Zika virus infection induces ultrastructural alterations, mitochondrial dysfunction and oxidative stress in human trophoblast HTR-8/SVneo

Background: Zika fever gained importance in Brazil in 2015 due to its association with congenital syndrome. Although Zika virus (ZIKV) crosses the placenta and infects the fetus, its pathogenesis remains incompletely understood. This study investigated the effects of ZIKV infection in HTR-8/SVneo trophoblast cells. Methods: ), was analyzed by RT-qPCR. Protein expression (SOD, CAT, NRF2), enzymatic activities (SOD, CAT), and oxidative damage markers (8-OHdG, MDA, NO) were assessed by immunofluorescence and/or colorimetric assays. Results: transcripts were reduced, protein immunolabeling and SOD activity were increased, whereas CAT activity was decreased. Elevated levels of 8-OHdG, MDA, and NO confirmed oxidative stress. Conclusion: ZIKV infection induces mitochondrial dysfunction, oxidative stress, and impaired mitophagy in HTR-8/SVneo trophoblast cells, highlighting mitochondrial dysfunction as a major component of the cellular response to ZIKV infection in trophoblast cells.