ArticleScience advances2025
Influenza A virus subverts the LC3-pericentrin dynein adaptor complex for host cytoplasm entry.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Population genomics of yellow-eyed penguins uncovers subspecies divergence and candidate genes linked to respiratory distress syndrome.Nature ecology & evolution · 2026Article
- Hijacking a cellular highway: non-lipidated LC3 proteins and PCNT (pericentrin) drive influenza a virus uncoating.Autophagy · 2026Article
- Visualising viral interactions and mechanisms at the nanoscale with expansion microscopy.Npj viruses · 2026Review
- Orchestrating immunopathology: the spectrum of programmed cell death pathways co-opted by influenza a virus in pulmonary immunity.Frontiers in immunology · 2026Review
- Host-Microbe Interactions: Understanding the Mechanism of Autophagy in Viral Replication and Immune Evasion.Veterinary sciences · 2025Review
- Virus infection and vesicle trafficking.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) enters host cells via endocytosis, and fusion of the viral particles (VPs) at endosomes releases the viral ribonucleoproteins (vRNPs) into the cytoplasm. This uncoating step that is vital for IAV infection remains to be fully understood. The aggresome processing machinery (APM) plays a relevant but not essential role in this. Here, we reveal a mechanism in which light chain 3 proteins (LC3s) and pericentrin (PCNT) form an adaptor complex that is required for vRNPs binding to the dynein 1 and IAV uncoating at endosomes. This function of LC3s and PCNT is independent from their established role in autophagy and centrosome assembly, respectively. LC3s or PCNT depletion severely impairs IAV cytoplasm entry and infection, which can be further inhibited by additional silencing of histone deacetylase 6, an APM component. Collectively, our results show that IAV has adopted two redundant strategies to hijack the dynein biomolecular motors and facilitate VP uncoating.
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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.