ArticleViruses2022
A Single Mutation at Position 120 in the Envelope Protein Attenuates Tembusu Virus in Ducks.
Article in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Duplication of specialized cis-acting elements SLI and SLIII in the viral RNA 3'UTR enables mosquito-borne orthoflavivirus adaptation to avian hosts.Nucleic acids research · 2026Article
- Article
- Review
- Computational Analysis Predicts Correlations among Amino Acids in SARS-CoV-2 Proteomes.Biomedicines · 2023Article
- Chicken-origin Cluster 3.2 Tembusu virus exhibits higher infectivity than duck-origin Cluster 2 Tembusu virus in chicks.Frontiers in veterinary science · 2023Article
- Pathogenesis of Cluster 1 Duck Tembusu Virus in Ducks Reveals the Impact of Viral Genotype on Pathogenicity and Disease Severity.Transboundary and emerging diseases · 2023Article
- Generation and characterization of chimeric Tembusu viruses containing pre-membrane and envelope genes of Japanese encephalitis virus.Frontiers in microbiology · 2023Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A live attenuated duck Tembusu virus (TMUV) vaccine FX2010-180P (180P) was successfully utilized to prevent TMUV infections in ducks in China. Compared with wild-type TMUV, 180P was highly attenuated and lost transmissibility in ducks. However, the mechanism of the attenuation of 180P remains poorly understood. To explore the key molecular basis of attenuation, chimeric and site mutant viruses in the background of the wild-type TMUV-FX2010 (FX) strain were rescued, and the replication, tissue tropism, and transmissibility were characterized in ducks. The results show that the envelope (E) protein was responsible for attenuation and loss of transmission in ducks. Further studies showed that a D120N amino acid mutation located in domain II of the E protein was responsible for the attenuation and transmissibility loss of 180P in ducks. The D120N substitution resulted in an extra high-mannose type N-linked glycosylation (NLG) in the E protein of 180P compared with the wild-type TMUV, which might restrict the tissue tropism and transmissibility of TMUV in ducks. Our findings elucidate that N120 in the E protein is a key molecular basis of TMUV attenuation in ducks and provide new insight into the role of NLG in TMUV tissue tropism and transmissibility.
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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.