ArticleJournal of virology2012
Rift Valley fever virus strain MP-12 enters mammalian host cells via caveola-mediated endocytosis.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed.
- Potent neutralization of Rift Valley fever virus mediated by monoclonal antibodies via concurrent inhibition of attachment and fusion.Emerging microbes & infections · 2026Article
- Review
- Review
- The lipopeptide Pam3CSK4 inhibits Rift Valley fever virus infection and protects from encephalitis.PLoS pathogens · 2024Article
- Newcastle disease virus activates diverse signaling pathways via Src to facilitate virus entry into host macrophages.Journal of virology · 2024Article
- Evaluation of Inactivation Methods for Rift Valley Fever Virus in Mouse Microglia.Pathogens (Basel, Switzerland) · 2024Article
- Making Rift Valley Fever Viral Particles Fluorescent.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Humoral immunity to phlebovirus infection.Annals of the New York Academy of Sciences · 2023Review
- Segmented, Negative-Sense RNA Viruses of Humans: Genetic Systems and Experimental Uses of Reporter Strains.Annual review of virology · 2023Review
- Rift Valley Fever Virus-Infection, Pathogenesis and Host Immune Responses.Pathogens (Basel, Switzerland) · 2023Review
- Multifunctional human monoclonal antibody combination mediates protection against Rift Valley fever virus at low doses.Nature communications · 2023Article
- Review
- Review
- Polyamine-Linked Cholesterol Incorporation in Rift Valley Fever Virus Particles Promotes Infectivity.ACS infectious diseases · 2022Article
- Immunology Meets Bioengineering: Improving the Effectiveness of Glioblastoma Immunotherapy.Cancers · 2022Review
- Studies in the antiviral molecular mechanisms of 25-hydroxycholesterol: Disturbing cholesterol homeostasis and post-translational modification of proteins.European journal of pharmacology · 2022Review
- MAVS mediates a protective immune response in the brain to Rift Valley fever virus.PLoS pathogens · 2022Article
- Immunocompromised Cas9 transgenic mice for rapidMolecular therapy. Methods & clinical development · 2021Article
- Newcastle Disease Virus Entry into Chicken Macrophages via a pH-Dependent, Dynamin and Caveola-Mediated Endocytic Pathway That Requires Rab5.Journal of virology · 2021Article
- Potent neutralization of Rift Valley fever virus by human monoclonal antibodies through fusion inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
1 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rift Valley fever virus (RVFV) is a zoonotic pathogen capable of causing serious morbidity and mortality in both humans and livestock. The lack of efficient countermeasure strategies, the potential for dispersion into new regions, and the pathogenesis in humans and livestock make RVFV a serious public health concern. The receptors, cellular factors, and entry pathways used by RVFV and other members of the family Bunyaviridae remain largely uncharacterized. Here we provide evidence that RVFV strain MP-12 uses dynamin-dependent caveola-mediated endocytosis for cell entry. Caveolae are lipid raft domains composed of caveolin (the main structural component), cholesterol, and sphingolipids. Caveola-mediated endocytosis is responsible for the uptake of a wide variety of host ligands, as well as bacteria, bacterial toxins, and a number of viruses. To determine the cellular entry mechanism of RVFV, we used small-molecule inhibitors, RNA interference (RNAi), and dominant negative (DN) protein expression to inhibit the major mammalian cell endocytic pathways. Inhibitors and RNAi specific for macropinocytosis and clathrin-mediated endocytosis had no effect on RVFV infection. In contrast, inhibitors of caveola-mediated endocytosis, and RNAi targeted to caveolin-1 and dynamin, drastically reduced RVFV infection in multiple cell lines. Expression of DN caveolin-1 also reduced RVFV infection significantly, while expression of DN EPS15, a protein required for the assembly of clathrin-coated pits, and DN PAK-1, an obligate mediator of macropinocytosis, had no significant impact on RVFV infection. These results together suggest that the primary mechanism of RVFV MP-12 uptake is dynamin-dependent, caveolin-1-mediated endocytosis.
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