ArticleThe European respiratory journal2021
Influenza virus infection increases ACE2 expression and shedding in human small airway epithelial cells.
Article in The European respiratory journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Angiotensin converting enzyme 2 level and its significance in COVID-19 and other diseases patients.European journal of clinical investigation · 2023Pooled it
- Interactions of SARS-CoV-2, influenza and respiratory syncytial virus influence epidemic timing and risk.Communications medicine · 2026Article
- PEBL, a component-based Chinese medicine, reduces virus-induced acute lung injury by targeting FXR to decrease ACE2 levels.Journal of advanced research · 2026Article
- Influenza-Infected Pigs Are Not Susceptible to SARS-CoV-2 Infection.Pathogens (Basel, Switzerland) · 2026Article
- Local and systemic host responses to influenza and concurrent or sequential SARS-CoV-2 infection.Frontiers in cellular and infection microbiology · 2026Review
- Article
- Ciliated cells promote high infectious potential of influenza A virus through the efficient intracellular activation of hemagglutinin.Journal of virology · 2025Article
- Profiling of proteases involved in SARS-CoV-2 pathogenesis in human saliva: Influence of age and gender.Journal, genetic engineering & biotechnology · 2025Article
- ACE2 shedding exacerbates sepsis-induced gut leak via loss of microbial metabolite 5-methoxytryptophan.Microbiome · 2025Article
- The Role of the CX3CR1-CX3CL1 Axis in Respiratory Syncytial Virus Infection and the Triggered Immune Response.International journal of molecular sciences · 2024Review
- Establishing Air-Liquid Interface (ALI) Airway Culture Models for Infectious Disease Research.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Influenza viral infection is a risk factor for severe illness in COVID-19 patients: a nationwide population-based cohort study.Emerging microbes & infections · 2023Article
- The Impact of Coronavirus Disease 2019 on Viral, Bacterial, and Fungal Respiratory Infections.Clinics in chest medicine · 2023Review
- The Immunosuppressive Roles of PD-L1 during Influenza A Virus Infection.International journal of molecular sciences · 2023Article
- P38 MAPK activated ADAM17 mediates ACE2 shedding and promotes cardiac remodeling and heart failure after myocardial infarction.Cell communication and signaling : CCS · 2023Article
- Article
- How the Competition for Cysteine May Promote Infection of SARS-CoV-2 by Triggering Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Article
- IgG autoantibodies against ACE2 in SARS-CoV-2 infected patients.Journal of medical virology · 2023Article
- Sequential infections with rhinovirus and influenza modulate the replicative capacity of SARS-CoV-2 in the upper respiratory tract.Emerging microbes & infections · 2022Article
- SARS-CoV-2 versus other minor viral infection on kidney injury in asymptomatic and mildly symptomatic patients.Virulence · 2022Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPatients with coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) demonstrate high rates of co-infection with respiratory viruses, including influenza A (IAV), suggesting pathogenic interactions.
methodsWe investigated how IAV may increase the risk of COVID-19 lung disease, focusing on the receptor angiotensin-converting enzyme (ACE)2 and the protease TMPRSS2, which cooperate in the intracellular uptake of SARS-CoV-2.
resultsWe found, using single-cell RNA sequencing of distal human nondiseased lung homogenates, that at baseline, ACE2 is minimally expressed in basal, goblet, ciliated and secretory epithelial cells populating small airways. We focused on human small airway epithelial cells (SAECs), central to the pathogenesis of lung injury following viral infections. Primary SAECs from nondiseased donor lungs apically infected (at the air-liquid interface) with IAV (up to 3×10
conclusionThese results indicate that IAV amplifies the expression of molecules necessary for SARS-CoV-2 infection of the distal lung. Furthermore, post-translational changes in ACE2 by IAV may increase vulnerability to lung injury such as acute respiratory distress syndrome during viral co-infections. These findings support efforts in the prevention and treatment of influenza infections during the COVID-19 pandemic.
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