ArticleCell insight2026
Targeting the ICAM-1/LFA-1 adhesion axis attenuates lethal Crimean-Congo hemorrhagic fever virus infection.
Article in Cell insight, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Crimean-Congo hemorrhagic fever virus (CCHFV) is a highly pathogenic tick-borne bunyavirus. Infection and dysfunction of the vascular endothelium are likely key factors in CCHFV pathogenesis, yet the underlying mechanisms remain poorly understood. Using a mouse model, we demonstrated that CCHFV directly infects vascular endothelium, leading to marked activation and damage, as evidenced by the upregulation of adhesion molecules. To further investigate this phenomenon, we performed a quantitative proteomics study on CCHFV-infected human umbilical vein endothelial cells (HUVECs), confirming a significant upregulation of cell adhesion molecular pathways. Notably, the key adhesion molecule intercellular adhesion molecule 1 (ICAM-1) was prominently induced upon infection, which was transcriptionally dependent on NF-κB. ICAM-1 interacts with its receptor integrin (LFA-1) on leukocytes to mediate firm adhesion and transmigration, thereby driving inflammatory responses. Using an established
Indexed as
Identifiers
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.