ArticleThe Journal of infectious diseases2017
CD-loop Extension in Zika Virus Envelope Protein Key for Stability and Pathogenesis.
Article in The Journal of infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Review
- Identifying crucial E-protein residues responsible for unusual stability of Zika virus envelope.Biophysical journal · 2021Article
- The key amino acids of E protein involved in early flavivirus infection: viral entry.Virology journal · 2021Review
- Article
- Zika virus infection enhances future risk of severe dengue disease.Science (New York, N.Y.) · 2020Article
- Protective and enhancing interactions among dengue viruses 1-4 and Zika virus.Current opinion in virology · 2020Review
- Role of Zika Virus Envelope Protein Domain III as a Target of Human Neutralizing Antibodies.mBio · 2019Article
- Article
- Shortening of Zika virus CD-loop reduces neurovirulence while preserving antigenicity.PLoS neglected tropical diseases · 2019Article
- Probing Zika Virus Neutralization Determinants with Glycoprotein Mutants Bearing Linear Epitope Insertions.Journal of virology · 2018Article
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
With severe disease manifestations including microcephaly, congenital malformation, and Guillain-Barré syndrome, Zika virus (ZIKV) remains a persistent global public health threat. Despite antigenic similarities with dengue viruses, structural studies have suggested the extended CD-loop and hydrogen-bonding interaction network within the ZIKV envelope protein contribute to stability differences between the viral families. This enhanced stability may lead to the augmented infection, disease manifestation, and persistence in body fluids seen following ZIKV infection. To examine the role of these motifs in infection, we generated a series of ZIKV recombinant viruses that disrupted the hydrogen-bonding network (350A, 351A, and 350A/351A) or the CD-loop extension (Δ346). Our results demonstrate a key role for the ZIKV extended CD-loop in cell-type-dependent replication, virion stability, and in vivo pathogenesis. Importantly, the Δ346 mutant maintains similar antigenicity to wild-type virus, opening the possibility for its use as a live-attenuated vaccine platform for ZIKV and other clinically relevant flaviviruses.
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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.