Authors: Izabela A. Rodenhuis-Zybert, Hilde M. van der Schaar, Júlia M. da Silva Voorham, Heidi van der Ende-Metselaar, Huan-Yao Lei, Jan Wilschut, Jolanda M. Smit
DOI: 10.1371/journal.ppat.1000718
Abstract Summary
Dengue-infected cells release immature virions that are normally non-infectious. However, researchers discovered that antibodies against prM protein—elevated during secondary infections—transform these immature particles into highly infectious agents. This occurs when prM antibodies help immature virions enter immune cells, where furin enzyme activates them. This mechanism may explain severe dengue in secondary infections.
Why Brain? 🧠
Immature dengue virus particles become highly infectious when bound by antibodies, potentially explaining severe disease in secondary infections or infants born to immune mothers.
The image is AI-generated for illustrative purposes only. Courtesy of Midjourney.
