ArticleVeterinary microbiology2010
Critical role of cholesterol in bovine herpesvirus type 1 infection of MDBK cells.
Article in Veterinary microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Rotavirus C Replication in Porcine Intestinal Enteroids Reveals Roles for Cellular Cholesterol and Sialic Acids.Viruses · 2022Article
- Nutraceutical Curcumin with Promising Protection against Herpesvirus Infections and Their Associated Inflammation: Mechanisms and Pathways.Microorganisms · 2021Review
- Curcumin as an Antiviral Agent.Viruses · 2020Review
- Induction of the Unfolded Protein Response during Bovine Alphaherpesvirus 1 Infection.Viruses · 2020Article
- Role of Sphingomyelin in Alphaherpesvirus Entry.Journal of virology · 2019Article
- Cellular cholesterol is required for porcine nidovirus infection.Archives of virology · 2017Article
- The role of phospholipase C signaling in bovine herpesvirus 1 infection.Veterinary research · 2017Article
- Critical role of the lipid rafts in caprine herpesvirus type 1 infection in vitro.Virus research · 2016Article
- Cholesterol-rich lipid rafts play an important role in the Cyprinid herpesvirus 3 replication cycle.Veterinary microbiology · 2015Article
- Role of the lipid rafts in the life cycle of canine coronavirus.The Journal of general virology · 2015Article
- Critical role of cellular cholesterol in bovine rotavirus infection.Virology journal · 2014Article
- A cholesterol tag at the N terminus of the relatively broad-spectrum fusion inhibitory peptide targets an earlier stage of fusion glycoprotein activation and increases the peptide's antiviral potency in vivo.Journal of virology · 2013Article
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Authors and funding
6 authors.
Funding
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Abstract
Cholesterol is involved in the life cycle of many viruses. Here, we examined the role of cholesterol for both viral envelope and target cell membrane for bovine herpesvirus type 1 (BoHV-1) infection. Cholesterol depletion by pretreatment of Madin-Darby bovine kidney (MDBK) cells with a cholesterol-sequestering drug methyl-beta-cyclodextrin (MbetaCD), inhibited the production of BoHV-1 in a dose-dependent manner. This inhibitory effect was partially reversed by cholesterol replenishment, indicating that the reduction was caused by cholesterol depletion. Cholesterol depletion at the post-entry stage only had a mild effect on the virus production. However, cell membrane cholesterol depletion did not reduce the virus attachment. In addition, treatment of BoHV-1 particles with MbetaCD also reduced the virus infectivity significantly and the effect was partially reversed by addition of exogenous cholesterol. Taken together, these data implicated that cell membrane cholesterol mainly contributed to BoHV-1 entry into MDBK cells and the viral envelope cholesterol was also essential for the virus infectivity.
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