ArticlePLoS pathogens2010
Transforming growth factor-β: activation by neuraminidase and role in highly pathogenic H5N1 influenza pathogenesis.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed, 143 citations in OpenAlex.
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- Positive Regulation of Cellular Proteins by Influenza Virus for Productive Infection.International journal of molecular sciences · 2025Review
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- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
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- Longitudinal transcriptome analysis reveals distinct gene expression patterns in traditional Chinese medicine syndromes of upper respiratory tract infections.Frontiers in genetics · 2024Article
- Analysis of miRNA expression in the trachea of Ri chicken infected with the highly pathogenic avian influenza H5N1 virus.Journal of veterinary science · 2023Article
- Airway proteolytic control of pneumococcal competence.PLoS pathogens · 2023Article
- Phenotypic effects of mutations observed in the neuraminidase of human origin H5N1 influenza A viruses.PLoS pathogens · 2023Article
- Aromatic amino acid metabolites alter interferon signaling and influenza pathogenesis.Frontiers in molecular biosciences · 2023Article
- Co-infection of the respiratory epithelium, scene of complex functional interactions between viral, bacterial, and human neuraminidases.Frontiers in microbiology · 2023Review
- Inhibitors of the Sialidase NEU3 as Potential Therapeutics for Fibrosis.International journal of molecular sciences · 2022Review
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43 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
Transforming growth factor-beta (TGF-β), a multifunctional cytokine regulating several immunologic processes, is expressed by virtually all cells as a biologically inactive molecule termed latent TGF-β (LTGF-β). We have previously shown that TGF-β activity increases during influenza virus infection in mice and suggested that the neuraminidase (NA) protein mediates this activation. In the current study, we determined the mechanism of activation of LTGF-β by NA from the influenza virus A/Gray Teal/Australia/2/1979 by mobility shift and enzyme inhibition assays. We also investigated whether exogenous TGF-β administered via a replication-deficient adenovirus vector provides protection from H5N1 influenza pathogenesis and whether depletion of TGF-β during virus infection increases morbidity in mice. We found that both the influenza and bacterial NA activate LTGF-β by removing sialic acid motifs from LTGF-β, each NA being specific for the sialic acid linkages cleaved. Further, NA likely activates LTGF-β primarily via its enzymatic activity, but proteases might also play a role in this process. Several influenza A virus subtypes (H1N1, H1N2, H3N2, H5N9, H6N1, and H7N3) except the highly pathogenic H5N1 strains activated LTGF-β in vitro and in vivo. Addition of exogenous TGF-β to H5N1 influenza virus-infected mice delayed mortality and reduced viral titers whereas neutralization of TGF-β during H5N1 and pandemic 2009 H1N1 infection increased morbidity. Together, these data show that microbe-associated NAs can directly activate LTGF-β and that TGF-β plays a pivotal role protecting the host from influenza pathogenesis.
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