ArticleJournal of virology2008
West Nile virus entry requires cholesterol-rich membrane microdomains and is independent of alphavbeta3 integrin.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
78 citing papers in PubMed, 138 citations in OpenAlex.
- West Nile virus: epidemiology, prevention, clinical features, diagnosis, treatment, and open research questions.Annals of medicine · 2026Review
- CALR-dependent endoplasmic reticulum N-glycoprotein maturation promotes Japanese encephalitis virus entry and replication.Cell & bioscience · 2026Article
- Review
- Arboviruses in Cancer therapy: pros and cons.Journal of neurovirology · 2026Review
- West Nile virus unmasked: from gene variability to future challenges.Frontiers in cellular and infection microbiology · 2025Review
- Glycerophospholipid remodeling is critical for orthoflavivirus infection.Nature communications · 2024Article
- Two novel compounds inhibit Flavivirus infectionJournal of virology · 2024Article
- Zika virus prM protein contains cholesterol binding motifs required for virus entry and assembly.Nature communications · 2023Article
- ARF1 with Sec7 Domain-Dependent GBF1 Activates Coatomer Protein I To Support Classical Swine Fever Virus Entry.Journal of virology · 2022Article
- αVβ3 Integrin Expression Is Essential for Replication of Mosquito and Tick-Borne Flaviviruses in Murine Fibroblast Cells.Viruses · 2021Article
- Role of Lipid Transfer Proteins (LTPs) in the Viral Life Cycle.Frontiers in microbiology · 2021Review
- Anti-flavivirus Properties of Lipid-Lowering Drugs.Frontiers in physiology · 2021Review
- Role of Lipid Rafts in Pathogen-Host Interaction - A Mini Review.Frontiers in immunology · 2021Review
- Membrane Rafts: Portals for Viral Entry.Frontiers in microbiology · 2021Review
- Zika Virus Targets Glioblastoma Stem Cells through a SOX2-Integrin αCell stem cell · 2020Article
- Characterization of Zika Virus Endocytic Pathways in Human Glioblastoma Cells.Frontiers in microbiology · 2020Article
- Targeting Lipid Rafts as a Strategy Against Coronavirus.Frontiers in cell and developmental biology · 2020Review
- Lipophilic statins inhibit Zika virus production in Vero cells.Scientific reports · 2019Article
- Cellular cholesterol abundance regulates potassium accumulation within endosomes and is an important determinant in bunyavirus entry.The Journal of biological chemistry · 2019Article
- The Role of Host Cytoskeleton in Flavivirus Infection.Virologica Sinica · 2019Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
West Nile virus (WNV) has been the leading cause of viral encephalitis in the United States since 1999. The endocytic processes involved in the internalization of infectious WNV by various cell types are not well characterized, and the involvement of cholesterol-rich membrane microdomains, or lipid rafts, in the life cycle of WNV has not been investigated previously. In this study, we found that the depletion of cellular cholesterol levels by brief treatment with methyl-beta-cyclodextrin resulted in a 100-fold reduction of the titers of infectious WNV released into the culture supernatant, as well as a reduction in the number of WNV genome copies in the cholesterol-depleted cells. The addition of exogenous cholesterol to cholesterol-depleted cells reversed this effect. Cholesterol depletion postinfection did not affect WNV growth, suggesting that the effect occurs at the level of WNV entry. We also showed that while WNV entry did not require alphavbeta3 integrin and focal adhesion kinase, WNV particles failed to be internalized by cholesterol-depleted cells. Finally, we showed the colocalization of the WNV envelope protein and cholera toxin B, which is internalized in a lipid raft-dependent pathway, in microdomain clusters at the plasma membrane. These data suggest that WNV utilizes lipid rafts during initial stages of internalization and that the lipid rafts may contain a factor(s) that may enhance WNV endocytosis.
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.