ArticlePLoS pathogens2025
TfR1 facilitates influenza virus endocytosis and uncoating by interacting with NA and M1 via extracellular and intracellular domains.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
- Identification of Prohibitin (PHB) as an Entry Factor of Highly Pathogenic Coronaviruses Using Metabolic Glycoengineering and Photo-Crosslinking Techniques.Emerging microbes & infections · 2026Article
- Transferrin receptor 1 is required for efficient hepatitis E virus production.PLoS pathogens · 2026Article
- Transferrin receptor 1 binds human parvovirus B19 VP1u to facilitate entry.Nature communications · 2026Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
An intriguing enigma in virology is the utilization of transferrin receptor 1 (TfR1) by various viruses as an entry portal into host cells, a mechanism that remains relatively underexplored. In this study, we report a strategy to investigate the multifaceted aspects of viral entry, using Influenza A viruses (IAVs) as a model system. By decorating the sialylated viral envelope with photo-crosslinking moieties, we identify and elucidate the pivotal role of TfR1 in this process. Our results demonstrate that TfR1 initially functions as a receptor, interacting with the viral neuraminidase (NA) through its extracellular apical domain, thereby initiating viral endocytosis. Subsequently, TfR1 acts as a matrix degradator, engaging its intracellular stop-transfer sequence with the viral matrix protein 1 (M1), which in turn triggers proteasome- and aggresome-mediated nucleocapsid uncoating. The identification of the molecular interactions between TfR1 and NA, as well as the reciprocal degradation of TfR1 and M1 not only illuminates a cellular pathway that enriches our understanding of viral entry mechanisms but also presents exciting avenues for the development of innovative antiviral strategies beyond IAVs.
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Registered trials
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