ArticleJournal of medical virology2012
Increased replication of respiratory syncytial virus in the presence of cytokeratin 8 and 18.
Article in Journal of medical virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Crosstalk between vimentin and keratins in viral infection: Implications across the viral life cycle.Virulence · 2026Review
- Human beta defensin-3 mediated activation of β-catenin during human respiratory syncytial virus infection: interaction of HBD3 with LDL receptor-related protein 5.Frontiers in microbiology · 2023Article
- Species-specific transcriptomic changes upon respiratory syncytial virus infection in cotton rats.Scientific reports · 2022Article
- Chronic E-Cigarette Aerosol Inhalation Alters the Immune State of the Lungs and Increases ACE2 Expression, Raising Concern for Altered Response and Susceptibility to SARS-CoV-2.Frontiers in physiology · 2021Article
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
No grant is acknowledged in the PubMed record.
Abstract
Previously, it was reported that productive viral infection, viral protein synthesis, and viral RNA replication of respiratory syncytial virus (RSV) operated efficiently in two human epithelial cell lines (HEp-2 and A549), but not in a human mast-cell line, HMC-1. Based on these observations, it was hypothesized that HMC-1 cells lack the machinery required for RSV replication. To identify the host factors required for RSV replication, cDNA subtraction using A549, HEp-2, and HMC-1 cells was performed, and cytokeratin 18 (C18) was identified as a candidate host factor. Because C18 is generally expressed in simple epithelia with cytokeratin 8 (C8), HMC-1 cells that constitutively express C18 and C8 (HMC-1-C8/18) were established to evaluate the role of C8/18 in RSV replication. In HMC-1-C8/18 cells, RSV RNA replication was increased, and the amount of infective virus produced was also increased in the cellular fraction after RSV spinoculation, whereas RSV production was decreased in A549 cells in which C18 expression was knocked down. These data suggest that the replication of RSV increases in the presence of C8/18.
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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.