ArticleJournal of innate immunity2013
TLR7 contributes to the rapid progression but not to the overall fatal outcome of secondary pneumococcal disease following influenza A virus infection.
Article in Journal of innate immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Propofol directly binds to and inhibits TLR7.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Article
- TLR7 Expression Aggravates Invasive Pulmonary Aspergillosis by Suppressing Anti-Infection and immunity · 2021Article
- Sequential targeting of interferon pathways for increased host resistance to bacterial superinfection during influenza.PLoS pathogens · 2021Article
- Virus-Induced Changes of the Respiratory Tract Environment Promote Secondary Infections WithFrontiers in cellular and infection microbiology · 2021Review
- Resolved Influenza A Virus Infection Has Extended Effects on Lung Homeostasis and Attenuates Allergic Airway Inflammation in a Mouse Model.Microorganisms · 2020Article
- Article
- Article
- RIG-I Signaling via MAVS Is Dispensable for Survival in Lethal Influenza InfectionMediators of inflammation · 2018Article
- Respiratory Influenza A Virus Infection Triggers Local and Systemic Natural Killer Cell ActivationFrontiers in immunology · 2018Article
- Chronic lung inflammation primes humoral immunity and augments antipneumococcal resistance.Scientific reports · 2017Article
- Article
- Review
- Desialylation of airway epithelial cells during influenza virus infection enhances pneumococcal adhesion via galectin binding.Molecular immunology · 2015Article
Corrections and comments
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Authors and funding
12 authors at 8 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased risk for bacterial superinfections substantially contributes to the mortality caused by influenza A virus (IAV) epidemics. While the mechanistic basis for this lethal synergism is still insufficiently understood, immune modulation through the viral infection has been shown to be involved. Since the pattern-recognition receptor (PRR) toll-like receptor 7 (TLR7) is a major sensor for the viral genome, we studied how IAV recognition by TLR7 influences the development of secondary pneumococcal infection. In a mouse model of IAV, TLR7-deficient hosts induced a potent antiviral response and showed unchanged survival. In secondary pneumococcal infection during acute influenza, TLR7ko mice showed a fatal outcome similar to wild-type (WT) hosts, despite significantly delayed disease progression. Also, when bacterial superinfection occurred after virus clearance, WT and TLR7-deficient hosts showed similar mortality, even though we found the phagocytic activity of alveolar macrophages isolated from IAV-pre-infected hosts to be enhanced in TLR7ko over WT mice. Thus, we show that a virus-sensing PRR modulates the progression of secondary pneumococcal infection following IAV. However, the fatal overall outcome in WT as well as TLR7ko hosts suggests that processes distinct from TLR7-triggering override the contribution of this single PRR.
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