ArticleNature medicine2024
Spatially resolved single-cell atlas unveils a distinct cellular signature of fatal lung COVID-19 in a Malawian population.
Article in Nature medicine, 2024. 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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Who cites it
7 citing papers in PubMed.
- BLASE: bulk linkage analysis for single cell experiments - teasing out the secrets of bulk transcriptomics with trajectory analysis.BMC methods · 2026Article
- Differential effects of SARS-CoV-2-targeted infection of ATII, club cells, and macrophages on lung immunopathology and antiviral responses.Mucosal immunology · 2026Article
- Pathogen-specific immune responses might underlie divergent outcomes of coronavirus and influenza infection in the natural porcine host.Communications biology · 2026Article
- Machine Learning Identification of Cell-Type-Specific Molecular Signatures Distinguishing COVID-19 from Other Lower Respiratory Tract Diseases.Life (Basel, Switzerland) · 2026Article
- Persistent pneumococcal colonisation in antiretroviral-treated HIV infection is associated with nasal inflammation.Nature communications · 2025Article
- Airway Immune Signatures in Severe and Fatal Infection with COVID-19.American journal of respiratory cell and molecular biology · 2025Article
- Secreted Phosphoprotein 1 in Lung Diseases.Metabolites · 2025Review
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47 authors.
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Abstract
Postmortem single-cell studies have transformed understanding of lower respiratory tract diseases (LRTDs), including coronavirus disease 2019 (COVID-19), but there are minimal data from African settings where HIV, malaria and other environmental exposures may affect disease pathobiology and treatment targets. In this study, we used histology and high-dimensional imaging to characterize fatal lung disease in Malawian adults with (n = 9) and without (n = 7) COVID-19, and we generated single-cell transcriptomics data from lung, blood and nasal cells. Data integration with other cohorts showed a conserved COVID-19 histopathological signature, driven by contrasting immune and inflammatory mechanisms: in US, European and Asian cohorts, by type I/III interferon (IFN) responses, particularly in blood-derived monocytes, and in the Malawian cohort, by response to IFN-γ in lung-resident macrophages. HIV status had minimal impact on histology or immunopathology. Our study provides a data resource and highlights the importance of studying the cellular mechanisms of disease in underrepresented populations, indicating shared and distinct targets for treatment.
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