ArticleJournal of immunology research2021
The Ablation of Envelope Protein Glycosylation Enhances the Neurovirulence of ZIKV and Cell Apoptosis in Newborn Mice.
Article in Journal of immunology research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Beyond the Capsid: How Can Post-Translational Modifications Modulate the Multifunctionality of the Orthoflavivirus Capsid Protein?Molecules (Basel, Switzerland) · 2026Review
- ZIKV envelope protein is a strong blocker of early directional differentiation in the neural lineage.Communications biology · 2026Article
- Evolution of Zika virus inVirus evolution · 2025Article
- An accumulated mutation gained in mosquito cells enhances Zika virus virulence and fitness in mice.Journal of virology · 2024Article
- Viral Protein Accumulation of Zika Virus Variants Links with Regulation of Innate Immunity for Differential Control of Viral Replication, Spread, and Response to Interferon.Journal of virology · 2023Article
- Coronavirus accessory protein ORF3 biology and its contribution to viral behavior and pathogenesis.iScience · 2023Review
- Glycosylation of viral proteins: Implication in virus-host interaction and virulence.Virulence · 2022Review
- Animal Model of Severe Fever With Thrombocytopenia Syndrome Virus Infection.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zika virus (ZIKV) has attracted the wide global attention due to its causal link to microcephaly. In this study, two amino acid (aa) mutation (E143K and R3394K) were identified at the fourth generation (named ZKC2P4) during the serial passage of ZIKV-Asian lineage ZKC2/2016 strain in the newborn mouse brain, while another seven aa deletions in envelope (E) protein were detected in ZKC2P6. ZKC2P6 is a novel nonglycosylated E protein Asian ZIKV we first identified and provides the first direct supporting evidence that glycosylation motif could be lost during the passage in neonatal mice. To study the impact of E protein glycosylation ablation, we compared the pathogenicity of ZKC2P6 with that of ZKC2P4. The results showed that the loss of E protein glycosylation accelerated the disease progression, as evidenced by an earlier weight loss and death, a thinner cerebral cortex, and more serious tissue lesions and inflammation/necrosis. Furthermore, ZKC2P6 exhibited a greater ability to replicate and caused severer cell apoptosis than that of ZKC2P4. Therefore, the ablation of E glycosylation generally enhances the neurovirulence of ZIKV and cell apoptosis in newborn mice.
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Registered trials
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