ArticleJCI insight2024
Chikungunya virus infection disrupts lymph node lymphatic endothelial cell composition and function via MARCO.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- Lymphatic Endothelial Cells in Health and Disease.MedComm · 2026Review
- Chikungunya virus persists in joint-associated macrophages and promotes chronic disease in mice.Nature microbiology · 2026Article
- Immune features and clinical characteristics of chikungunya fever in children: differences from adults and across pediatric age groups.Frontiers in pediatrics · 2026Review
- Review
- Medullary stromal cells define small intestinal lymph node identity in humans and mice.Cell reports · 2025Article
- A specific gene expression program underlies antigen archiving by lymphatic endothelial cells in mammalian lymph nodes.Nature communications · 2025Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 5 countries.
Funding
Abstract
Infection with chikungunya virus (CHIKV) causes disruption of draining lymph node (dLN) organization, including paracortical relocalization of B cells, loss of the B cell-T cell border, and lymphocyte depletion that is associated with infiltration of the LN with inflammatory myeloid cells. Here, we found that, during the first 24 hours of infection, CHIKV RNA accumulated in MARCO-expressing lymphatic endothelial cells (LECs) in both the floor and medullary LN sinuses. The accumulation of viral RNA in the LN was associated with a switch to an antiviral and inflammatory gene expression program across LN stromal cells, and this inflammatory response - including recruitment of myeloid cells to the LN - was accelerated by CHIKV-MARCO interactions. As CHIKV infection progressed, both floor and medullary LECs diminished in number, suggesting further functional impairment of the LN by infection. Consistent with this idea, antigen acquisition by LECs, a key function of LN LECs during infection and immunization, was reduced during pathogenic CHIKV infection.
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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.