Journal of Clinical and Cellular Immunology
Open Access
ISSN: 2155-9899
ISSN: 2155-9899
Segundo Mesa Castillo
Psychiatric Hospital of Havana, Cuba
Posters & Accepted Abstracts: J Clin Cell Immunol
The neurodevelopmental theory in the etiology of schizophrenia is considered one of the most consistent at present. Evidence from epidemiological and neuropathological studies indicates that the pathogenic process that culminates in the development of schizophrenia are initiated early in life and has been associated with a variety of prenatal environmental insults to the developing brain, including infection. Although the infectious agents have been proposed as one of the risk factors for schizophrenia the data on the association of a specific infectious agent with prenatal brain evidence is absent. Understanding of the structural abnormalities would allow a better identification of neurodevelopmental processes that contribute to risk for schizophrenia. We have hypothesized that at ultrahigh-risk fetuses would have alterations at the cellular level that would let us differentiate them from the comparison subjects. A reappraisal of our ultrastructural studies carried out in samples of the left temporal lobe of fetuses at ultra-high risk of developing schizophrenia is presented. The findings obtained are compatible with an active infection of the central nervous system by herpes simplex hominis type I [HSV1] virus. The present results are the first direct evidence that demonstrates the presence of this virus in the central nervous system of fetuses from schizophrenic mothers in the critical period of fetal development. The importance of this finding can have practical applications in the prevention of the illness keeping in mind its direct relation to the etiology and physiopathology of schizophrenia.
E-mail: segundo@infomed.sld.cu