To the Editor: We appreciate the comments of Dr. Vedeniapin, which call attention to the fact that it is unlikely that a prenatal infection alone can account for the fluctuations in the clinical state of schizophrenia over the long-term course of the illness.

He also introduces a mechanism for potential effects of infection in patients with schizophrenia: the small interfering RNA-induced silencing complex. Such a mechanism may not only account for changes in the expression of the illness over time but also introduces a target to be investigated for genetic polymorphisms that may interact with infectious exposures.

It should be acknowledged, however, that while such a mechanism might relate to an infectious process in the brain of a patient with schizophrenia, it probably would not explain the effect of most prenatal infectious exposures that have been associated with schizophrenia, since, as noted in our review article, most of these infections do not appear to infect the fetal brain.

Regardless, this could represent an important new lead in the discovery of pathogenic microbes that might predispose an individual to schizophrenia.