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ZIKV Strains Elicit Different Inflammatory and Anti-Viral Responses in Microglia Cells

In recent years, the Zika Virus (ZIKV) has caused pandemic outbreaks associated with a high rate of congenital ZIKV syndrome (CZS). Although all strains associated with worldwide outbreaks derive from the Asian lineage, the reasons for their enhanced spread and severity are not fully understood. In...

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Detalles Bibliográficos
Autores principales: de Oliveira, Fernanda Bellaniza Caminha, Freire, Vanessa Paola Alves Sampaio de Sá, Coelho, Sharton Vinicius Antunes, Meuren, Lana Monteiro, Palmeira, Julys da Fonseca, Cardoso, Ana Luísa, Neves, Francisco de Assis Rocha, Ribeiro, Bergmann Morais, Argañaraz, Gustavo Adolfo, de Arruda, Luciana Barros, Argañaraz, Enrique Roberto
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10303021/
https://www.ncbi.nlm.nih.gov/pubmed/37376550
http://dx.doi.org/10.3390/v15061250
Descripción
Sumario:In recent years, the Zika Virus (ZIKV) has caused pandemic outbreaks associated with a high rate of congenital ZIKV syndrome (CZS). Although all strains associated with worldwide outbreaks derive from the Asian lineage, the reasons for their enhanced spread and severity are not fully understood. In this study, we conducted a comparative analysis of miRNAs (miRNA-155/146a/124) and their cellular targets (SOCS1/3, SHP1, TRAF6, IRAK1), as well as pro- and anti-inflammatory and anti-viral cytokines (IL-6, TNF-α, IFN-γ, IL-10, and IFN-β) and peroxisome proliferator-activated receptor γ (PPAR-γ) expression in BV2 microglia cells infected with ZIKV strains derived from African and Asian lineages (ZIKV(MR766) and ZIKV(PE243)). BV2 cells were susceptible to both ZIKV strains, and showed discrete levels of viral replication, with delayed release of viral particles without inducing significant cytopathogenic effects. However, the ZIKV(MR766) strain showed higher infectivity and replicative capacity, inducing a higher expression of microglial activation markers than the ZIKV(PE243) strain. Moreover, infection with the ZIKV(MR766) strain promoted both a higher inflammatory response and a lower expression of anti-viral factors compared to the ZIKV(PE243) strain. Remarkably, the ZIKK(PE243) strain induced significantly higher levels of the anti-inflammatory nuclear receptor—PPAR-γ. These findings improve our understanding of ZIKV-mediated modulation of inflammatory and anti-viral innate immune responses and open a new avenue to explore underlining mechanisms involved in the pathogenesis of ZIKV-associated diseases.