ArticleIn vitro cellular & developmental biology. Animal2010
Entry of bovine viral diarrhea virus into ovine cells occurs through clathrin-dependent endocytosis and low pH-dependent fusion.
Article in In vitro cellular & developmental biology. Animal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Host cell factors involved in classical swine fever virus entry.Veterinary research · 2023Review
- Review
- Article
- ADAM17 is an essential attachment factor for classical swine fever virus.PLoS pathogens · 2021Article
- Host receptors: the key to establishing cells with broad viral tropism for vaccine production.Critical reviews in microbiology · 2020Review
- 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
- Cell Walls and the Convergent Evolution of the Viral Envelope.Microbiology and molecular biology reviews : MMBR · 2015Review
- Suppression of influenza A virus replication in human lung epithelial cells by noncytotoxic concentrations bafilomycin A1.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Prolonged activity of the pestiviral RNase Erns as an interferon antagonist after uptake by clathrin-mediated endocytosis.Journal of virology · 2014Article
- Structural models of the membrane anchors of envelope glycoproteins E1 and E2 from pestiviruses.Virology · 2014Article
- Crystal structure of glycoprotein E2 from bovine viral diarrhea virus.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although mechanisms of bovine viral diarrhea virus (BVDV) entry into bovine cells have been elucidated, little is known concerning pestivirus entry and receptor usage in ovine cells. In this study, we determined the entry mechanisms of BVDV-1 and BVDV-2 in sheep fetal thymus cells. Both BVDV-1 and BVDV-2 infections were inhibited completely by chlorpromazine, beta-methyl cyclodextrin, sucrose, bafilomycin A1, chloroquine, and ammonium chloride. Simultaneous presence of reducing agent and low pH resulted in marked loss of BVDV infectivity. Moreover, BVDV was unable to fuse with ovine cell membrane by the presence of reducing agent or low pH alone, while combination of both led to fusion at low efficiency. Furthermore, sheep fetal thymus cells acutely infected with BVDV-1 or BVDV-2 were found protected from heterologous BVDV infection. Taken together, our results showed for the first time that entry of both BVDV-1 and BVDV-2 into ovine cells occurred through clathrin-dependent endocytosis, endosomal acidification, and low pH-dependent fusion following an activation step, besides suggesting the involvement of a common ovine cellular receptor during attachment and entry.
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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.