ArticleProceedings of the National Academy of Sciences of the United States of America2021
Primary differentiated respiratory epithelial cells respond to apical measles virus infection by shedding multinucleated giant cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Distinct Humoral Response Development to Measles Virus Across Vaccine Platforms.The Journal of infectious diseases · 2026Article
- Airway epithelia clear rhinovirus infection via two waves of cell extrusion.Science advances · 2026Article
- Evidence of Mpox clade IIb infection in primary human alveolar epithelium.Emerging microbes & infections · 2025Article
- Acute induction of IFNα is responsible for the attenuation of the live measles vaccine.bioRxiv : the preprint server for biology · 2025Article
- Detection of Live Attenuated Measles Virus in the Respiratory Tract Following Subcutaneous Measles-Mumps-Rubella Vaccination.The Journal of infectious diseases · 2025Article
- Sphingosine-1-phosphate signaling mediates shedding of measles virus-infected respiratory epithelial cells.Journal of virology · 2025Article
- Epithelial-to-mesenchymal transition and live cell extrusion contribute to measles virus release from human airway epithelia.Journal of virology · 2025Article
- Article
- Live imaging of airway epithelium reveals that mucociliary clearance modulates SARS-CoV-2 spread.Nature communications · 2024Article
- What's going on with measles?Journal of virology · 2024Review
- Measles Infection Dose Responses: Insights from Mathematical Modeling.Bulletin of mathematical biology · 2024Article
- The epithelium takes the stage in asthma and inflammatory bowel diseases.Frontiers in cell and developmental biology · 2024Review
- Brain tropism acquisition: The spatial dynamics and evolution of a measles virus collective infectious unit that drove lethal subacute sclerosing panencephalitis.PLoS pathogens · 2023Article
- Antiviral responses in a Jamaican fruit bat intestinal organoid model of SARS-CoV-2 infection.Nature communications · 2023Article
- Modelling BK Polyomavirus dissemination and cytopathology using polarized human renal tubule epithelial cells.PLoS pathogens · 2023Article
- Mechanosensitive extrusion of Enterovirus A71-infected cells from colonic organoids.Nature microbiology · 2023Article
- Canine Distemper Virus Alters Defense Responses in an Ex Vivo Model of Pulmonary Infection.Viruses · 2023Article
- Article
- Nebulized fusion inhibitory peptide protects cynomolgus macaques from measles virus infection.Nature communications · 2022Article
- Nebulized fusion inhibitory peptide protects cynomolgus macaques from measles virus infection.Research square · 2022Article
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5 authors.
Funding
Abstract
Measles virus (MeV) is highly infectious by the respiratory route and remains an important cause of childhood mortality. However, the process by which MeV infection is efficiently established in the respiratory tract is controversial with suggestions that respiratory epithelial cells are not susceptible to infection from the apical mucosal surface. Therefore, it has been hypothesized that infection is initiated in lung macrophages or dendritic cells and that epithelial infection is subsequently established through the basolateral surface by infected lymphocytes. To better understand the process of respiratory tract initiation of MeV infection, primary differentiated respiratory epithelial cell cultures were established from rhesus macaque tracheal and nasal tissues. Infection of these cultures with MeV from the apical surface was more efficient than from the basolateral surface with shedding of viable MeV-producing multinucleated giant cell (MGC) syncytia from the surface. Despite presence of MGCs and infectious virus in supernatant fluids after apical infection, infected cells were not detected in the adherent epithelial sheet and transepithelial electrical resistance was maintained. After infection from the basolateral surface, epithelial damage and large clusters of MeV-positive cells were observed. Treatment with fusion inhibitory peptides showed that MeV production after apical infection was not dependent on infection of the basolateral surface. These results are consistent with the hypothesis that MeV infection is initiated by apical infection of respiratory epithelial cells with subsequent infection of lymphoid tissue and systemic spread.
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