A review of epidemiologic and translational studies on prenatal infection and schizophrenia reveals that gestational exposure to infection may contribute to the etiology of schizophrenia. Recent studies have moved from ecologic designs to investigations using reliable biomarkers in individual pregnancies, identifying specific infections, such as influenza, toxoplasmosis, and herpes simplex virus type 2 (HSV-2), that may increase schizophrenia risk. Animal models of maternal immune activation have shown behavioral, neurochemical, and neurophysiologic abnormalities consistent with schizophrenia. Human and animal studies are exploring the cellular and molecular mechanisms by which prenatal infection affects neurodevelopment and increases schizophrenia susceptibility. The review discusses epidemiologic evidence, including ecologic and birth cohort studies, and highlights the interaction between prenatal infection and genetic variants. It also addresses the implications for prevention and the need for new research approaches. The review emphasizes the potential of these findings to identify susceptibility loci in genetic studies and to inform public health strategies. The role of cytokines, such as interleukin-8 and tumor necrosis factor-alpha, in the pathogenesis of schizophrenia is also discussed. The review concludes that prenatal infection may play a significant role in the etiology of schizophrenia, and further research is needed to clarify the mechanisms and develop effective prevention strategies.A review of epidemiologic and translational studies on prenatal infection and schizophrenia reveals that gestational exposure to infection may contribute to the etiology of schizophrenia. Recent studies have moved from ecologic designs to investigations using reliable biomarkers in individual pregnancies, identifying specific infections, such as influenza, toxoplasmosis, and herpes simplex virus type 2 (HSV-2), that may increase schizophrenia risk. Animal models of maternal immune activation have shown behavioral, neurochemical, and neurophysiologic abnormalities consistent with schizophrenia. Human and animal studies are exploring the cellular and molecular mechanisms by which prenatal infection affects neurodevelopment and increases schizophrenia susceptibility. The review discusses epidemiologic evidence, including ecologic and birth cohort studies, and highlights the interaction between prenatal infection and genetic variants. It also addresses the implications for prevention and the need for new research approaches. The review emphasizes the potential of these findings to identify susceptibility loci in genetic studies and to inform public health strategies. The role of cytokines, such as interleukin-8 and tumor necrosis factor-alpha, in the pathogenesis of schizophrenia is also discussed. The review concludes that prenatal infection may play a significant role in the etiology of schizophrenia, and further research is needed to clarify the mechanisms and develop effective prevention strategies.