ArticleFrontiers in microbiology2021
Influenza B Virus Infection Is Enhanced Upon Heterotypic Co-infection With Influenza A Virus.
Article in Frontiers in microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Nucleocapsid-like cryo-EM structure of influenza B virus.PLoS pathogens · 2026Article
- Respiratory viral coinfections: interactions, mechanisms and clinical implications.Nature reviews. Microbiology · 2025Review
- Experimental Models to Investigate Viral and Cellular Dynamics in Respiratory Viral Co-Infections.Microorganisms · 2025Review
- 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
- Respiratory Viral Coinfections: Insights into Epidemiology, Immune Response, Pathology, and Clinical Outcomes.Pathogens (Basel, Switzerland) · 2024Review
- Potential co-infection of influenza A, influenza B, respiratory syncytial virus, andFrontiers in medicine · 2023Article
- Treatment of Respiratory Viral Coinfections.Epidemiologia (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homotypic co-infections with influenza viruses are described to increase genetic population diversity, to drive viral evolution and to allow genetic complementation. Less is known about heterotypic co-infections between influenza A (IAV) and influenza B (IBV) viruses. Previous publications showed that IAV replication was suppressed upon co-infection with IBV. However, the effect of heterotypic co-infections on IBV replication was not investigated. To do so, we produced by reverse genetics a pair of replication-competent recombinant IAV (A/WSN/33) and IBV (B/Brisbane/60/2008) expressing a GFP and mCherry fluorescent reporter, respectively. A549 cells were infected simultaneously or 1 h apart at a high MOI with IAV-GFP or IBV-mCherry and the fluorescence was measured at 6 h post-infection by flow cytometry. Unexpectedly, we observed that IBV-mCherry infection was enhanced upon co-infection with IAV-GFP, and more strongly so when IAV was added 1 h prior to IBV. The same effect was observed with wild-type viruses and with various strains of IAV. Using UV-inactivated IAV or type-specific antiviral compounds, we showed that the enhancing effect of IAV infection on IBV infection was dependent on transcription/replication of the IAV genome. Our results, taken with available data in the literature, support the hypothesis that the presence of IAV proteins can enhance IBV genome expression and/or complement IBV defective particles.
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