ArticleFrontiers in microbiology2016
Duck Tembusu Virus Exhibits Pathogenicity to Kunming Mice by Intracerebral Inoculation.
Article in Frontiers in microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 55 citations in OpenAlex.
- Exosomes mediate intercellular transmission of Tembusu virus via the NS4A-Rab27a axis.Veterinary research · 2026Article
- Development and Humanization of a Camelid-Derived Neutralizing Nanobody Targeting Botulinum Neurotoxin Type A.International journal of nanomedicine · 2026Article
- The A487 residue in the E protein of duck Tembusu virus significantly enhances viral replication and increases its neurovirulence in Kunming mice.Journal of virology · 2025Article
- Natural fatal infection of Tembusu virus in bottlenose dolphins in Thailand.Scientific reports · 2025Article
- Article
- Duck Tembusu virus NS3 protein induces apoptosis by activating the PERK/PKR pathway and mitochondrial pathway.Journal of virology · 2023Article
- Duck Tembusu virus induces incomplete autophagy via the ERK/mTOR and AMPK/mTOR signalling pathways to promote viral replication in neuronal cells.Veterinary research · 2023Article
- Comparative study of the pathogenicity of the mosquito origin strain and duck origin strain of Tembusu virus in ducklings and three-week-old mice.Virologica Sinica · 2023Article
- Isolation and characterization of a novel goose ovaritis-associated cluster 3 Tembusu virus.Poultry science · 2023Article
- 34-kDa salivary protein enhances duck Tembusu virus infectivity in the salivary glands of Aedes albopictus by modulating the innate immune response.Scientific reports · 2023Article
- Ultrastructural study of the duck brain infected with duck Tembusu virus.Frontiers in microbiology · 2023Article
- Stem-Loop I of the Tembusu Virus 3'-Untranslated Region Is Responsible for Viral Host-Specific Adaptation and the Pathogenicity of the Virus in Mice.Microbiology spectrum · 2022Article
- Tembusu Virus entering the central nervous system caused nonsuppurative encephalitis without disrupting the blood-brain barrier.Journal of virology · 2021Article
- Duck Tembusu Virus Infection Promotes the Expression of Duck Interferon-Induced Protein 35 to Counteract RIG-I Antiviral Signaling in Duck Embryo Fibroblasts.Frontiers in immunology · 2021Article
- Article
- Determinants of duck Tembusu virus NS2A/2B polyprotein procession attenuated viral replication and proliferation in vitro.Scientific reports · 2020Article
- Innate immune responses to duck Tembusu virus infection.Veterinary research · 2020Review
- Binding of Duck Tembusu Virus Nonstructural Protein 2A to Duck STING Disrupts Induction of Its Signal Transduction Cascade To Inhibit Beta Interferon Induction.Journal of virology · 2020Article
- Article
- Autophagy Promotes Duck Tembusu Virus Replication by Suppressing p62/SQSTM1-Mediated Innate Immune Responses In Vitro.Vaccines · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, Kunming mice were used as the animal models to study the pathogenicity of TMUV. Three groups of 3-week-old female Kunming mice (n = 15 mice per group) were infected with the SDSG strain of TMUV in 50 μL allantoic fluid (10(4.8) ELD50/0.2 ml) respectively by the intracerebral (i.c.), subcutaneous (s.c.) and intranasal (i.n.) routes. The control group (n = 15 mice) was inoculated with 50 μL sterile phosphate-buffered saline. Clinical signs, gross, and microscopic lesions, viral loads in different tissues, and serum antibody titers were examined and recorded. Kunming mice infected intracerebrally showed typical clinical symptoms, including severe hindlimb paralysis, weight loss and death. Only dead mice presented severe intestinal mucosal edema. No gross lesions were observed in mice sequentially euthanized. However, microscopic lesions in the brain, spleen, liver, kidney, and lung were very typical including varying degrees of viral encephalitis, lymphocytes depletion, liver cell necrosis and nephritis, etc. Viral loads in different tissues were detected by the SYBR Green I real-time PCR assay. Viral loads in the brain, liver, and spleen were first detected and maintained a longer time, which indicated that these organs may be the target organs of TMUV. The level of viral loads was consistent with the severity of clinical signs and microscopic lesions in different tissues. The neutralizing antibody began to seroconvert at 8 dpi. Clinical signs, microscopic lesions, viral loads and serum neutralizing antibodies weren't observed in other groups. In summary, TMUV can cause systemic infections and death in Kunming mice by i.c., which provides some experimental basis for further study of the significance of TMUV in public health.
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