Small extracellular vesicles from the human endothelial cell line EA.hy 926 exert a self-cell activation and modulate DENV-2 genome replication and infection in naïve endothelial cells
María-Angélica Calderón-Peláez, L. Johana Madroñero, Jaime E. Castellanos, Myriam L. Velandia-Romero
TL;DR
This study shows that small extracellular vesicles from infected endothelial cells can activate healthy cells and reduce dengue virus replication, offering potential for new treatments.
Contribution
The study reveals that sEVs from DENV-2-infected cells modulate infection and protect against endothelial barrier disruption in naïve cells.
Findings
Infected cells produce more EVs containing viral peptides and proteins involved in proteasome activity.
sEVs from infected cells reduce DENV-2 replication and protect against barrier disruption in naïve cells.
Y-RNAs and specific miRs in sEVs may regulate the dengue virus genome.
Abstract
Extracellular vesicles (EVs) play crucial roles in cell signaling and communication, transporting molecules that convey a message to target cells. During infectious diseases, EVs can also carry viral molecules that may contribute to viral spread, as previously reported for dengue virus (DENV). EVs from infected endothelial cells (EC) may harbor viral segments and various sets of molecules that could contribute to endothelial dysfunction during severe dengue. However, the effect of these EVs on non-infected EC (NIC) remain unknown. We characterized the EVs produced by the human EC line EA.hy 926 infected with DENV-2 and assessed their functional impact on polarized NIC. Results showed that infection induced an increased in the quantity of produced EVs, which differentially carried proteins mainly involved in proteosome activity, along with a peptide of the NS5 viral protein.…
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Taxonomy
TopicsPoverty, Education, and Child Welfare · Global Educational Policies and Reforms