Influence of Zika Virus in mechanisms related of cytotoxicity, cell adhesion, apoptosis and inflammatory markers on glioblastoma cells

Glioblastoma (GBM) is one of the most common brain tumors in adults. Despite the presence of available treatments, it remains one of the most lethal and difficult tumors to treat such that most patients die within two years. Studies reported that infection with Zika virus (ZIKV) causes inhibition of cell proliferation as well as induction of apoptosis; moreover, these manifestations show a predilection for developing neuronal cells. In the present study, two GBM cell lines U-138 and U-251 were infected with ZIKV at multiplicities of infection (MOI) 0.1, 0,01 and 0.001 and tested for cell viability, cell migration, cell adhesion, induction of apoptosis, interleukin levels, and cell surface markers (CD14 and CD73). Our study demonstrated that the ZIKV infection promotes loss of cell viability and increased apoptosis potential. It was not evidenced changes in cell migration, however, the two glioblastoma cell lines displayed increased the cell adhesion behavior. There was small increase in the IL-4 level in the U-251 cell line after exposure to ZIKV, with no change in relation to INF-γ levels. Furthermore, we observed an increase in the percentage of cells expressing the CD14 surface marker in both cell lines and increased CD73 expression in the U-251 cell line. Our results suggest that ZIKV may be associated with decrease of cell viability and increased CD73 expression, enhanced adherence, as well as increased apoptosis rates. Further investigations are required to explore the potential use of ZIKV in the treatment of GBM.