ArticlePLoS pathogens2017
Influenza virus differentially activates mTORC1 and mTORC2 signaling to maximize late stage replication.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
What it found
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Who cites it
73 citing papers in PubMed, 114 citations in OpenAlex.
- Influenza A deletion-containing viral genome production is altered by metabolites, metabolic signaling molecules, and cyanobacterial extracts.Applied and environmental microbiology · 2026Article
- Viral-host interactions mediated by the mTOR signaling pathway.Cell insight · 2026Review
- Lipidomic profiling of influenza A virus production in MDCK cells towards targeted clone selection.Scientific reports · 2026Article
- Lipid metabolism, viral infection, and antiviral immunity: a new host-pathogen interface.Frontiers in cellular and infection microbiology · 2026Review
- The ribosomal landscape in influenza A virus infection: from molecular mechanisms to clinical relevance.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Host PI3K inhibition via anti-cancer drug alpelisib influences Influenza A non-infectious particles and deletion-containing viral genomes.Cell communication and signaling : CCS · 2025Article
- Review
- Viral Reprogramming of Nucleotide Synthesis and Its Impact on Viral Infection.Journal of medical virology · 2025Review
- Metabolic Reprogramming in Respiratory Viral Infections: A Focus on SARS-CoV-2, Influenza, and Respiratory Syncytial Virus.Biomolecules · 2025Review
- Anti-Influenza Activity of 6BIGOE: Improved Pharmacological Profile After Encapsulation in PLGA Nanoparticles.International journal of molecular sciences · 2025Article
- Hypercapnia Increases Influenza A Virus Infection of Bronchial Epithelial Cells by Augmenting Cellular Cholesterol via mTOR and Akt.International journal of molecular sciences · 2025Article
- Positive Regulation of Cellular Proteins by Influenza Virus for Productive Infection.International journal of molecular sciences · 2025Review
- Deciphering Host-Virus Interactions and Advancing Therapeutics for Chronic Viral Infection.Viruses · 2025Review
- Orthoflavivirus infection and the mTOR signaling pathway.Frontiers in microbiology · 2025Review
- Quantitative analysis of proteomic changes in two monoclonal suspension MDCK cell lines infected with human influenza A virus (H1N1).PloS one · 2025Article
- Metabolic hijacking styles: a review of how viral life cycles dictate glucose metabolism reprogramming.Frontiers in microbiology · 2025Review
- Mammalian Target of Rapamycin Complex 1 Activation in Macrophages Contributes to Persistent Lung Inflammation following Respiratory Tract Viral Infection.The American journal of pathology · 2024Article
- Microglial- neuronal crosstalk in chronic viral infection through mTOR, SPP1/OPN and inflammasome pathway signaling.Frontiers in immunology · 2024Review
- Association of mTOR Pathway and Conformational Alterations in C-Reactive Protein in Neurodegenerative Diseases and Infections.Cellular and molecular neurobiology · 2023Review
- Multifaceted Nature of Lipid Droplets in Viral Interactions and Pathogenesis.Microorganisms · 2023Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Influenza A virus usurps host signaling factors to regulate its replication. One example is mTOR, a cellular regulator of protein synthesis, growth and motility. While the role of mTORC1 in viral infection has been studied, the mechanisms that induce mTORC1 activation and the substrates regulated by mTORC1 during influenza virus infection have not been established. In addition, the role of mTORC2 during influenza virus infection remains unknown. Here we show that mTORC2 and PDPK1 differentially phosphorylate AKT upon influenza virus infection. PDPK1-mediated phoshorylation of AKT at a distinct site is required for mTORC1 activation by influenza virus. On the other hand, the viral NS1 protein promotes phosphorylation of AKT at a different site via mTORC2, which is an activity dispensable for mTORC1 stimulation but known to regulate apoptosis. Influenza virus HA protein and down-regulation of the mTORC1 inhibitor REDD1 by the virus M2 protein promote mTORC1 activity. Systematic phosphoproteomics analysis performed in cells lacking the mTORC2 component Rictor in the absence or presence of Torin, an inhibitor of both mTORC1 and mTORC2, revealed mTORC1-dependent substrates regulated during infection. Members of pathways that regulate mTORC1 or are regulated by mTORC1 were identified, including constituents of the translation machinery that once activated can promote translation. mTORC1 activation supports viral protein expression and replication. As mTORC1 activation is optimal midway through the virus life cycle, the observed effects on viral protein expression likely support the late stages of influenza virus replication when infected cells undergo significant stress.
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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 OpenQuestion graph.