ArticleEMBO molecular medicine2023
mAb therapy controls CNS-resident lyssavirus infection via a CD4 T cell-dependent mechanism.
Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Peripheral human mAb therapy yields modulation of neuroinflammation and long-term functional recovery from lyssavirus infection.Emerging microbes & infections · 2026Article
- Breaking the Silent Barrier: Engineering Antibodies for Brain-Targeted Rabies Immunotherapy.Pharmaceutics · 2026Review
- Biological barriers underlying the extremely high fatality of symptomatic rabies: neuroinvasion, immune evasion, and blood-brain barrier restriction.Frontiers in immunology · 2026Review
- A SynB1-conjugated antibody cocktail crosses the blood-brain barrier to produce a therapeutic effect on rabies.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Targeting SARM1 as a novel neuroprotective therapy in neurotropic viral infections.Journal of neuroinflammation · 2025Article
- Review
- Toward the Development of a Pan-Lyssavirus Vaccine.Viruses · 2024Article
- Human Rabies Treatment-From Palliation to Promise.Viruses · 2024Review
- mAb therapy controls CNS-resident lyssavirus infection via a CD4 T cell-dependent mechanism.EMBO molecular medicine · 2023Article
- Establishment of a longitudinal pre-clinical model of lyssavirus infection.Journal of virological methods · 2020Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 3 countries.
Funding
Abstract
Infections with rabies virus (RABV) and related lyssaviruses are uniformly fatal once virus accesses the central nervous system (CNS) and causes disease signs. Current immunotherapies are thus focused on the early, pre-symptomatic stage of disease, with the goal of peripheral neutralization of virus to prevent CNS infection. Here, we evaluated the therapeutic efficacy of F11, an anti-lyssavirus human monoclonal antibody (mAb), on established lyssavirus infections. We show that a single dose of F11 limits viral load in the brain and reverses disease signs following infection with a lethal dose of lyssavirus, even when administered after initiation of robust virus replication in the CNS. Importantly, we found that F11-dependent neutralization is not sufficient to protect animals from mortality, and a CD4 T cell-dependent adaptive immune response is required for successful control of infection. F11 significantly changes the spectrum of leukocyte populations in the brain, and the FcRγ-binding function of F11 contributes to therapeutic efficacy. Thus, mAb therapy can drive potent neutralization-independent T cell-mediated effects, even against an established CNS infection by a lethal neurotropic virus.
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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.