ArticleThe Journal of general virology2012
Infection of human alveolar macrophages by human coronavirus strain 229E.
Article in The Journal of general virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- [Pulmonary innate immune response in Sars-cov-2 infection]Revista de la Facultad de Ciencias Medicas (Cordoba, Argentina) · 2022Pooled it
- Macrophage Immune Responses in Viral Infections: Functional Plasticity and Therapeutic Targeting.Journal of microbiology and biotechnology · 2026Review
- UHRF1 restricts HCoV-229E infection through epigenetic silencing of the viral receptor APN.Nature communications · 2025Article
- Human Coronavirus-229E Hijacks Key Host-Cell RNA-Processing Complexes for Replication.Journal of proteome research · 2025Article
- Interplay between respiratory viruses and cilia in the airways.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Collectins and Ficolins.Advances in experimental medicine and biology · 2025Review
- Differential immunoregulation by human surfactant protein A variants determines severity of SARS-CoV-2-induced lung disease.Frontiers in immunology · 2025Article
- The Effects of Different Respiratory Viruses on the Oxidative Stress Marker Levels in an In Vitro Model: A Pilot Study.International journal of molecular sciences · 2024Article
- Surfactant Protein A Inhibits Human Rhinovirus C Binding and Infection of Airway Epithelial Cells from Pediatric Asthma.Viruses · 2024Article
- Host Cell Proteases Involved in Human Respiratory Viral Infections and Their Inhibitors: A Review.Viruses · 2024Review
- Article
- Human surfactant protein A inhibits SARS-CoV-2 infectivity and alleviates lung injury in a mouse infection model.Frontiers in immunology · 2024Article
- More tools for our toolkit: The application of HEL-299 cells and dsRNA-nanoparticles to study human coronaviruses in vitro.Virus research · 2022Article
- Nonproductive exposure of PBMCs to SARS-CoV-2 induces cell-intrinsic innate immune responses.Molecular systems biology · 2022Article
- Review
- Antiviral therapy for COVID-19: Derivation of optimal strategy based on past antiviral and favipiravir experiences.Pharmacology & therapeutics · 2022Review
- Alveolar macrophages protect mice from MERS-CoV-induced pneumonia and severe disease.Veterinary pathology · 2022Article
- Pulmonary surfactant as a versatile biomaterial to fight COVID-19.Journal of controlled release : official journal of the Controlled Release Society · 2022Review
- Insights Gained Into the Treatment of COVID19 by Pulmonary Surfactant and Its Components.Frontiers in immunology · 2022Review
- Exercise-induced myokines downregulates the ACE2 level in bronchial epithelial cells: Implications for SARS-CoV-2 prevention.PloS one · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Human coronavirus strain 229E (HCoV-229E) commonly causes upper respiratory tract infections. However, lower respiratory tract infections can occur in some individuals, indicating that cells in the distal lung are susceptible to HCoV-229E. This study determined the virus susceptibility of primary cultures of human alveolar epithelial cells and alveolar macrophages (AMs). Fluorescent antibody staining indicated that HCoV-229E could readily infect AMs, but no evidence was found for infection in differentiated alveolar epithelial type II cells and only a very low level of infection in type II cells transitioning to the type I-like cell phenotype. However, a human bronchial epithelial cell line (16HBE) was readily infected. The innate immune response of AMs to HCoV-229E infection was evaluated for cytokine production and interferon (IFN) gene expression. AMs secreted significant amounts of tumour necrosis factor alpha (TNF-α), regulated on activation normal T-cell expressed and secreted (RANTES/CCL5) and macrophage inflammatory protein 1β (MIP-1β/CCL4) in response to HCoV-229E infection, but these cells exhibited no detectable increase in IFN-β or interleukin-29 in mRNA levels. AMs from smokers had reduced secretion of TNF-α compared with non-smokers in response to HCoV-229E infection. Surfactant protein A (SP-A) and SP-D are part of the innate immune system in the distal lung. Both surfactant proteins bound to HCoV-229E, and pre-treatment of HCoV-229E with SP-A or SP-D inhibited infection of 16HBE cells. In contrast, there was a modest reduction in infection in AMs by SP-A, but not by SP-D. In summary, AMs are an important target for HCoV-229E, and they can mount a pro-inflammatory innate immune response to infection.
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What OpenQuestion holds
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.