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This study examines the mechanisms by which ZIKV infects placental cells, including trophoblasts and Hofbauer macrophages, through the engagement of specific cellular receptors such as AXL and T\u2010cell immunoglobulin and mucin (TIM), while simultaneously evading host immune defenses. Although the placental immune system employs interferon signaling and innate immune cells to restrict viral replication, ZIKV disrupts these pathways, promoting chronic inflammation and structural damage within placental tissue. These morphofunctional alterations impair fetal nutrient exchange and facilitate vertical transmission, leading to severe adverse outcomes such as congenital Zika syndrome (CZS), intrauterine growth restriction, and preterm birth. Importantly, pregnancy outcomes appear to depend on a delicate balance between the timing of maternal infection and the effectiveness of the local immune response. 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