ArticleNature microbiology2021
Restriction factor compendium for influenza A virus reveals a mechanism for evasion of autophagy.
Article in Nature microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 45 citations in OpenAlex.
- Deciphering the rules of regulated cell death subroutines by in silico methods.Journal of advanced research · 2026Review
- A functional genomics-pharmacotranscriptomics framework identifies host-directed anti-influenza agents.iScience · 2026Article
- Research Progress on Avian Influenza Virus and Autophagy: A Review.Pathogens (Basel, Switzerland) · 2026Review
- Sorting Nexin 10 Mediates Endosomal Acidification and Autophagy to Promote Influenza A Virus Infection.Viruses · 2026Article
- The molecular mechanisms of autophagy-virus interactions: from antiviral defense to viral counterstrategies.FEMS microbiology reviews · 2026Review
- Multi-omics to study chronic respiratory diseases and viral infections.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Integrative multi-omics analysisiScience · 2025Article
- TRIM45 restricts influenza virus infection through modulating the chaperone-mediated autophagic degradation of viral PB2 protein.PLoS pathogens · 2025Article
- Rab27a regulates the transport of influenza virus membrane proteins to the plasma membrane.Nature communications · 2025Article
- Influenza A virus induces PI4P production at the endoplasmic reticulum in an ATG16L1-dependent manner to promote the egress of viral ribonucleoproteins.PLoS biology · 2025Article
- Host cellular protein RAB33B facilitates influenza viral replication and modulates M2 trafficking by enhancing autophagy.Veterinary research · 2025Article
- hnRNPM regulates influenza A virus replication through distinct mechanisms in human and avian cells: implications for cross-species transmission.Journal of virology · 2025Article
- Influenza A virus subverts the LC3-pericentrin dynein adaptor complex for host cytoplasm entry.Science advances · 2025Article
- Proteomic Analysis of Differentially Expressed Proteins in A549 Cells Infected with H9N2 Avian Influenza Virus.International journal of molecular sciences · 2025Article
- Virus infection and vesicle trafficking.Frontiers in immunology · 2025Review
- Regulation of viral replication by host restriction factors.Frontiers in immunology · 2025Review
- An interferon-stimulated long non-coding RNA USP30-AS1 as an immune modulator in influenza A virus infection.PLoS pathogens · 2025Article
- Inhibition of SARS-CoV-2 growth in the lungs of mice by a peptide-conjugated morpholino oligomer targeting viral RNA.Molecular therapy. Nucleic acids · 2024Article
- Conference Report: LPMHealthcare Emerging Viruses 2023 (EVOX23): Pandemics-Learning from the Past and Present to Prepare for the Future.Pathogens (Basel, Switzerland) · 2024Article
- Regulation of Autophagosome-Lysosome Fusion by Human Viral Infections.Pathogens (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
30 authors at 9 institutions in 2 countries.
Funding
Abstract
The fate of influenza A virus (IAV) infection in the host cell depends on the balance between cellular defence mechanisms and viral evasion strategies. To illuminate the landscape of IAV cellular restriction, we generated and integrated global genetic loss-of-function screens with transcriptomics and proteomics data. Our multi-omics analysis revealed a subset of both IFN-dependent and independent cellular defence mechanisms that inhibit IAV replication. Amongst these, the autophagy regulator TBC1 domain family member 5 (TBC1D5), which binds Rab7 to enable fusion of autophagosomes and lysosomes, was found to control IAV replication in vitro and in vivo and to promote lysosomal targeting of IAV M2 protein. Notably, IAV M2 was observed to abrogate TBC1D5-Rab7 binding through a physical interaction with TBC1D5 via its cytoplasmic tail. Our results provide evidence for the molecular mechanism utilised by IAV M2 protein to escape lysosomal degradation and traffic to the cell membrane, where it supports IAV budding and growth.
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Registered trials
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 Socratic graph.