ArticleThe Journal of clinical investigation2008
Measles virus blind to its epithelial cell receptor remains virulent in rhesus monkeys but cannot cross the airway epithelium and is not shed.
Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
143 citing papers in PubMed, 1 synthesis or guideline pooled it, 235 citations in OpenAlex.
- Peste des petits ruminants in Africa: Meta-analysis of the virus isolation in molecular epidemiology studies.The Onderstepoort journal of veterinary research · 2019Pooled it
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- Engineering precision oncology: Targeting tumors and immune cells with lentiviral vectors.Molecular therapy. Oncology · 2026Review
- Three paradoxical paradigms of measles virus.PLoS pathogens · 2026Article
- Epithelial-to-mesenchymal transition and live cell extrusion contribute to measles virus release from human airway epithelia.Journal of virology · 2025Article
- The measles virus matrix F50S mutation from a lethal case of subacute sclerosing panencephalitis promotes receptor-independent neuronal spread.Journal of virology · 2025Article
- What's going on with measles?Journal of virology · 2024Review
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- Rational attenuation of canine distemper virus (CDV) to develop a morbillivirus animal model that mimics measles in humans.Journal of virology · 2024Article
- Brain tropism acquisition: The spatial dynamics and evolution of a measles virus collective infectious unit that drove lethal subacute sclerosing panencephalitis.PLoS pathogens · 2023Article
- Interferon-independent processes constrain measles virus cell-to-cell spread in primary human airway epithelial cells.Microbiology spectrum · 2023Article
- Metagenomics-enabled reverse-genetics assembly and characterization of myotis bat morbillivirus.Nature microbiology · 2023Article
- Article
- Advances in RNA Viral Vector Technology to Reprogram Somatic Cells: The Paramyxovirus Wave.Molecular diagnosis & therapy · 2022Review
- Updates on Measles Incidence and Eradication: Emphasis on the Immunological Aspects of Measles Infection.Medicina (Kaunas, Lithuania) · 2022Review
- Overcoming the Barrier of the Respiratory Epithelium during Canine Distemper Virus Infection.mBio · 2022Article
- The Communication between Ocular Surface and Nasal Epithelia in 3D Cell Culture Technology for Translational Research: A Narrative Review.International journal of molecular sciences · 2021Review
- M protein of subacute sclerosing panencephalitis virus, synergistically with the F protein, plays a crucial role in viral neuropathogenicity.The Journal of general virology · 2021Article
- Zoonotic potential of a novel bat morbillivirus.Research square · 2021Article
- Measles virus exits human airway epithelia within dislodged metabolically active infectious centers.PLoS pathogens · 2021Article
83 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
The current model of measles virus (MV) pathogenesis implies that apical infection of airway epithelial cells precedes systemic spread. An alternative model suggests that primarily infected lymphatic cells carry MV to the basolateral surface of epithelial cells, supporting MV shedding into the airway lumen and contagion. This model predicts that a mutant MV, unable to enter cells through the unidentified epithelial cell receptor (EpR), would remain virulent but not be shed. To test this model, we identified residues of the MV attachment protein sustaining EpR-mediated cell fusion. These nonpolar or uncharged polar residues defined an area located near the binding site of the signaling lymphocytic activation molecule (SLAM), the receptor for MV on lymphatic cells. We then generated an EpR-blind virus maintaining SLAM-dependent cell entry and inoculated rhesus monkeys intranasally. Hosts infected with the selectively EpR-blind MV developed rash and anorexia while averaging slightly lower viremia than hosts infected with wild-type MV but did not shed virus in the airways. The mechanism restricting shedding was characterized using primary well-differentiated human airway epithelial cells. Wild-type MV infected columnar epithelial cells bearing tight junctions only when applied basolaterally, while the EpR-blind virus did not infect these cells. Thus, EpR is probably a basolateral protein, and infection of the airway epithelium is not essential for systemic spread and virulence of MV.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.