Reactive Oxygen Species (ROS) Are Not a Key Determinant for Zika Virus-Induced Apoptosis in SH-SY5Y Neuroblastoma Cells

Autor(es)

de Mendonca-Vieira, Leila Rodrigues ^[1] ; Anibal-Silva, Conceicao Elidianne ^[2] ; Menezes-Neto, Armando ^[1] ; Neves Azevedo, Elisa de Almeida ^[1] ; Zanluqui, Nagela Ghabdan ^[3] ; Schatzmann Peron, Jean Pierre ^[3] ; de Oliveira Franca, Rafael Freitas ^[1]

Afiliação do(s) autor(es)

^[1] Oswaldo Cruz Fdn Fiocruz, Aggeu Magalhaes Inst, BR-50740465 Recife, PE - Brazil

^[2] Univ Sao Paulo, Ribeirao Preto Med Sch, BR-14049900 Ribeirao Preto - Brazil

^[3] Univ Sao Paulo, Inst Biomed Sci, Dept Immunol, BR-05508000 Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Viruses-Basel; v. 13, n. 11 NOV 2021.
• Citações Web of Science: 0

Resumo

Introduction: ZIKV is a highly neurotropic virus that can cause the death of infected neuroprogenitor cells through mitochondrial damage and intrinsic apoptotic signaling. In this context, the role of reactive oxygen species (ROS) in neuronal cell death caused by ZIKV still remains elusive. Objective: We aimed at evaluating the role of these cellular components in the death of human undifferentiated neuroblastoma cell line infected with ZIKV. Results: ZIKV infection resulted in the extensive death of SH-SY5Y cells with the upregulation of several genes involved in survival and apoptotic responses as well as the colocalization of mitochondrial staining with ZIKV Envelope (E) protein. Notably, levels of intracellular reactive oxygen species (ROS) were not altered during ZIKV infection in undifferentiated SH-SY5Y cells, and consistent with these results, the treatment of infected cells with the widely studied ROS scavenger N-acetylcysteine (NAC) did not prevent cell death in these cells. Conclusion: Altogether, our results suggest that excessive ROS production is not the main trigger of SH-SY5Y cells death in ZIKV infection. (AU)

• Processo FAPESP: 16/07371-2 - Caracterização do papel de linfócitos T CD8+ na infecção por Zika vírus
• Beneficiário: Nagela Ghabdan Zanluqui
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 17/22504-1 - O papel dos receptores TAM e seus ligantes, Gas6 e Pros1, na Síndrome Congênita do Zika Vírus Experimental
• Beneficiário: Jean Pierre Schatzmann Peron
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 17/26170-0 - Neuroimunobiologia em modelo experimental de Encefalomielite Autoimune e Síndrome Congênita do Zika Vírus: fisiopatogenia, susceptibilidade, terapia celular, vacinação
• Beneficiário: Carolina Demarchi Munhoz
• Modalidade de apoio: Auxílio à Pesquisa - Temático