ReviewFrontiers in cellular and infection microbiology2026
Reframing clathrin-mediated viral entry: evidence standards, context dependence and host-directed vulnerabilities.
Review in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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5 authors.
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Abstract
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
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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.