ArticleMicrobiology spectrum2025
Cholesterol-rich lipid rafts mediate endocytosis as a common pathway for respiratory syncytial virus entry into different host cells.
Article in Microbiology spectrum, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Intravital Depletion of Cholesterol Reduces Membrane Dynamics and Increases Mechanosensitivity in Osteocytes In Vivo.bioRxiv : the preprint server for biology · 2026Article
- Article
- Polyphenols fromMembranes · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
The entry of respiratory syncytial virus (RSV) into host cells is a multifaceted process involving viral adsorption, interaction of viral glycoproteins with cellular receptors, and utilization of various invasion pathways. Despite these complexities, our understanding of potential common pathways facilitating RSV entry remains limited. In this study, we demonstrate that endocytosis via cholesterol-rich lipid rafts is a common mechanism utilized by various RSV genotypes in different cell types. Specifically, RSV strains A2, B18537, and the currently epidemic ON1 strains all employ this mechanism to gain entry into human cell lines, including HEp-2, A549, and primary human bronchial epithelial cells. Cellular receptors binding to viral fusion glycoprotein were recruited to cholesterol-rich lipid rafts, leading to actin rearrangement and endosome formation, which facilitated viral entry. Furthermore, reducing cholesterol levels using methyl-β-cyclodextrin, simvastatin, or terbinafine inhibited RSV infection. Notably, combining simvastatin with an RSV fusion protein inhibitor (AK0529) resulted in enhanced antiviral effects both
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