ArticlePloS one2013
Mechanisms of HIV entry into the CNS: increased sensitivity of HIV infected CD14+CD16+ monocytes to CCL2 and key roles of CCR2, JAM-A, and ALCAM in diapedesis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
118 citing papers in PubMed, 1 synthesis or guideline pooled it, 161 citations in OpenAlex.
- Genome-wide association study of CSF levels of 59 alzheimer's disease candidate proteins: significant associations with proteins involved in amyloid processing and inflammation.PLoS genetics · 2014Pooled it
- Normalization of Soluble CD163 Levels After Institution of Antiretroviral Therapy During Acute HIV Infection Tracks with Fewer Neurological Abnormalities.The Journal of infectious diseases · 2018Trial
- Improved Cognitive Performance and Reduced Monocyte Activation in Virally Suppressed Chronic HIV After Dual CCR2 and CCR5 Antagonism.Journal of acquired immune deficiency syndromes (1999) · 2018Trial
- JAM-A and ALCAM are therapeutic targets to inhibit diapedesis across the BBB of CD14+CD16+ monocytes in HIV-infected individuals.Journal of leukocyte biology · 2015Trial
- Brain viral reservoir seeding and neurological metabolic dysregulation in early-life immunodeficiency virus infection.Brain pathology (Zurich, Switzerland) · 2026Article
- Soluble TREM2 Mediates Blood Brain Barrier Permeability through Astrocyte Reactivity.Research square · 2026Article
- Identification of distinct HIV reservoir phenotypes and associated immune landscapes.JCI insight · 2026Article
- HIV transgenic mouse monocytes display increasedJournal of virology · 2026Article
- Review
- Latent HIV Reservoirs in the Central Nervous System: Mechanisms, Barriers, and Therapeutic Approaches.ACS infectious diseases · 2026Review
- HIV Infection, Neurotoxicity, Inflammation, Premature Aging, and Therapeutic Challenges to PLWH: An Overview.International journal of molecular sciences · 2026Review
- Redirecting the route: Monocyte-mediated delivery of oHSV-1 across a human BBB-on-chip model.Materials today. Bio · 2025Article
- Chronic Neuroplasticity Changes Following Neurotropic Viral Infection: Mechanisms and Implications.Cellular and molecular neurobiology · 2025Review
- EcoHIV Infection Promotes Atherosclerosis Progression in LDLR-Deficient Mice.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- JAM-A: Adhesion Receptor and Signaling Regulator in Atherosclerosis.Current atherosclerosis reports · 2025Review
- Review
- HTLV-1-infected cells drive the differentiation of monocytes into macrophages in vitro.BMC immunology · 2025Article
- HIV Cerebrospinal Fluid Escape: Interventions for the Management, Current Evidence and Future Perspectives.Tropical medicine and infectious disease · 2025Review
- Influence of plasma exosomes from women living with HIV Stratified by HAND on monocyte subpopulations from healthy women without HIV.Journal of neurovirology · 2025Article
- Single-cell analysis of CD14Frontiers in immunology · 2025Article
58 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
As HIV infected individuals live longer, the prevalence of HIV associated neurocognitive disorders is increasing, despite successful antiretroviral therapy. CD14(+)CD16(+) monocytes are critical to the neuropathogenesis of HIV as they promote viral seeding of the brain and establish neuroinflammation. The mechanisms by which HIV infected and uninfected monocytes cross the blood brain barrier and enter the central nervous system are not fully understood. We determined that HIV infection of CD14(+)CD16(+) monocytes resulted in their highly increased transmigration across the blood brain barrier in response to CCL2 as compared to uninfected cells, which did not occur in the absence of the chemokine. This exuberant transmigration of HIV infected monocytes was due, at least in part, to increased CCR2 and significantly heightened sensitivity to CCL2. The entry of HIV infected and uninfected CD14(+)CD16(+) monocytes into the brain was facilitated by significantly increased surface JAM-A, ALCAM, CD99, and PECAM-1, as compared to CD14(+) cells that are CD16 negative. Upon HIV infection, there was an additional increase in surface JAM-A and ALCAM on CD14(+)CD16(+) monocytes isolated from some individuals. Antibodies to ALCAM and JAM-A inhibited the transmigration of both HIV infected and uninfected CD14(+)CD16(+) monocytes across the BBB, demonstrating their importance in facilitating monocyte transmigration and entry into the brain parenchyma. Targeting CCR2, JAM-A, and ALCAM present on CD14(+)CD16(+) monocytes that preferentially infiltrate the CNS represents a therapeutic strategy to reduce viral seeding of the brain as well as the ongoing neuroinflammation that occurs during HIV pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.