ArticleCommunications biology2023
COVID-19 and influenza infections mediate distinct pulmonary cellular and transcriptomic changes.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- IRF7 Protects Against Severe Influenza A Infection Independently of TLR7 Recognition in Mice.Viruses · 2026Article
- The emerging role of TLR7-mediated signaling in respiratory viral infections and autoimmune diseases.Cellular and molecular life sciences : CMLS · 2026Review
- Characterization of subchronic lung and brain consequences caused by mouse-adapted SARS-CoV-2 and influenza A infection of C57BL6 mice.Frontiers in immunology · 2026Article
- Respiratory long COVID in aged hamsters features impaired lung function post-exercise with bronchiolization and fibrosis.Nature communications · 2025Article
- Translating insights into therapies for Long Covid.Science translational medicine · 2024Review
- Chronic lung inflammation and CK14+ basal cell proliferation induce persistent alveolar-bronchiolization in SARS-CoV-2-infected hamsters.EBioMedicine · 2024Article
- Deficiency of Tlr7 and Irf7 in mice increases the severity of COVID-19 through the reduced interferon production.Communications biology · 2024Article
- Enhanced complement activation and MAC formation accelerates severe COVID-19.Cellular and molecular life sciences : CMLS · 2024Article
- Article
- Emerging role of complement in COVID-19 and other respiratory virus diseases.Cellular and molecular life sciences : CMLS · 2024Review
- Aging is associated with an insufficient early inflammatory response of lung endothelial cells in SARS-CoV-2 infection.Frontiers in immunology · 2024Article
- How Neutrophils Shape the Immune Response: Reassessing Their Multifaceted Role in Health and Disease.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
Abstract
SARS-CoV-2 infection can cause persistent respiratory sequelae. However, the underlying mechanisms remain unclear. Here we report that sub-lethally infected K18-human ACE2 mice show patchy pneumonia associated with histiocytic inflammation and collagen deposition at 21 and 45 days post infection (DPI). Transcriptomic analyses revealed that compared to influenza-infected mice, SARS-CoV-2-infected mice had reduced interferon-gamma/alpha responses at 4 DPI and failed to induce keratin 5 (Krt5) at 6 DPI in lung, a marker of nascent pulmonary progenitor cells. Histologically, influenza- but not SARS-CoV-2-infected mice showed extensive Krt5+ "pods" structure co-stained with stem cell markers Trp63/NGFR proliferated in the pulmonary consolidation area at both 7 and 14 DPI, with regression at 21 DPI. These Krt5+ "pods" structures were not observed in the lungs of SARS-CoV-2-infected humans or nonhuman primates. These results suggest that SARS-CoV-2 infection fails to induce nascent Krt5+ cell proliferation in consolidated regions, leading to incomplete repair of the injured lung.
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Registered trials
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