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Lynn E. DeLisi, MD
Clinical Neurogenetics Branch National Institute of Mental Health Bldg 10, Room 3N/220 Bethesda, MD 20205

Arch Gen Psychiatry. 1986;43(2):189-190.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

In the February 1985 ARCHIVES, Roos et al¹ attempted to refute the viral hypothesis of schizophrenia with results from a cerebrospinal fluid immunoglobulin study that failed to show elevations in immunoglobulin titers in schizophrenic and depressed patients compared with controls. In chronic persistent viral infections of the central nervous system (CNS), however, total immunoglobulin concentrations may not be elevated, but may be normal or even decreased.^2,3 Partial immunodeficiency may actually precede the infection, causing increased susceptibility to some viruses. What is more pertinent to the viral hypothesis is the increased titers of antibodies specific to certain viruses, such as has been reported with herpes class viruses in schizophrenia.^4,5 The lack of oligoclonal banding in the study by Roos et al¹ is the most notable finding they have reported that refutes the role of a viral infection in this disorder, since this would . . . [Full Text PDF of this Article]

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