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Viral infections of the respiratory tract can lead to chronic lung injury through immunopathological mechanisms that remain unclear. Communities of commensal bacteria colonising the respiratory tract, known as the respiratory tract microbiota, are altered in viral infections, which can contribute to inflammation, lung epithelial damage and subsequent development of lung disease. Emerging evidence on post-viral lung injury suggests an interplay between viral infections, immune responses and airway microbiota composition in the development of viral-induced lung diseases. In this review, we present the clinical characteristics of post-viral lung injury, along with the underlying immunopathological mechanisms and host-bacteria interactions, with a focus on influenza virus, respiratory syncytial virus and coronaviruses. Additionally, considering the important role of the airway microbiota in viral-induced pulmonary sequelae, we suggest key areas for future research on respiratory microbiota involvement in the development of post-viral lung diseases.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11973713 | PMC |
http://dx.doi.org/10.1183/23120541.00560-2024 | DOI Listing |
Int J Mol Sci
August 2025
Department of Translational Medical Sciences, Section of Cardiology, University of Campania Luigi Vanvitelli, 80131 Naples, Italy.
Long COVID is a persistent post-viral syndrome with the significant involvement of both the cardiovascular and pulmonary systems, often extending well beyond the acute phase of SARS-CoV-2 infection. Emerging evidence has highlighted a spectrum of chronic alterations, including endothelial dysfunction, microvascular inflammation, perivascular fibrosis, and in some cases, the persistence of viral components in the cardiac and pulmonary tissues. At the molecular level, a sustained inflammatory milieu-characterized by elevated pro-inflammatory cytokines such as interleukin 6 (IL-6)-and chronic platelet hyperreactivity contribute to a prothrombotic state.
View Article and Find Full Text PDFClin Microbiol Rev
July 2025
Centre for Inflammation Research, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh BioQuarter, Edinburgh, United Kingdom.
SUMMARYRespiratory viral infections cause extensive cell death in the lung epithelium, resulting from both direct viral action and exuberant immune responses. Recovery following viral infection requires rapid and coordinated repair programs, ensuring the replacement of the damaged tissue through proliferation, migration, and differentiation of respiratory epithelial progenitor cells. Viral infection and the resulting inflammatory milieu alter host gene expression.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
June 2025
State Key Laboratory of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou University of Chinese Medicine; Guangzhou 510080, China.
Objectives: To explore the therapeutic mechanism of extract for treatment of Post-Viral Pneumonia Pulmonary Fibrosis (PPF).
Methods: The chemical constituents of extracts were identified using UHPLC-Q-TOF-MS/MS. Mouse models of pulmonary fibrosis established by tracheal instillation of bleomycin were treated with Arctium lappa extract, and body weight changes were recorded and lung tissue pathology was examined using HE and Masson staining.
Aberrant epithelial regeneration and immune remodeling are hallmarks of chronic lung diseases such as idiopathic pulmonary fibrosis (IPF), COPD, and post-viral syndromes. Yet how cellular context shapes these trajectories remains unresolved. We present a tunable, primary rat-derived lung organoid model that systematically varies immune, epithelial, and mesenchymal inputs to reveal how composition alone dictates epithelial plasticity and macrophage polarization.
View Article and Find Full Text PDFJ Clin Med
April 2025
Division of Pediatric Pulmonology, Allergy and Endocrinology, Department of Pediatrics and Adolescent Medicine, Comprehensive Centre of Pediatrics, Medical University of Vienna, 1090 Vienna, Austria.
Patients with chronic lung diseases, such as cystic fibrosis, were considered a risk group for a severe course of coronavirus disease 2019 at the beginning of the pandemic. However, mounting evidence suggests that this group may not face an elevated risk for a severe SARS-CoV-2 infection. : Here, we present data on the incidence and clinical course of SARS-CoV-2 infections in a single pediatric CF centre in Austria.
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