Zika virus exposure affects neuron-glia communication in the hippocampal slices of adult rats

• Autor(a) principal: Bobermin, Larissa Daniele
• Data de Publicação: 2020
• Outros Autores: Quincozes-Santos, André, Santos, Camila Leite, Varela, Ana Paula Muterle, Teixeira, Thais Fumaco, Wartchow, Krista Minéia, Lissner, Lílian Juliana, Silva, Amanda da, Thomaz, Natalie Katherine, Santi, Lucélia, Silva, Walter Orlando Beys da, Roehe, Paulo Michel, Sesterheim, Patrícia, Guimaraes, Jorge Almeida, Goncalves, Carlos Alberto Saraiva, Souza, Diogo Onofre Gomes de
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRGS
• Texto Completo: http://hdl.handle.net/10183/217251
• topic: Infecção por Zika virus; Neuroglia; Hipocampo; NF-kappa B; Comunicação celular

Zika virus (ZIKV) infection during pregnancy was associated with microcephaly in neonates, but clinical and experimental evidence indicate that ZIKV also causes neurological complications in adults. However, the changes in neuron-glial communication, which is essential for brain homeostasis, are still unknown. Here, we report that hippocampal slices from adult rats exposed acutely to ZIKV showed significant cellular alterations regarding to redox homeostasis, inflammatory process, neurotrophic functions and molecular signalling pathways associated with neurons and glial cells. Our findings support the hypothesis that ZIKV is highly neurotropic and its infection readily induces an inflammatory response, characterized by an increased expression and/or release of pro-inflammatory cytokines. We also observed changes in neural parameters, such as adenosine receptor A2a expression, as well as in the release of brain-derived neurotrophic factor and neuron-specific enolase, indicating plasticity synaptic impairment/neuronal damage. In addition, ZIKV induced a glial commitment, with alterations in specific and functional parameters such as aquaporin 4 expression, S100B secretion and glutathione synthesis. ZIKV also induced p21 senescence-associated gene expression, indicating that ZIKV may induce early senescence. Taken together, our results indicate that ZIKV-induced neuroinflammation, involving nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor κB (NFκB) pathways, affects important aspects of neuron-glia communication. Therefore, although ZIKV infection is transient, long-term consequences might be associated with neurological and/or neurodegenerative diseases.