Zika virus impairs non-homologous end joining and exacerbates DNA damage in neural progenitors derived from Huntington's disease iPSCs via mutant huntingtin-elicited Ku70/Ku80 complex disruption.

ABSTRACT:

Background

Zika virus (ZIKV) preferentially infects neural progenitor cells (NPCs) and is associated with NPC depletion in neonates. However, the impacts of ZIKV infection on NPCs in the context of neurodegenerative disease such as Huntington's disease (HD) remains poorly understood.

Methods

To investigate the effects of ZIKV on NPCs from individuals with HD, induced pluripotent stem cells (iPSCs) derived from HD patients were differentiated into NPCs (HD-iPSC-NPCs) in vitro. The phenotypic characterization of HD-iPSC-NPCs was performed using reverse transcription polymerase chain reaction (RT-PCR), Western blotting, and immunocytochemistry. Additionally, potential interactions between Ku70 and huntingtin were assessed using proximity ligation assay (PLA) and co-immunoprecip

SUBMITTER: Chiu FL 

PROVIDER: S-EPMC12329916 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature