ArticleVirology2012
Mumps virus inhibits migration of primary human macrophages toward a chemokine gradient through a TNF-alpha dependent mechanism.
Article in Virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed, 3 citations in OpenAlex.
- Alveolar macrophages are early targets of mumps virus.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Paramyxovirus activation and inhibition of innate immune responses.Journal of molecular biology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Macrophages are an important cell type for regulation of immunity, and can play key roles in virus pathogenesis. Here we address the effect of infection of primary human macrophages with the related paramyxoviruses Parainfluenza virus 5 (PIV5) and Mumps virus (MuV). Monocyte-derived macrophages infected with PIV5 or MuV showed very little cytopathic effect, but were found to be defective in migration toward a gradient of chemokines such as macrophage colony stimulating factor (MCSF) and vascular endothelial growth factor (VEGF). For MuV infection, the inhibition of migration required live virus infection, but was not caused by a loss of chemokine receptors on the surface of infected cells. MuV-mediated inhibition of macrophage chemotaxis was through a soluble factor released from infected cells. MuV infection enhanced secretion of TNF-α, but not macrophage inhibitory factor (MIF). Antibody inhibition and add-back experiments demonstrated that TNF-α was both necessary and sufficient for MuV-mediate chemotaxis inhibition.
Indexed as
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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.