ArticleProceedings of the National Academy of Sciences of the United States of America2023
Human airway and nasal organoids reveal escalating replicative fitness of SARS-CoV-2 emerging variants.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed.
- Organoid-based evaluation of SA55 and Pemivibart against evolving SARS-CoV-2 variants.Emerging microbes & infections · 2026Article
- Delayed antiviral immune response in alveolar type 2 cells increases susceptibility to influenza virus in alveoli.Chinese medical journal · 2026Article
- Cattle and human organoids reveal 2.3.4.4b H5N1 cross-species transmission potential and neuraminidase-specific neutralizing antibodies in humans.Nature communications · 2026Article
- Organoids: From Bench to Bedside Applications.MedComm · 2026Review
- A precision-cut lung slice platform for evaluating respiratory virus replication dynamics.bioRxiv : the preprint server for biology · 2026Article
- Nasal Epithelial Organoids as Translational Platforms in Inflammatory, Infectious, and Precision Medicine Applications: A Systematic Review.Journal of clinical medicine · 2026Review
- TNF inhibits SARS-CoV-2 induced cell-cell fusion through activating the SDC4-RhoA signaling to promote actin bundles formation.Cell insight · 2026Article
- Advances in human respiratory organoid models for studying the pathogenesis and intervention strategies of COVID-19.Virologica Sinica · 2026Review
- Tropism, replication competence, and cellular responses of HAdV-14p1 in human airway organoids.iScience · 2026Article
- SARS-CoV-2 peptide fragments selectively dysregulate specific immune cell populations via Gaussian curvature targeting.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cathepsin S contributes to influenza-induced lung injury by driving inflammation, promoting apoptosis, and disrupting epithelial barrier integrity.Microbiology spectrum · 2026Article
- Current knowledge on the host-pathogen interactions of henipaviruses and novel platforms to enable further characterisation.EBioMedicine · 2026Review
- Engineering Organoid Platforms for Pathogenesis Research.Research (Washington, D.C.) · 2026Review
- Organoid: a promising solution to current challenges in cancer immunotherapy.npj biomedical innovations · 2025Review
- Article
- Organoid Models to Study Human Infectious Diseases.Cell proliferation · 2025Review
- Experimental Models to Investigate Viral and Cellular Dynamics in Respiratory Viral Co-Infections.Microorganisms · 2025Review
- MERS-CoV and SARS-CoV-2 infection in diverse human lung organoid-derived cultures.Journal of virology · 2025Article
- Article
- The Mac1 ADP-ribosylhydrolase is a Therapeutic Target for SARS-CoV-2.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The high transmissibility of SARS-CoV-2 Omicron subvariants was generally ascribed to immune escape. It remained unclear whether the emerging variants have gradually acquired replicative fitness in human respiratory epithelial cells. We sought to evaluate the replicative fitness of BA.5 and earlier variants in physiologically active respiratory organoids. BA.5 exhibited a dramatically increased replicative capacity and infectivity than B.1.1.529 and an ancestral strain wildtype (WT) in human nasal and airway organoids. BA.5 spike pseudovirus showed a significantly higher entry efficiency than that carrying WT or B.1.1.529 spike. Notably, we observed prominent syncytium formation in BA.5-infected nasal and airway organoids, albeit elusive in WT- and B.1.1.529-infected organoids. BA.5 spike-triggered syncytium formation was verified by lentiviral overexpression of spike in nasal organoids. Moreover, BA.5 replicated modestly in alveolar organoids, with a significantly lower titer than B.1.1.529 and WT. Collectively, the higher entry efficiency and fusogenic activity of BA.5 spike potentiated viral spread through syncytium formation in the human airway epithelium, leading to enhanced replicative fitness and immune evasion, whereas the attenuated replicative capacity of BA.5 in the alveolar organoids may account for its benign clinical manifestation.
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