Author:
Orrego Miguel A.,Szczesniak Michal W.,Vasquez Carlos M.,Verastegui Manuela R.,Bustos Javier A.,Garcia Hector H.,Nash Theodore E., ,Garcia Hector H.,Gilman Robert H.,Gonzalez Armando E.,Verastegui Manuela,Zimic Mirko,Bustos Javier,O’Neal Seth E.,Rodriguez Silvia,Gonzalez Isidro,Saavedra Herbert,Sanchez Sofia,Martinez Manuel,Santivañez Saul,Mayta Holger,Castillo Yesenia,Pajuelo Monica,Arroyo Gianfranco,Chile Nancy,Toribio Luz,Orrego Miguel A.,Lopez Maria T.,Gomez Luis,Gavidia Cesar M.,Vargas-Calla Ana,Gonzales Eloy,Moyano Luz M.,Gamboa Ricardo,Muro Claudio,Vichez Percy,Handali Sukwan,Noh John,Nash Theodore E.,Friedland Jon
Abstract
AbstractSubarachnoid neurocysticercosis (SANCC) is caused by an abnormally transformed form of the metacestode or larval form of the tapeworm Taenia solium. In contrast to vesicular parenchymal and ventricular located cysts that contain a viable scolex and are anlage of the adult tapeworm, the subarachnoid cyst proliferates to form aberrant membranous cystic masses within the subarachnoid spaces that cause mass effects and acute and chronic arachnoiditis. How subarachnoid cyst proliferates and interacts with the human host is poorly understood, but parasite stem cells (germinative cells) likely participate. RNA-seq analysis of the subarachnoid cyst bladder wall compared to the bladder wall and scolex of the vesicular cyst revealed that the subarachnoid form exhibits activation of signaling pathways that promote proliferation and increased lipid metabolism. These adaptions allow growth in a nutrient-limited cerebral spinal fluid. In addition, we identified therapeutic drug targets that would inhibit growth of the parasite, potentially increase effectiveness of treatment, and shorten its duration.
Funder
Fogarty International Center
Publisher
Springer Science and Business Media LLC