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oai:figshare.com:article/34068954 2026-10-05T09:40:22Z category_303 portal_316 item_type_3 month_year_10_2026

Table 2_Reframing clathrin-mediated viral entry: evidence standards, context dependence and host-directed vulnerabilities.docx Qinying Wang (2805388) Liran Xu (17961809) Yangang Sun (8072717) Yuting Xia (2901131) Jingyu Yue (12314657) Clinical Microbiology AP-2 clathrin-coated pit clathrin-mediated endocytosis dynamin endosomal entry evidence hierarchy single-particle tracking viral entry <p>Viral entry is the first obligatory step of productive infection and a rational point for host-directed antiviral intervention. This structured narrative review synthesizes evidence from database searches and citation tracking performed up to 18 June 2026. Clathrin-mediated endocytosis (CME) can internalize virus-receptor complexes and deliver them to endosomal compartments that support penetration, fusion, capsid remodeling, uncoating or genome release. However, CME should be interpreted as a series of experimentally separable checkpoints rather than as a single pathway label. Viral use of CME varies with strain, receptor and cofactor availability, host-cell type, membrane composition, protease environment, inoculum size and synchronization conditions. Strict CME-dependent entry is assigned only when direct perturbation of core or proximal CME machinery, supported by rescue or an orthogonal approach, converges with stage-resolved evidence of productive virion progression through clathrin/AP-2-positive coated pits or vesicles and an early functional entry readout in a defined virus-receptor-cell context. Pharmacological findings are treated as supportive rather than universally mandatory when stronger direct mechanistic evidence is available. The review integrates receptor organization, cargo-specific adaptor recruitment, membrane lipids, particle geometry, actin dynamics and virus-induced remodeling with a transparent evidence framework that distinguishes CME-associated, CME-involved and CME-dependent entry. It further separates mechanistic probes from host-directed strategies targeting membrane sphingolipids, TPC2-dependent endolysosomal trafficking, NPC1/cholesterol homeostasis, PIKfyve and kinase-regulated trafficking. Translational priorities are framed as context-dependent opportunities requiring target engagement, disease-relevant models and in vivo validation rather than as validated consequences of global CME blockade.</p> 2026-10-05T09:40:22Z Dataset Dataset 10.3389/fcimb.2026.1929024.s002 https://figshare.com/articles/dataset/Table_2_Reframing_clathrin-mediated_viral_entry_evidence_standards_context_dependence_and_host-directed_vulnerabilities_docx/34068954 CC BY 4.0