ArticleFrontiers in microbiology2018
Analysis of Mouse Brain Transcriptome After Experimental Duvenhage Virus Infection Shows Activation of Innate Immune Response and Pyroptotic Cell Death Pathway.
Article in Frontiers in microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- A novel murine model of Sjögren's disease using lacrimal autoantigen.Frontiers in immunology · 2026Article
- Immunological findings of West Caucasian bat virus in an accidental host.Journal of virology · 2025Article
- Rabies Virus Infection Causes Pyroptosis of Neuronal Cells.International journal of molecular sciences · 2024Article
- Rabies virus infection is associated with variations in calbindin D-28K and calretinin mRNA expression levels in mouse brain tissue.Archives of virology · 2023Article
- Rabies virus uniquely reprograms the transcriptome of human monocyte-derived macrophages.Frontiers in cellular and infection microbiology · 2023Article
- Uncovering potential single nucleotide polymorphisms, copy number variations and related signaling pathways in primary Sjogren's syndrome.Bioengineered · 2021Article
- Early Transcriptional Changes in Rabies Virus-Infected Neurons and Their Impact on Neuronal Functions.Frontiers in microbiology · 2021Article
- Transcriptome Profile During Rabies Virus Infection: Identification of Human CXCL16 as a Potential New Viral Target.Frontiers in cellular and infection microbiology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rabies is an important neglected disease, characterized by invariably fatal encephalitis. Several studies focus on understanding the pathogenic mechanisms of the prototype lyssavirus rabies virus (RABV) infection, and little is known about the pathogenesis of rabies caused by other lyssaviruses. We sought to characterize the host response to Duvenhage virus infection and compare it with responses observed during RABV infection by gene expression profiling of brains of mice with the respective infections. We found in both infections differentially expressed genes leading to increased expression of type I interferons (IFNs), chemokines, and proinflammatory cytokines. In addition several genes of the IFN signaling pathway are up-regulated, indicating a strong antiviral response and activation of the negative feedback mechanism to limit type I IFN responses. Furthermore we provide evidence that in the absence of significant neuronal apoptotic death, cell death of neurons is mediated via the pyroptotic pathway in both infections. Taken together, we have identified several genes and/or pathways for both infections that could be used to explore novel approaches for intervention strategies against rabies.
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Registered trials
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