ArticleJournal of virology2005
Acid-resistant bovine pestivirus requires activation for pH-triggered fusion during entry.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 83 citations in OpenAlex.
- A Bovine Cell Line Resistant to Japanese Encephalitis Virus Entry but Permissive to Post-Entry Replication.Viruses · 2026Article
- Virus-neutralizing monoclonal antibodies against bovine viral diarrhea virus and classical swine fever virus target conformational and linear epitopes on E2 glycoprotein subdomains.Microbiology spectrum · 2025Article
- Structures of the Hepaci-, Pegi-, and Pestiviruses envelope proteins suggest a novel membrane fusion mechanism.PLoS biology · 2023Article
- Review
- Article
- Viral Traits and Cellular Knock-Out Genotype Affect Dependence of BVDV on Bovine CD46.Pathogens (Basel, Switzerland) · 2021Article
- Evaluating Large Spontaneous Deletions in a Bovine Cell Line Selected for Bovine Viral Diarrhea Virus Resistance.Viruses · 2021Article
- The EViruses · 2021Article
- ADAM17 is an essential attachment factor for classical swine fever virus.PLoS pathogens · 2021Article
- Real Time Analysis of Bovine Viral Diarrhea Virus (BVDV) Infection and Its Dependence on Bovine CD46.Viruses · 2020Article
- Functional expression and characterization of the envelope glycoprotein E1E2 heterodimer of hepatitis C virus.PLoS pathogens · 2019Article
- Fluorophore labelled BVDV: a novel tool for the analysis of infection dynamics.Scientific reports · 2019Article
- Cell-to-Cell Transmission Is the Main Mechanism Supporting Bovine Viral Diarrhea Virus Spread in Cell Culture.Journal of virology · 2019Article
- Regulated Entry of Hepatitis C Virus into Hepatocytes.Viruses · 2017Review
- Classical Swine Fever-An Updated Review.Viruses · 2017Review
- Entry of Classical Swine Fever Virus into PK-15 Cells via a pH-, Dynamin-, and Cholesterol-Dependent, Clathrin-Mediated Endocytic Pathway That Requires Rab5 and Rab7.Journal of virology · 2016Article
- Fusion of Enveloped Viruses in Endosomes.Traffic (Copenhagen, Denmark) · 2016Review
- Morphology and Molecular Composition of Purified Bovine Viral Diarrhea Virus Envelope.PLoS pathogens · 2016Article
- Review
- Molecular characterization of E2 glycoprotein of classical swine fever virus: adaptation and propagation in porcine kidney cells.In vitro cellular & developmental biology. Animal · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The route of internalization of the pestivirus bovine viral diarrhea virus (BVDV) was studied by using different chemical and biophysical inhibitors of endocytosis. Expression of the dominant-negative mutant Dyn(K44A) of the GTPase dynamin in MDBK cells, as well as the treatment of the cells with chlorpromazine and beta-methyl-cyclodextrin inhibited BVDV entry. BVDV infection was also abolished by potassium (K+) depletion, hyperosmolarity, and different inhibitors of endosomal acidification. We conclude that BVDV likely enters the cell by clathrin-dependent endocytosis and that acidification initiates fusion with the endosomal membrane. Further studies revealed that BVDV was unable to undergo "fusion from without" at low pH. The finding that low pH is not sufficient to force adsorbed BVDV into fusion with the plasma membrane is compatible with the remarkable resistance of pestiviruses to inactivation by low pH. The importance of the abundant intra- and intermolecular disulfide bonds in BVDV glycoproteins for virus stability was studied by the use of reducing agents. The combination of dithiothreitol and acidic pH led to partial inactivation of BVDV and allowed fusion from without at low efficiency. Evidence is provided here that acid-resistant BVDV is destabilized during endocytosis to become fusogenic at an endosomal acidic pH. We suggest that destabilization of the virion occurs by breakage of disulfide bonds in the glycoproteins by an unknown mechanism.
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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.