ArticlePLoS pathogens2019
Long-term surviving influenza infected cells evade CD8+ T cell mediated clearance.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- NS-segment-based reporter influenza A viruses: engineering strategy, applications, and limitations.Journal of virology · 2026Review
- The role of T cells in influenza infection and vaccination.Virologica Sinica · 2026Review
- Pulmonary Microvascular Endothelial Antigen Presentation Activates resident CD8Research square · 2026Article
- Lung cell fates during influenza.Cell research · 2025Review
- Viral expansion after transfer is a primary driver of influenza A virus transmission bottlenecks.PLoS biology · 2025Article
- Lung structural cells are altered by infeluenza virus leading to rapid immune protection following re-challenge.Nature communications · 2025Article
- Viral expansion after transfer is a primary driver of influenza A virus transmission bottlenecks.bioRxiv : the preprint server for biology · 2025Article
- Influenza B virus infection alters the regenerative potential of murine alveolar type 2 pneumocytes.mBio · 2025Article
- Dynamic landscapes and protective immunity coordinated by influenza-specific lung-resident memory CD8Immunity · 2024Article
- Tropism for ciliated cells is the dominant driver of influenza viral burst size in the human airway.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Gasdermin D promotes influenza virus-induced mortality through neutrophil amplification of inflammation.Nature communications · 2024Article
- Intestinal tuft cell immune privilege enables norovirus persistence.Science immunology · 2024Article
- Segmented, Negative-Sense RNA Viruses of Humans: Genetic Systems and Experimental Uses of Reporter Strains.Annual review of virology · 2023Review
- New Insights into the Alveolar Epithelium as a Driver of Acute Respiratory Distress Syndrome.Biomolecules · 2022Review
- Respiratory Influenza Virus Infection Causes Dynamic Tuft Cell and Innate Lymphoid Cell Changes in the Small Intestine.Journal of virology · 2022Article
- Calprotectin (S100A8/A9) Is an Innate Immune Effector in Experimental Periodontitis.Infection and immunity · 2021Article
- Exacerbation of Influenza A Virus Disease Severity by Respiratory Syncytial Virus Co-Infection in a Mouse Model.Viruses · 2021Article
- Stromal-immune cell crosstalk fundamentally alters the lung microenvironment following tissue insult.Immunology · 2021Review
- Article
- Synthetic Virology: Building Viruses to Better Understand Them.Cold Spring Harbor perspectives in medicine · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Influenza A virus (IAV) is a seasonal pathogen with the potential to cause devastating pandemics. IAV infects multiple epithelial cell subsets in the respiratory tract, eliciting damage to the lungs. Clearance of IAV is primarily dependent on CD8+ T cells, which must balance control of the infection with immunopathology. Using a virus expressing Cre recombinase to permanently label infected cells in a Cre-inducible reporter mouse, we previously discovered infected club cells that survive both lytic virus replication and CD8+ T cell-mediated clearance. In this study, we demonstrate that ciliated epithelial cells, type I and type II alveolar cells can also become survivor cells. Survivor cells are stable in the lung long-term and demonstrate enhanced proliferation compared to uninfected cells. When we investigated how survivor cells evade CD8+ T cell killing we observed that survivor cells upregulated the inhibitory ligand PD-L1, but survivor cells did not use PD-L1 to evade CD8+ T cell killing. Instead our data suggest that survivor cells are not inherently resistant to CD8+ T cell killing, but instead no longer present IAV antigen and cannot be detected by CD8+ T cells. Finally, we evaluate the failure of CD8+ T cells to kill these previously infected cells. This work demonstrates that additional cell types can survive IAV infection and that these cells robustly proliferate and are stable long term. By sparing previously infected cells, the adaptive immune system may be minimizing pathology associated with IAV infection.
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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.