ArticleJournal of virology2013
Nipah virus entry and egress from polarized epithelial cells.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 58 citations in OpenAlex.
- Deadbolt Drug Discovery: Locking the Door to Class 1 Viral Entry by Small Molecules.ACS infectious diseases · 2026Review
- Cryo-electron tomography of Nipah virus structural protein complexes in virus-like particles.bioRxiv : the preprint server for biology · 2026Article
- Nipah virus: pathogenesis, genome, diagnosis, and treatment.Applied microbiology and biotechnology · 2025Review
- Host cell lectins ASGR1 and DC-SIGN jointly with TMEM106B confer ACE2 independence and imdevimab resistance to SARS-CoV-2 pseudovirus with spike mutation E484D.Journal of virology · 2025Article
- Nipah Virus-Associated Neuropathology in African Green Monkeys During Acute Disease and Convalescence.The Journal of infectious diseases · 2025Article
- Histopathological and immunohistochemical characterization of lesions in the golden Syrian hamster model of Nipah virus infection (Bangladesh strain).Frontiers in veterinary science · 2025Article
- An Updated Review on Nipah Virus Infection with a Focus on Encephalitis, Vasculitis, and Therapeutic Approaches.Current topics in medicinal chemistry · 2025Review
- Vascular dysfunction in hemorrhagic viral fevers: opportunities for organotypic modeling.Biofabrication · 2024Review
- Article
- Development of immortalized rhesus macaque kidney cells supporting infection with a panel of viruses.PloS one · 2023Article
- Article
- Measles and Nipah virus assembly: Specific lipid binding drives matrix polymerization.Science advances · 2022Article
- Review
- Infection of polarized bovine respiratory epithelial cells by bovine viral diarrhea virus (BVDV).Virulence · 2021Article
- Negative-sense RNA viruses: An underexplored platform for examining virus-host lipid interactions.Molecular biology of the cell · 2021Review
- Article
- Article
- Nano-based approach to combat emerging viral (NIPAH virus) infection.Nanomedicine : nanotechnology, biology, and medicine · 2019Review
- Nipah virus induces two inclusion body populations: Identification of novel inclusions at the plasma membrane.PLoS pathogens · 2019Article
- Tetherin Inhibits Nipah Virus but Not Ebola Virus Replication in Fruit Bat Cells.Journal of virology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Highly pathogenic Nipah virus (NiV) infections are transmitted via airway secretions and urine, commonly via the respiratory route. Epithelial surfaces represent important replication sites in both primary and systemic infection phases. NiV entry and spread from polarized epithelial cells therefore determine virus entry and dissemination within a new host and influence virus shedding via mucosal surfaces in the respiratory and urinary tract. To date, there is no knowledge regarding the entry and exit sites of NiV in polarized epithelial cells. In this report, we show for the first time that NiV can infect polarized kidney epithelial cells (MDCK) from both cell surfaces, while virus release is primarily restricted to the apical plasma membrane. Substantial amounts of basolateral infectivity were detected only after infection with high virus doses, at time points when the integrity of the cell monolayer was largely disrupted as a result of cell-to-cell fusion. Confocal immunofluorescence analyses of envelope protein distribution at early and late infection stages suggested that apical virus budding is determined by the polarized sorting of the NiV matrix protein, M. Studies with stably M-expressing and with monensin-treated cells furthermore demonstrated that M protein transport is independent from the glycoproteins, implying that the M protein possesses an intrinsic apical targeting signal.
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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.