ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Suppression of influenza A virus replication in human lung epithelial cells by noncytotoxic concentrations bafilomycin A1.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.
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Who cites it
52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.
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- Investigation ofMedicina (Kaunas, Lithuania) · 2019Pooled it
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- MHC class II functions as a host-specific entry receptor for representative human and swine H3N2 influenza A viruses.Nature communications · 2026Article
- Drug-induced phospholipidosis as an artifact in antiviral drug repurposing.bioRxiv : the preprint server for biology · 2025Article
- Evaluation of Autophagy in Conjunctival Fibroblasts.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Assessment of Autophagy in Leishmania Parasites.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Inhibition of RAN attenuates influenza a virus replication and nucleoprotein nuclear export.Emerging microbes & infections · 2024Article
- Lassa virus Z protein hijacks the autophagy machinery for efficient transportation by interrupting CCT2-mediated cytoskeleton network formation.Autophagy · 2024Article
- Proteomic and genetic analyses of influenza A viruses identify pan-viral host targets.Nature communications · 2023Article
- Upregulation of galectin-3 in influenza A virus infection promotes viral RNA synthesis through its association with viral PA protein.Journal of biomedical science · 2023Article
- The cytosolic N-terminal domain of V-ATPase a-subunits is a regulatory hub targeted by multiple signals.Frontiers in molecular biosciences · 2023Review
- The battle for autophagy between host and influenza A virus.Virulence · 2022Review
- Erythromycin Estolate Is a Potent Inhibitor Against HCoV-OC43 by Directly Inactivating the Virus Particle.Frontiers in cellular and infection microbiology · 2022Article
- Myxobacteria as a Source of New Bioactive Compounds: A Perspective Study.Pharmaceutics · 2021Review
- The V-ATPaseInternational journal of molecular sciences · 2021Review
- Autophagy: A Friend or Foe in Allergic Asthma?International journal of molecular sciences · 2021Review
- Autophagy, Unfolded Protein Response, and Neuropilin-1 Cross-Talk in SARS-CoV-2 Infection: What Can Be Learned from Other Coronaviruses.International journal of molecular sciences · 2021Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Subcellular trafficking within host cells plays a critical role in viral life cycles, including influenza A virus (IAV). Thus targeting relevant subcellular compartments holds promise for effective intervention to control the impact of influenza infection. Bafilomycin A1 (Baf-A1), when used at relative high concentrations (≥10 nM), inhibits vacuolar ATPase (V-ATPase) and reduces endosome acidification and lysosome number, thus inhibiting IAV replication but promoting host cell cytotoxicity. We tested the hypothesis that much lower doses of Baf-A1 also have anti-IAV activity, but without toxic effects. Thus we assessed the antiviral activity of Baf-A1 at different concentrations (0.1-100 nM) in human alveolar epithelial cells (A549) infected with IAV strain A/PR/8/34 virus (H1N1). Infected and mock-infected cells pre- and cotreated with Baf-A1 were harvested 0-24 h postinfection and analyzed by immunoblotting, immunofluorescence, and confocal and electron microscopy. We found that Baf-A1 had disparate concentration-dependent effects on subcellular organelles and suppressed affected IAV replication. At concentrations ≥10 nM Baf-A1 inhibited acid lysosome formation, which resulted in greatly reduced IAV replication and release. Notably, at a very low concentration of 0.1 nM that is insufficient to reduce lysosome number, Baf-A1 retained the capacity to significantly impair IAV nuclear accumulation as well as IAV replication and release. In contrast to the effects of high concentrations of Baf-A1, very low concentrations did not exhibit cytotoxic effects or induce apoptotic cell death, based on morphological and FACS analyses. In conclusion, our results reveal that low-concentration Baf-A1 is an effective inhibitor of IAV replication, without impacting host cell viability.
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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.