ArticleBioactive materials2026
Cord blood natural killer cell-derived extracellular vesicles inhibit Zika virus infectivity through ITGB2/perforin-mediated envelope disruption in vitro and in vivo.
Article in Bioactive materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- MiR-1290 in natural killer cell derived extracellular vesicles: a pathogenic mediator of lupus nephritis and therapeutic target for th17 regulation.Journal of nanobiotechnology · 2026Article
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
No grant is acknowledged in the PubMed record.
Abstract
Zika virus (ZIKV) can traverse the placental barrier, leading to fetal microcephaly and congenital zika syndrome (CZS). The viral E protein mediates host-cell interactions and infection. Here, we demonstrated that cord blood natural killer cell-derived extracellular vesicles (CBNK-EVs) potently inhibit ZIKV infection in vitro without compromising cellular viability. Mechanistically, CBNK-EVs engage ZIKV through ITGB2, a surface-enriched integrin that interacts with the viral E protein, facilitating nanoparticle-virion contact or membrane fusion. This interaction triggers antiviral activity via perforins within extracellular vesicles (EVs), resulting in diminished viral infectivity. Notably, CBNK-EVs not only effectively crossed the placental barrier to protect fetuses from ZIKV-induced pathologies, but also reduced the ZIKV burden in IFN-deficient murine models and decreased CZS incidence and mortality. Additionally, either blockade of ITGB2 with a monoclonal antibody or chelation of Ca
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.