ArticleJournal of virology2022
Respiratory Syncytial Virus Protects Bystander Cells against Influenza A Virus Infection by Triggering Secretion of Type I and Type III Interferons.
Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 29 citations in OpenAlex.
- Innate airway responses shape permissiveness to human respiratory syncytial virus.Virus research · 2026Article
- Epidemiological analysis of pediatric respiratory pathogens in Hunan, China: a retrospective multicenter study from 2022 to 2024.BMC infectious diseases · 2025Article
- Post-COVID-19 Seasonality of Influenza, Respiratory Syncytial Virus, and SARS-CoV-2 Among Hospitalized Children in Western Iran: A Molecular Surveillance Study (2023-2024).Journal of epidemiology and global health · 2025Article
- Respiratory viral coinfections: interactions, mechanisms and clinical implications.Nature reviews. Microbiology · 2025Review
- Impact of RSV Infection in Transplant and Immunocompromised Population: Incidence and Co-Infections: Retrospective Analysis of a Single Centre.Journal of clinical medicine · 2025Article
- The added value of diagnostics to characterize age-specific patterns of respiratory viral infections and coinfections and to detect emerging threats.BMC infectious diseases · 2025Article
- Multiple Respiratory Virus Detection in Acute Respiratory Infection Patients in Mie Prefecture, Japan, 2021-2023.Viruses · 2025Article
- Exploring viral respiratory coinfections: Shedding light on pathogen interactions.PLoS pathogens · 2024Article
- Uncovering strain- and age-dependent innate immune responses to SARS-CoV-2 infection in air-liquid-interface cultured nasal epithelia.iScience · 2024Article
- The Characteristics of the Influenza Virus Epidemic Around the SARS-CoV-2 Epidemic Period in the Pudong New Area of Shanghai.Journal of epidemiology and global health · 2024Article
- Single-cell analysis reveals an antiviral network that controls Zika virus infection in human dendritic cells.Journal of virology · 2024Article
- The intersection of hostMicrobiology and molecular biology reviews : MMBR · 2024Review
- Antagonism between viral infection and innate immunity at the single-cell level.PLoS pathogens · 2023Article
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- Mathematical modeling of regulatory networks of intracellular processes - Aims and selected methods.Computational and structural biotechnology journal · 2023Review
- Epigenetic control of type III interferon expression by 8-oxoguanine and its reader 8-oxoguanine DNA glycosylase1.Frontiers in immunology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We observed the interference between two prevalent respiratory viruses, respiratory syncytial virus (RSV) and influenza A virus (IAV) (H1N1), and characterized its molecular underpinnings in alveolar epithelial cells (A549). We found that RSV induces higher levels of interferon beta (IFN-β) production than IAV and that IFN-β priming confers higher-level protection against infection with IAV than with RSV. Consequently, we focused on the sequential infection scheme of RSV and then IAV. Using A549 wild-type (WT), IFNAR1 knockout (KO), IFNLR1 KO, and IFNAR1-IFNLR1 double-KO cell lines, we found that both IFN-β and IFN-λ are necessary for maximum protection against subsequent infection. Immunostaining revealed that preinfection with RSV partitions the cell population into a subpopulation susceptible to subsequent infection with IAV and an IAV-proof subpopulation. Strikingly, the susceptible cells turned out to be those already compromised and efficiently expressing RSV, whereas the bystander, interferon-primed cells are resistant to IAV infection. Thus, virus-virus exclusion at the cell population level is not realized through direct competition for a shared ecological niche (single cell) but rather is achieved with the involvement of specific cytokines induced by the host's innate immune response.
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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.