ArticleJournal of medical virology2025
Persistent Human T-Lymphotropic Virus Type 1 (HTLV-1) Infection in the Placenta of Pregnant Women.
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 3 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.
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Who cites it
3 citing papers in PubMed.
- Placenta models for HIV-1-ART-nicotine comorbidity research: advances and remaining challenges.Cell death discovery · 2026Review
- Observational
- Persistent Human T-Lymphotropic Virus Type 1 (HTLV-1) Infection in the Placenta of Pregnant Women.Journal of medical virology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
Mother-to-child transmission (MTCT) is the primary route of human T-lymphotropic virus type 1 (HTLV-1) infection. Although formula feeding reduces breastfeeding-associated transmission, MTCT still occurs, implicating pregnancy or delivery as key transmission windows. In this study, placental tissues from nine HTLV-1-positive mothers were analyzed using DNA/RNAscope, revealing low HTLV-1 DNA and RNA levels and a low RNA/DNA ratio, consistent with latent infection in the placenta and potentially explaining the low MTCT rate. Elevated interferon (IFN)-β levels were observed in infected placentas compared to seronegative controls, while IFNα, IFNγ, and IFITM expression remained unchanged. Concurrently, sustained IFNβ expression in infected placentas suggests its dual roles in HTLV-1 pathogenesis: suppressing viral replication while potentially disrupting placental homeostasis through chronic inflammation. In vitro modeling using BeWo cells or primary trophoblasts cocultured with HTLV-1-infected MT-2 cells demonstrated syncytin-1-mediated viral entry, confirmed by HTLV-1 p19 detection in both trophoblasts. Of note, HTLV-1 transmission was abolished by a syncytin-1-specific fusion inhibitor HRB1, underscoring syncytin-1's essential role in cell-to-cell transmission of HTLV-1. Thus, this study identifies syncytin-1 as a therapeutic target to block vertical transmission and highlights the need to balance antiviral responses with placental integrity in HTLV-1 management.
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Registered trials
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