority of Ki-67+ nuclei were localized to CD163+ macrophages in perivascular cuffs and lesions. The proliferative capacity of Ki-67+ perivascular macrophages (PVM) was confirmed by their nuclear incorporation of bromodeoxyuridine. Examining SIVE lesions, using double-label immunofluorescence with antibodies against SIV-Gag-p28 and Ki-67, showed that the population of Ki-67+ cells were productively infected and expanded proportionally with lesions. Altogether, this study shows that there are subpopulations of resident PVM that express Ki-67 and are SIV-infected, suggesting a mechanism of macrophage accumulation in the brain via PVM proliferation.
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Registered trials
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