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Zika virus (ZIKV) is a member of the Flavivirus family. ZIKV infection ranges from asymptomatic to a mild disease in adults. However, in 2015, ZIKV infection became a public health emergency in the Americas associated with neurological alterations such as Guillain-Barré syndrome (GBS) in adults and congenital zika syndrome (CZS). By blocking type I IFN interferon signaling pathways, ZIKV evades the immune system and infects cells expressing the T cell immunoglobulin mucin domain-1 (TIM-1) and TAM (Tyro3, AXL, and Mer) receptors, such as neural progenitor cells. Moreover, ZIKV seems to orchestrate a process of astrocytic hypoxia that leads to the production of reactive oxygen species (ROS), mitochondrial DNA (mtDNA) fragmentation, and apoptosis. In recent decades, the active participation of mitochondria in the immuno-inflammatory response has been reported in several pathologies. In this context, mtDNA seems to have an essential role in triggering the innate immune response by activating inflammasomes, activating the cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING) pathway, and also activating toll-like receptors that lead to IFN production and viral clearance. Here, we present an overview of some mechanisms of inflammatory response present in ZIKV infection, which contributes to mitochondrial dysfunction, mtDNA release, and tissue damage.