ArticleFrontiers in cellular and infection microbiology2023
Rabies virus uniquely reprograms the transcriptome of human monocyte-derived macrophages.
Article in Frontiers in cellular and infection microbiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Langerhans cells as targets of rabies virus immune evasion.The Journal of general virology · 2026Article
- Biological barriers underlying the extremely high fatality of symptomatic rabies: neuroinvasion, immune evasion, and blood-brain barrier restriction.Frontiers in immunology · 2026Review
- Article
- Immunohistochemical investigation of canine lymph nodes collected during a rabies outbreak in South Africa.The Journal of general virology · 2025Article
- Temporally integrated multiomics analysis elucidates intricate regulatory mechanisms of ASFV in a wild boar lung-derived clonal cell line.Veterinary research · 2025Article
- Selective inhibition of rabies virus gene expression by human miRNAs: a therapeutic approach using the 7mer-m8 model.Virus genes · 2025Article
- A comparative analysis of the dendritic cell response upon exposure to different rabies virus strains.PLoS neglected tropical diseases · 2025Article
- Comparative Transcriptomics Analysis of Foot-and-Mouth Disease Virus-Infected Cell Model Systems.Veterinary sciences · 2025Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are amongst the first immune cells that encounter rabies virus (RABV) at virus entry sites. Activation of macrophages is essential for the onset of a potent immune response, but insights into the effects of RABV on macrophage activation are scarce. In this study we performed high-throughput sequencing on RNA extracted from macrophages that were exposed to RABV for 48 hours, and compared their transcriptional profiles to that of non-polarized macrophages (M0), and macrophages polarized towards the canonical M1, M2a and M2c phenotypes. Our analysis revealed that RABV-stimulated macrophages show high expression of several M1, M2a and M2c signature genes. Apart from their partial resemblance to these phenotypes, unbiased clustering analysis revealed that RABV induces a unique and distinct polarization program. Closer examination revealed that RABV induced multiple pathways related to the interferon- and antiviral response, which were not induced under other classical polarization strategies. Surprisingly, our data show that RABV induces an activated rather than a fully suppressed macrophage phenotype, triggering virus-induced activation and polarization. This includes multiple genes with known antiviral (e.g. APOBEC3A, IFIT/OAS/TRIM genes), which may play a role in anti-RABV immunity.
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