ArticleVeterinary microbiology2013
Rabies virus glycoprotein is an important determinant for the induction of innate immune responses and the pathogenic mechanisms.
Article in Veterinary microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 67 citations in OpenAlex.
- TRIM7 Inhibits Rabies Virus Replication by Promoting K48-Linked Ubiquitination and Degradation of RABV-M.Emerging microbes & infections · 2026Article
- Combined Glycoprotein Mutations in Rabies Virus Promote Astrocyte Tropism and Protective CNS Immunity in Mice.Viruses · 2026Article
- Geographic Distribution of Rabies Virus and Genomic Sequence Alignment of Wild and Vaccine Strains, Kenya.Emerging infectious diseases · 2024Article
- TRIM44 Promotes Rabies Virus Replication by Autophagy-Dependent Mechanism.International journal of molecular sciences · 2024Article
- TMP269, a small molecule inhibitor of class IIa HDAC, suppresses RABV replicationFrontiers in microbiology · 2023Article
- Looking at the Pathogenesis of the Rabies Lyssavirus Strain Pasteur Vaccins through a Prism of the Disorder-Based Bioinformatics.Biomolecules · 2022Article
- Regulation of innate immune responses by rabies virus.Animal models and experimental medicine · 2022Review
- Production, purification, and characterization of recombinant rabies virus glycoprotein expressed in PichiaPink™ yeast.Biotechnology reports (Amsterdam, Netherlands) · 2022Article
- Review
- Early diagnosis of rabies virus infection by RPA-CRISPR techniques in a rat model.Archives of virology · 2021Article
- Preexposure and Postexposure Prophylaxis of Rabies With Adeno-Associated Virus Expressing Virus-Neutralizing Antibody in Rodent Models.Frontiers in microbiology · 2021Article
- Inflammatory response and MAPK and NF-κB pathway activation induced by natural street rabies virus infection in the brain tissues of dogs and humans.Virology journal · 2020Article
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- Change in the Single Amino Acid Site 83 in Rabies Virus Glycoprotein Enhances the BBB Permeability and Reduces Viral Pathogenicity.Frontiers in cell and developmental biology · 2020Article
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- Serine residues at positions 162 and 166 of the rabies virus phosphoprotein are critical for the induction of oxidative stress in rabies virus infection.Journal of neurovirology · 2017Article
- Critical Role of K1685 and K1829 in the Large Protein of Rabies Virus in Viral Pathogenicity and Immune Evasion.Journal of virology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Our previous studies have suggested that street and fixed rabies viruses (RABVs) induce diseases in the mouse model via different mechanisms. In the present study, attempts were made to determine if it is the glycoprotein (G) that is responsible for the observed differences in the pathogenic mechanisms. To this end, an infectious clone from fixed virus B2c was established and used as a backbone for exchange of the G from street viruses. The rate of viral replication, expression of viral proteins, and the induction of innate immune responses were compared in cells or in mice infected with each of the viruses. Furthermore, the infiltration of inflammatory cells into the CNS and the enhancement of blood-brain barrier (BBB) permeability were also compared. It was found that fixed viruses induced stronger innate immune responses (expression of chemokines, infiltration of inflammatory cells, and enhancement of BBB permeability) than street RABV or recombinant viruses expressing the G from street RABVs. Fixed viruses induce disease via an immune-mediated pathogenic mechanism while street viruses or recombinant viruses expressing the G from street RABVs induce diseases via a mechanism other than immune-mediated pathogenesis. Therefore, RABV G is an important determinant for the induction of innate immune responses and consequently the pathogenic mechanisms.
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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.