ArticleThe Journal of infectious diseases2012
Influenza A viruses target type II pneumocytes in the human lung.
Article in The Journal of infectious diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
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Who cites it
125 citing papers in PubMed.
- Macrophages orchestrate antiviral defense and epithelial repair in a human iPSC-derived alveolar air-liquid interface.JCI insight · 2026Article
- Generation of an Induced Pluripotent Stem Cell-Derived Alveolar Type II In Vitro Model to Study Influenza A Virus Infection and Drug Treatments.Advanced healthcare materials · 2026Article
- TLR7-mediated inflammation drives PD-L1 upregulation and T cell exhaustion during influenza A virus infection.iScience · 2026Article
- Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Lung cell fates during influenza.Cell research · 2025Review
- The long reach of influenza and other respiratory viruses: from acute epithelial injury to post-viral lung disease.Clinical microbiology reviews · 2025Review
- Age Matters: Key Contributors to Interferon Toxicity in Infants During Influenza Virus Infection.Viruses · 2025Review
- The Originally Established PBE Cell Line as a Reliable In Vitro Model for Investigating SIV Infection and Immunity.International journal of molecular sciences · 2025Article
- Epigenetic changes and serotype-specific responses of alveolar type II epithelial cells to Streptococcus pneumoniae in resolving influenza A virus infection.Cell communication and signaling : CCS · 2025Article
- Bioprinted Four-Cell-Type Lung Model for Viral Infection Studies Under Air-Liquid Interface Conditions.International journal of molecular sciences · 2025Article
- Lung surfactant reducesMicrobiology spectrum · 2025Article
- Influenza virus-induced type I interferons disrupt alveolar epithelial repair and tight junction integrity in the developing lung.Mucosal immunology · 2025Article
- Cryopreservation of human lung tissue for 3D ex vivo analysis.Respiratory research · 2025Review
- Aging shapes infection profiles of influenza A virus and SARS-CoV-2 in human precision-cut lung slices.Respiratory research · 2025Article
- A Novel In Vitro Primary Human Alveolar Model (AlveolAir™) for H1N1 and SARS-CoV-2 Infection and Antiviral Screening.Microorganisms · 2025Article
- Article
- Alveolar Macrophages in Viral Respiratory Infections: Sentinels and Saboteurs of Lung Defense.International journal of molecular sciences · 2025Review
- Molecular characterisation of influenza B virus from the 2017/18 season in primary models of the human lung reveals improved adaptation to the lower respiratory tract.Emerging microbes & infections · 2024Article
- Differential transcriptomic host responses in the early phase of viral and bacterial infections in human lung tissue explants ex vivo.Respiratory research · 2024Article
- The deadly dance of alveolar macrophages and influenza virus.European respiratory review : an official journal of the European Respiratory Society · 2024Review
65 more citing papers are in PubMed but not listed here.
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17 authors.
Funding
Abstract
backgroundHighly pathogenic avian H5N1 influenza viruses preferentially infect alveolar type II pneumocytes in human lung. However, it is unknown whether this cellular tropism contributes to high viral virulence because the primary target cells of other influenza viruses have not been systematically studied.
methodsWe provide the first comparison of the replication, tropism, and cytokine induction of human, highly pathogenic avian influenza A virus subtype H5N1 and other animal influenza A viruses in primary human lung organ cultures.
resultsSubytpe H5N1 and human-adapted subtype H1N1 and H3N2 viruses replicated efficiently in the lung tissue, whereas classic swine and low-pathogenicity avian viruses propagated only poorly. Nevertheless, all viruses examined were detected almost exclusively in type II pneumocytes, with a minor involvement of alveolar macrophages. Infection with avian viruses that have a low and high pathogenicity provoked a pronounced induction of cytokines and chemokines, while human and pandemic H1N1-2009 viruses triggered only weak responses.
conclusionsThese findings show that differences in the pathogenic potential of influenza A viruses in the human lung cannot be attributed to a distinct cellular tropism. Rather, high or low viral pathogenicity is associated with a strain-specific capacity to productively replicate in type II pneumocytes and to cope with the induced cytokine response.
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