ArticleJournal of biomedical science2024
The glycosylation deficiency of flavivirus NS1 attenuates virus replication through interfering with the formation of viral replication compartments.
Article in Journal of biomedical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- The oligosaccharyltransferase TaOST1B promotes viral infection by enhancement of RNA silencing suppression in wheat.Nature communications · 2026Article
- Divergent roles of Hsp70 chaperones in orthoflavivirus protein secretion and virion formation.Npj viruses · 2026Article
- Roles of non-structural protein 1 in dengue virus replication and immunomodulation in vivo.The Journal of veterinary medical science · 2026Article
- Application of Orthoflavivirus Pseudovirus Technology in Antiviral Research.International journal of molecular sciences · 2026Review
- Hiding in plain sight: Genomic and phenotypic characterization of mosquito-borne Bussuquara virus.PLoS neglected tropical diseases · 2025Article
- The Sweet Aspects of Orthoflavivirus Treatment Design and Vaccine Development.Journal of medical virology · 2025Review
- N-glycosylation of the PEDV spike protein modulates viral replication and pathogenicity.Veterinary research · 2025Article
- Development of a Noninfectious Japanese Encephalitis Virus Replicon for Antiviral Drug Screening and Gene Function Studies.Viruses · 2025Article
- Attenuating Mutations in Usutu Virus: Towards Understanding Orthoflavivirus Virulence Determinants and Live Attenuated Vaccine Design.Vaccines · 2025Article
- TRIM14 restricts tembusu virus infection through degrading viral NS1 protein and activating type I interferon signaling.PLoS pathogens · 2025Article
- The Japanese encephalitis virus NS1 protein concentrates ER membranes in a cytoskeleton-independent manner to facilitate viral replication.Journal of virology · 2025Article
- Towards a Universal Translator: Decoding the PTMs That Regulate Orthoflavivirus Infection.Viruses · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundFlavivirus is a challenge all over the world. The replication of flavivirus takes place within membranous replication compartments (RCs) derived from endoplasmic reticulum (ER). Flavivirus NS1 proteins have been proven essential for the formation of viral RCs by remodeling the ER. The glycosylation of flavivirus NS1 proteins is important for viral replication, yet the underlying mechanism remains unclear.
methodsHeLa cells were used to visualize the ER remodeling effects induced by NS1 expression. ZIKV replicon luciferase assay was performed with BHK-21 cells. rZIKV was generated from BHK-21 cells and the plaque assay was done with Vero Cells. Liposome co-floating assay was performed with purified NS1 proteins from 293T cells.
resultsWe found that the glycosylation of flavivirus NS1 contributes to its ER remodeling activity. Glycosylation deficiency of NS1, either through N-glycosylation sites mutations or tunicamycin treatment, compromises its ER remodeling activity and interferes with viral RCs formation. Disruption of NS1 glycosylation results in abnormal aggregation of NS1, rather than reducing its membrane-binding activity. Consequently, deficiency in NS1 glycosylation impairs virus replication.
conclusionsIn summary, our results highlight the significance of NS1 glycosylation in flavivirus replication and elucidate the underlying mechanism. This provides a new strategy for combating flavivirus infections.
Indexed as
Identifiers
What OpenQuestion holds
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.