ArticleViruses2025
MCP-1 Reduction by L-SIGN Expression in Dengue Virus-Infected Liver Endothelial Cells.
Article in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it.
- Mechanistic constraints in dengue severity: a systematic review with evidence stratification and agent-based evaluation of logical sufficiency.Frontiers in immunology · 2026Pooled it
- Multilayer Fluorescent Immunoassay for Early and Sensitive Dengue Virus Detection Using Host and Viral Biomarkers.Bioconjugate chemistry · 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
(1) Background: The C-type lectin domain family 4 member M (CLEC4M, also known as L-SIGN) is a crucial pathogen-recognition receptor for the dengue virus (DENV). Our previous study has exhibited a polymorphism in its extracellular neck region, specifically within the long tandem repeats of exon 4, which correlates with DHF in DENV infection and causes liver damage. (2) Methods: Using monocyte-derived dendritic cells (MDDCs) and SK-HEP1 liver endothelial cell lines to compare viral replication relative to L-SIGN expression. (3) Results: Results indicated that SK-HEP1 cells were more susceptible to DENV infection than MDDCs, and L-SIGN transfection significantly increased viral replication in SK-HEP1 cell lines. The study also found that L-SIGN-enhanced DENV infection is mediated by the decrease in monocyte chemoattractant protein-1 (MCP-1) but not interferon gamma inducible protein-10 (IP-10). These findings reveal that L-SIGN-induced DENV infection leads to reduced MCP-1 levels, which, in turn, enhances DENV replication velocity. (4) Conclusions: This study offers insights into the molecular mechanisms of DENV replication and identifies potential therapeutic targets involving MCP-1 and L-SIGN pathways.
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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.