Viral Infection

Numerous studies have shown that in utero exposure to viruses during the second trimester of gestation is associated with increased risk of developing schizophrenia (O'Reilly, 1994). Precisely which virus(es) may be risk factors is unknown since it is impossible to do antibody titers from a gestational exposure that occurred 20 or 30 years before. Studies that have examined the incidence of schizophrenia following influenza epidemics of 1954, 1957, and 1959 in Australia and Japan have revealed positive associations between gestational exposure to this virus and development of schizophrenia. Reports of viral diseases from 1920 to 1955 in Connecticut and Massachusetts found associations between the development of schizophrenia and gestational exposure to the measles, varicella-zoster, and polio viruses (Torrey et al., 1988). Studies have also found that individuals exposed to rubella in utero, during the 1964 rubella epidemic, had a substantially greater risk of developing nonaffective psychosis than nonexposed subjects (Brown et al., 2000).

There are several other risk factors for schizophrenia that may also be related to viral infections. For instance, there is an increased prevalence of schizophrenia among individuals born in late winter-early spring. Many viral infections peak at certain times of the year, and it is likely, as in the case of other seasonal diseases such as anencephaly and mental retardation, that this can explain the seasonality of schizophrenia. Being born or raised in an urban area also increases one's chance of developing schizophrenia, which may be explained by greater exposure to infectious agents in densely populated areas (Lobato et al., 2001).

Recently, endogenous retroviruses have also been suggested as a possible etio-logical factor in schizophrenia. Retrovirus can infect brain cells, integrate into their cellular deoxyribonucleic acid (DNA), and cause long-term alterations in brain function. Possible transcripts of these viruses have been found in higher levels in the brains of schizophrenia patients than unaffected individuals (Yolken et al., 2000).

Understanding the causes of schizophrenia is made more difficult by several factors: our relative lack of knowledge about how the abnormal genes and environmental factors function in brain development; the likelihood that schizophrenia is more than one disease—that is, more than one underlying biological abnormality may cause similar symptoms; the fact that studies of genes and studies of environmental factors are rarely done in the same people; and the evidence that what is inherited is not just schizophrenia but a range of behavioral, physical, and cognitive abnormalities (the schizophrenia spectrum). There may be more than one "causal pathway" to schizophrenia, that is, different people may have the disorder due to different causes. Because the causes of schizophrenia are poorly understood, it remains possible that all of the following causal pathways lead to schizophrenia:

1. Everyone who has both genes A and B will have a schizophrenia spectrum disorder.

2. People with gene A have a schizophrenia spectrum disorder only if their mothers have a severe stress at a critical period during pregnancy.

3. If a mother has a sufficiently severe stress at the right time during gestation, anyone will have a schizophrenia spectrum disorder.

Other possibilities exist, and it is possible that each particular form of schizophrenia may have one or more of these causal pathways.

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