ArticlePLoS pathogens2011
HIV-1 replication in the central nervous system occurs in two distinct cell types.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers.
What it found
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Who cites it
183 citing papers in PubMed, 241 citations in OpenAlex.
- HIV-1 in lymph nodes is maintained by cellular proliferation during antiretroviral therapy.The Journal of clinical investigation · 2019Trial
- Compartmentalized replication of R5 T cell-tropic HIV-1 in the central nervous system early in the course of infection.PLoS pathogens · 2015Trial
- The brain as an HIV reservoir: Recent findings using autopsy tissues from people with HIV.PLoS pathogens · 2026Review
- A New Type of Nonsuppressible Viremia Produced by HIV-Infected Macrophage.The Journal of infectious diseases · 2026Article
- Smoldering in the sanctuary: HIV-associated brain injury in the ART era.The Journal of clinical investigation · 2026Review
- Coreceptor usage of plasma and cerebrospinal fluid-derived HIV-1 subtype C variants.Virology journal · 2026Article
- Neurosymptomatic Cerebrospinal Fluid Escape Is a Central Nervous System-Focused Form of Antiretroviral Therapy Treatment Failure.Open forum infectious diseases · 2026Article
- HIV-1 latency: From acquaintance to confidant.Journal of virus eradication · 2025Review
- Article
- HIV-1 Tat protein alters medial prefrontal cortex neuronal activity and recognition memory.iScience · 2025Article
- Neurovirulent and non-neurovirulent strains of HIV-1 and their Tat proteins induce differential cytokine-chemokine profiles.NeuroImmune pharmacology and therapeutics · 2025Article
- Shared interactions of six neurotropic viruses with 38 human proteins: a computational and literature-based exploration of viral interactions and hijacking of human proteins in neuropsychiatric disorders.Discover mental health · 2025Article
- HIV Cerebrospinal Fluid Escape: Interventions for the Management, Current Evidence and Future Perspectives.Tropical medicine and infectious disease · 2025Review
- Viruses and the Brain-A Relationship Prone to Trouble.Viruses · 2025Review
- Longitudinal CNS and systemic T-lymphocyte and monocyte activation before and after antiretroviral therapy beginning in primary HIV infection.Frontiers in immunology · 2025Article
- Repurposing lapatinib as a triple antagonist of chemokine receptors 3, 4, and 5.Molecular pharmacology · 2025Article
- Postmortem Analysis of Dolutegravir, Tenofovir, Lamivudine, and Efavirenz Penetration in Multiple Central Nervous System Compartments.The Journal of infectious diseases · 2024Article
- Neurosymptomatic HIV-1 CSF escape is associated with replication in CNS T cells and inflammation.The Journal of clinical investigation · 2024Article
- Changes in cerebrospinal fluid proteins across the spectrum of untreated and treated chronic HIV-1 infection.PLoS pathogens · 2024Article
- Characterization of HIV variants from paired Cerebrospinal fluid and Plasma samples in primary microglia and CD4Journal of neurovirology · 2024Article
123 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system (CNS) can lead to the development of HIV-1-associated dementia (HAD). We examined the virological characteristics of HIV-1 in the cerebrospinal fluid (CSF) of HAD subjects to explore the association between independent viral replication in the CNS and the development of overt dementia. We found that genetically compartmentalized CCR5-tropic (R5) T cell-tropic and macrophage-tropic HIV-1 populations were independently detected in the CSF of subjects diagnosed with HIV-1-associated dementia. Macrophage-tropic HIV-1 populations were genetically diverse, representing established CNS infections, while R5 T cell-tropic HIV-1 populations were clonally amplified and associated with pleocytosis. R5 T cell-tropic viruses required high levels of surface CD4 to enter cells, and their presence was correlated with rapid decay of virus in the CSF with therapy initiation (similar to virus in the blood that is replicating in activated T cells). Macrophage-tropic viruses could enter cells with low levels of CD4, and their presence was correlated with slow decay of virus in the CSF, demonstrating a separate long-lived cell as the source of the virus. These studies demonstrate two distinct virological states inferred from the CSF virus in subjects diagnosed with HAD. Finally, macrophage-tropic viruses were largely restricted to the CNS/CSF compartment and not the blood, and in one case we were able to identify the macrophage-tropic lineage as a minor variant nearly two years before its expansion in the CNS. These results suggest that HIV-1 variants in CSF can provide information about viral replication and evolution in the CNS, events that are likely to play an important role in HIV-associated neurocognitive disorders.
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What OpenQuestion holds
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.