EV-A71 vesicles weaken the brain barrier in experimental models
Cell experiments and neonatal mice link enterovirus A71 infection to a route that weakens the blood–brain barrier. Vesicles released by infected cells carry small RNAs that suppress Notch1 signalling. The peer-reviewed study also found elevated RNA levels in severe childhood cases, but the patient comparison was observational and no treatment was tested in children.
Science··Midday
A distant route to brain vessels
Enterovirus A71 can weaken the barrier around the brain through packages released by infected cells elsewhere in the body. In a peer-reviewed study, cell experiments and neonatal mice showed that these extracellular vesicles, tiny membrane-bound carriers, reached brain vessels and increased leakage. Blood samples from children provided an additional observational comparison. The finding identifies an indirect route by which infection could help the virus enter the central nervous system.[1], [2]
Small RNAs interfere with a protective signal
The vesicles carried members of the miR-30 and miR-34 families, small RNA molecules that regulate gene activity. These reduced Notch1 signalling in cells lining brain blood vessels, disrupting connections that normally restrict passage. Tests included both a flat endothelial-cell layer and three-dimensional cultures incorporating other barrier-supporting cells. Activating Notch1 with the experimental agent JAG1 improved barrier measurements in the models; treated mice also had less leakage and lower viral burden in the brain.[1]
Children’s samples add an association
The clinical sampling included 24 healthy children, 23 mild cases and 21 severe cases. Vesicle-associated RNA levels were higher in the severe group, supporting a possible link with disease severity. That comparison cannot establish which process caused severe illness. No child received the experimental intervention. Other contents of the vesicles may contribute to the barrier changes, and the proposed blood markers still require testing in independent patient groups.[1]
