RETROVIRUS REACTIVITY OF PERINATAL SERA FROM MOTHERS WHOSE CHILDRENDEVELOPED SCHIZOPHRENIA

human endogenous retroviruses may contribute to the etiology of some cases of

schizophrenia (Yolken et al., Brain Res. Rev. 31, 193-199, 2000).  To

further characterize the relationship between retroviruses and schizophrenia, we

have undertaken a systematic analysis of retrovirus exposure, as assessed by

virus reactive serum antibodies, in various populations of patients with

schizophrenia or matched controls.  We showed previously by ELISA and

Western blot analyses that antibodies against non-human primate retroviruses,

predominately directed against gag encoded proteins, were present at

significantly greater frequencies in patients with acute onset schizophrenia

compared with unaffected controls (Lillehoj, et. al., J. Neurovirol. 6, 492-497,

2000). The antigenic determinants reacting with these antibodies presumably

originated from regions of gag genes conserved between monkey and human

retroviruses.  While our initial study lended support to the hypothesis

that replication of a human retrovirus in patients with schizophrenia may

explain some of the clinical and epidemiological features of this disease, we

examined a relatively small group of patients (n=38) selected from a clinical

population at the University of Heidelberg, Germany. In this follow-up study, we

extended our initial observations by analysis of the larger, more diverse

patient population: (1) a panel of sera from Chinese schizophrenia patients and

matched controls (N=40), (2) a set of matched sera from monozgotic twins

discordant for schizophrenia (N=50), and (3) a collection of perinatal sera from

mothers whose children subsequently were followed for development of

schizophrenia (N=86).  Of these 3 populations, the perinatal sera gave the

most interesting results. By MPMV ELISA, all control samples (N=41) had OD450