This review discusses the emerging literature on the role of prenatal infection in the etiology of schizophrenia, highlighting epidemiologic, clinical, and preclinical studies. Early studies relied on ecological data, such as influenza epidemics, but these findings were often inconsistent and lacked confirmation of maternal infection during pregnancy. More recent studies have used biomarkers to document specific infections, such as influenza, *Toxoplasma gondii*, and herpes simplex virus type 2 (HSV-2), and have found associations with an elevated risk of schizophrenia. Preclinical studies in animal models have revealed behavioral, neurochemical, and neurophysiological abnormalities consistent with observations in schizophrenia. The authors discuss the potential mechanisms by which in utero exposure to infection contributes to schizophrenia risk, including unique and common effects. They also explore the implications of this research for prevention and public health practices, suggesting that reducing prenatal exposure to infections could potentially lower the incidence of schizophrenia. The review emphasizes the need for further research to identify specific microbial risk factors and to understand the critical windows of vulnerability during pregnancy.This review discusses the emerging literature on the role of prenatal infection in the etiology of schizophrenia, highlighting epidemiologic, clinical, and preclinical studies. Early studies relied on ecological data, such as influenza epidemics, but these findings were often inconsistent and lacked confirmation of maternal infection during pregnancy. More recent studies have used biomarkers to document specific infections, such as influenza, *Toxoplasma gondii*, and herpes simplex virus type 2 (HSV-2), and have found associations with an elevated risk of schizophrenia. Preclinical studies in animal models have revealed behavioral, neurochemical, and neurophysiological abnormalities consistent with observations in schizophrenia. The authors discuss the potential mechanisms by which in utero exposure to infection contributes to schizophrenia risk, including unique and common effects. They also explore the implications of this research for prevention and public health practices, suggesting that reducing prenatal exposure to infections could potentially lower the incidence of schizophrenia. The review emphasizes the need for further research to identify specific microbial risk factors and to understand the critical windows of vulnerability during pregnancy.