ArticleThe Journal of general virology2020
Passage of influenza A/H3N2 viruses in human airway cells removes artefactual variants associated with neuraminidase-mediated binding.
Article in The Journal of general virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
The trial behind it
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
9 citing papers in PubMed, 10 citations in OpenAlex.
- Chronic opioid use is associated with higher antibody response to influenza vaccination in people living with HIV.Frontiers in immunology · 2025Article
- Receptor Binding Properties of Neuraminidase for influenza A virus: An Overview of Recent Research Advances.Virulence · 2023Review
- New insights into the neuraminidase-mediated hemagglutination activity of influenza A(H3N2) viruses.Antiviral research · 2023Article
- Kinetic analysis of paramyxovirus-sialoglycan receptor interactions reveals virion motility.PLoS pathogens · 2023Article
- Antivirals Targeting the Neuraminidase.Cold Spring Harbor perspectives in medicine · 2022Review
- Do Vaccines Need a Gender Perspective? Influenza Says Yes!Frontiers in immunology · 2021Article
- Leveraging 3D Model Systems to Understand Viral Interactions with the Respiratory Mucosa.Viruses · 2020Review
- Human Organs-on-Chips for Virology.Trends in microbiology · 2020Review
- Adaptation of influenza viruses to human airway receptors.The Journal of biological chemistryReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serological assays with modern influenza A/H3N2 viruses have become problematic due to the progressive reduction in the ability of viruses of this subtype to bind and agglutinate red blood cells (RBCs). This is due to reduced ability of the viral haemagglutinin (HA) glycoprotein to bind to the sialic acid-containing receptors presented by these cells. Additionally, as a result of reduced HA-mediated binding in cell culture, modern A/H3N2 viruses often acquire compensatory mutations during propagation that enable binding of cellular receptors through their neuraminidase (NA) surface protein. Viruses that have acquired this NA-mediated binding agglutinate RBCs through their NA, confusing the results of serological assays designed to assess HA antigenicity. Here we confirm with a large dataset that the acquisition of mutations that confer NA binding of RBCs is a culture artefact, and demonstrate that modern A/H3N2 isolates with acquired NA-binding mutations revert to a clinical-like NA sequence after a single passage in human airway epithelial (HAE) cells.
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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.