ArticleJournal of virology2002
Apical budding of a recombinant influenza A virus expressing a hemagglutinin protein with a basolateral localization signal.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 56 citations in OpenAlex.
- Generation of an Induced Pluripotent Stem Cell-Derived Alveolar Type II In Vitro Model to Study Influenza A Virus Infection and Drug Treatments.Advanced healthcare materials · 2026Article
- RNA N6-methyladenosine methylation in influenza A virus infection.Frontiers in microbiology · 2024Review
- A mathematical model describing the localization and spread of influenza A virus infection within the human respiratory tract.PLoS computational biology · 2020Article
- Directional entry and release of Zika virus from polarized epithelial cells.Virology journal · 2019Article
- Cholesterol Binding to the Transmembrane Region of a Group 2 Hemagglutinin (HA) of Influenza Virus Is Essential for Virus Replication, Affecting both Virus Assembly and HA Fusion Activity.Journal of virology · 2019Article
- Article
- Review
- Apical Trafficking Pathways of Influenza A Virus HA and NA via Rab17- and Rab23-Positive Compartments.Frontiers in microbiology · 2019Article
- Influenza A Virus M2 Protein Apical Targeting Is Required for Efficient Virus Replication.Journal of virology · 2018Article
- Cytoplasmic tail of coronavirus spike protein has intracellular targeting signals.Journal of biosciences · 2017Article
- Lateral Organization of Influenza Virus Proteins in the Budozone Region of the Plasma Membrane.Journal of virology · 2017Article
- Alveolar Macrophages Prevent Lethal Influenza Pneumonia By Inhibiting Infection Of Type-1 Alveolar Epithelial Cells.PLoS pathogens · 2017Article
- NLRX1 prevents mitochondrial induced apoptosis and enhances macrophage antiviral immunity by interacting with influenza virus PB1-F2 protein.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Nipah virus entry and egress from polarized epithelial cells.Journal of virology · 2013Article
- Polar release of pathogenic Old World hantaviruses from renal tubular epithelial cells.Virology journal · 2012Article
- Canine distemper virus matrix protein influences particle infectivity, particle composition, and envelope distribution in polarized epithelial cells and modulates virulence.Journal of virology · 2011Article
- A review of mathematical models of influenza A infections within a host or cell culture: lessons learned and challenges ahead.BMC public health · 2011Article
- Evasion of natural killer cells by influenza virus.Journal of leukocyte biology · 2011Review
- Viral protein determinants of Lassa virus entry and release from polarized epithelial cells.Journal of virology · 2010Article
- Influenza virus morphogenesis and budding.Virus research · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Influenza virions bud preferentially from the apical plasma membrane of infected epithelial cells, by enveloping viral nucleocapsids located in the cytosol with its viral integral membrane proteins, i.e., hemagglutinin (HA), neuraminidase (NA), and M2 proteins, located at the plasma membrane. Because individually expressed HA, NA, and M2 proteins are targeted to the apical surface of the cell, guided by apical sorting signals in their transmembrane or cytoplasmic domains, it has been proposed that the polarized budding of influenza virions depends on the interaction of nucleocapsids and matrix proteins with the cytoplasmic domains of HA, NA, and/or M2 proteins. Since HA is the major protein component of the viral envelope, its polarized surface delivery may be a major force that drives polarized viral budding. We investigated this hypothesis by infecting MDCK cells with a transfectant influenza virus carrying a mutant form of HA (C560Y) with a basolateral sorting signal in its cytoplasmic domain. C560Y HA was expressed nonpolarly on the surface of infected MDCK cells. Interestingly, viral budding remained apical in C560Y virus-infected cells, and so did the location of NP and M1 proteins at late times of infection. These results are consistent with a model in which apical viral budding is a shared function of various viral components rather than a role of the major viral envelope glycoprotein HA.
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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.