ArticleJournal of medical virology2025
Monkeypox Virus Subverts the Inflammatory Response of Macrophages at the Maternal-Fetal Interface.
Article in Journal of medical virology, 2025. 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
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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
2 citing papers in PubMed.
- Review
- The evolving mpox threat (2022-2024): clade dynamics, immune evasion, and escalating global health challenges.Frontiers in cellular and infection microbiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Monkeypox is a viral zoonosis caused by the monkeypox virus (MPXV). Although the virus was identified decades ago, human immunity to MPXV infection has not been widely characterized. During MPXV infection, macrophages are recruited at the site of infection and are thought to contribute to the spread of the virus. Cases of MPXV vertical transmission were reported in infected pregnant women to the developing fetuses in utero resulting to high viral burden in placenta tissue and abortion. We aim to understand the impact of MPXV infection at the foeto-maternal interface by focusing on macrophages functions. Using full-term placental explant model, macrophages were recruited at site of infection. Isolated naive macrophages are permissive to MPXV infection and secrete high levels of pro-inflammatory cytokines associated with a strong M1 polarization profile. Analysis of antiviral gene expression reveals upregulation of IFNA and IFN-associated genes suggesting that MPXV induces the expression of some component of antiviral response from macrophages that are unable to clear the virus. Our study shows that macrophages are permissive to MPXV that subverts inflammatory and antiviral machinery without virus clearance. Such findings contribute to better knowledge of MPXV vertical transmission pathogenesis.
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Registered trials
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