Abstract

Schizophrenia is a highly disabling chronic mental illness. It is considerded as a neurodeveloppemental illness resulting from the interaction of genetic and environmental factors. Growing evidence supports the major role of prenatal infections and inflammation in the genesis of schizophrenia. The hypothesis including viral infections has been the subject of several studies and the role of parvovirus B19 (PB19) in the onset of the disease has been suggested. However, there is, up till now, no seroepidemiological evidence of his involvement. To determine the prevalence of parvovirus B19 (PB19) in schizophrenic patients and in control subjects and to examine clinical associations between viral prevalence, risk factors of infectious disease and clinical features. We carried out a case-control seroepidemiological study in the Psychiatry department of Farhat-Hached general hospital of Sousse (Tunisia). We recruited108 schizophrenic patients and 108 healthy controls free from any psychotic disorder and matched for age and sex. We collected sociodemographic data, medical history, axis I comorbid disorders and infectious risk factors. We assessed patients for psychopathology and severity of illness using respectively the Brief Psychiatric Rating Scale (BPRS), the Scale for the Assessment of Positive Symptoms (SAPS), the Scale for the Assessment of Negative Symptoms (SANS), the Positive and Negative Syndrome Scale (PANSS) and the Clinical Global Impressions (CGI). For each study participant, blood sample was collected and levels of IgG and IgM anti-PB19 were measured using the ELISA technique. The prevalence of IgG antibodies to PB19 was significantly higher in schizophrenic patients than in controls (73.1% vs 60.2%; P=0.04). There were no statistical differences between the two groups regarding the prevalence of IgM antibodies to PB19. No association was found between viral prevalence and sociodemographic data, risk factors for infection or clinical characteristics. The presence of PB19 antibodies was associated with a lower score on the PANSS negative subscale (P=0.04). No other signficative association were found. In our study, prevalence of IgG antibodies to PB19 was significantly higher in schizophrenic patients than in controls. This finding supports the hypothesis of the involvement of PB19 in schizophrenia. Further studies including both virological and immunological aspects are needed to better clarify the etiopathogenic mechanisms of schizophrenia which would challenge the management of this disease.

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