Effects of ZIKV + IgG+ complex on murine microglial cells

Background: Infection by Zika virus (ZIKV) is associated with damage to the Central Nervous System, such as Congenital Zika Syndrome1 . Due to its transplacental transmission, ZIKV induces neuroinflammation and microglial activation, resulting in lesions that can compromise neurodevelopment2-4. The fetus protection can be provided by maternal antibodies. However, this protection is still controversial5 . In this context, it is necessary to elucidate the effects of ZIKV and the mechanisms involved. Objectives: The present work aim to evaluate the role of the ZIKV+IgG+ complex in murine microglia cells (BV2). Design and setting: BV2 were exposed for 24 or 72 hours, to ZIKV, ZIKA-IgG+ or ZIKV+IgG+ complex. Methods: Effects of exposure to treatments were evaluated by MTT, oxidation of DCFHDA (ROS production)6 and mitochondrial membrane potential (Δ∴ϑ), measured by JC-17 assay. Results: It was observed that ZIKV-IgG+ and the ZIKV+IgG+ complex are cytotoxic to microglia, impairing the viability of these cells, altering Δ∴ϑ and inducing the production of ROS, especially in long-term exposure8,9. Negative action mediated by these antibodies may be a result of oxidative stress and a intervention in the Δ∴ϑ. Conclusion: ZIKV-IgG+ antibodies are harmful to microglia and these mechanisms may be related to the potential for ZIKV neuroinflammation.