In conclusion, these publications add to a body of literature suggesting that environmental exposures may play a more important role in the etiopathogenesis of schizophrenia than has been previously assumed. In addition to infection, environmental insults that have been implicated include nutritional deficiencies, fetal hypoxia, maternal stress, cannabis use, and childhood trauma (9). The promise of this work is underscored by the fact that many infectious exposures and other environmental insults are treatable and preventable. For example, several proven hygienic measures exist to prevent exposure to T. gondii, such as avoidance of undercooked meat, access to safe drinking water, and reducing contamination of cat litter boxes with oocysts. With regard to HSV1, however, there are no known preventive strategies and while antiviral medications such as acyclovir can reduce healing time, it does not prevent the immune response to this microbe (10), nor, as discussed by Prasad et al. (4), does it slow cingulate cortex neuronal loss in animal studies. Further prospective epidemiologic and clinical neuroscience studies are necessary to substantiate these findings, complemented by animal models on candidate pathogenic mechanisms.