ArticlePLoS pathogens2014
Anti-α4 antibody treatment blocks virus traffic to the brain and gut early, and stabilizes CNS injury late in infection.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 69 citations in OpenAlex.
- HIV Reservoirs in Brain parenchyma and Cerebrospinal Fluid During Suppressive ART: Same-Same or Very Different?Current HIV/AIDS reports · 2026Review
- α4 Integrin blockade impairs CD8+ T cell neuroimmune surveillance following SIV infection.The Journal of clinical investigation · 2026Article
- A Comparative Study of the Profile of Cognitive Impairment and Associated Factors among Subsets of Human Immunodeficiency Virus Patients in a Special Human Immunodeficiency Virus Clinic in South-East Nigeria.Annals of African medicine · 2026Article
- Resolving inflammation: The impact of antiretroviral therapy on macrophage traffic in and out of the CNS.PLoS pathogens · 2025Article
- T cell-mediated SIV dissemination into the CNS: a single-cell transcriptomic analysis.Journal of neuroinflammation · 2025Article
- Longitudinal CNS and systemic T-lymphocyte and monocyte activation before and after antiretroviral therapy beginning in primary HIV infection.Frontiers in immunology · 2025Article
- Microglia and macrophages alterations in the CNS during acute SIV infection: A single-cell analysis in rhesus macaques.PLoS pathogens · 2024Article
- Galectin-3, Galectin-9, and Interleukin-18 Are Associated with Monocyte/Macrophage Activation and Turnover More so than Simian Immunodeficiency Virus-Associated Cardiac Pathology or Encephalitis.AIDS research and human retroviruses · 2024Article
- Microglia and macrophages alterations in the CNS during acute SIV infection: a single-cell analysis in rhesus macaques.bioRxiv : the preprint server for biology · 2024Article
- Biotypes of Central Nervous System Complications in People With Human Immunodeficiency Virus: Virology, Immunology, and Neuropathology.The Journal of infectious diseases · 2023Article
- Simian immunodeficiency virus-infected rhesus macaques with AIDS co-develop cardiovascular pathology and encephalitis.Frontiers in immunology · 2023Article
- A Rationale and Approach to the Development of Specific Treatments for HIV Associated Neurocognitive Impairment.Microorganisms · 2022Review
- Neuroinflammatory transcriptional programs induced in rhesus pre-frontal cortex white matter during acute SHIV infection.Journal of neuroinflammation · 2022Article
- Developments in Neuroprotection for HIV-Associated Neurocognitive Disorders (HAND).Current HIV/AIDS reports · 2022Review
- Review
- Neuropathogenesis of HIV-1: insights from across the spectrum of acute through long-term treated infection.Seminars in immunopathology · 2022Review
- Persistent Inflammation and Non-AIDS Comorbidities During ART: Coming of the Age of Monocytes.Frontiers in immunology · 2022Review
- HIV infection is linked with reduced error-related default mode network suppression and poorer medication management abilities.Progress in neuro-psychopharmacology & biological psychiatry · 2021Article
- Advances in SIV/SHIV Non-Human Primate Models of NeuroAIDS.Pathogens (Basel, Switzerland) · 2021Review
- Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
Four SIV-infected monkeys with high plasma virus and CNS injury were treated with an anti-α4 blocking antibody (natalizumab) once a week for three weeks beginning on 28 days post-infection (late). Infection in the brain and gut were quantified, and neuronal injury in the CNS was assessed by MR spectroscopy, and compared to controls with AIDS and SIV encephalitis. Treatment resulted in stabilization of ongoing neuronal injury (NAA/Cr by 1H MRS), and decreased numbers of monocytes/macrophages and productive infection (SIV p28+, RNA+) in brain and gut. Antibody treatment of six SIV infected monkeys at the time of infection (early) for 3 weeks blocked monocyte/macrophage traffic and infection in the CNS, and significantly decreased leukocyte traffic and infection in the gut. SIV - RNA and p28 was absent in the CNS and the gut. SIV DNA was undetectable in brains of five of six early treated macaques, but proviral DNA in guts of treated and control animals was equivalent. Early treated animals had low-to-no plasma LPS and sCD163. These results support the notion that monocyte/macrophage traffic late in infection drives neuronal injury and maintains CNS viral reservoirs and lesions. Leukocyte traffic early in infection seeds the CNS with virus and contributes to productive infection in the gut. Leukocyte traffic early contributes to gut pathology, bacterial translocation, and activation of innate immunity.
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