By Bradley D. Pearce

The quest to find the etiology of schizophrenia has interested and pissed off researchers for greater than a century. in recent times, there was an accumulation of experimental and epidemiological proof assisting the position of viral infections in schizophrenia pathogenesis. This growing to be physique of proof has accrued to the purpose the place the mainstream clinical neighborhood can now not forget about it. Drawing on his study event in organic psychiatry and neurovirology, Dr. Pearce presents the 1st ebook committed solely to a serious appraisal of the viral speculation of schizophrenia.

This booklet is an enlightening and worthy source for psychiatrists, psychologists, neurobiologists, and their scholars. by way of integrating the most recent findings in virology and immunology with present innovations within the pathophysiology of the non-affective psychotic issues, this good illustrated quantity disentangles a number of the sub-theories of the viral speculation, and lays the foundation for extra targeted explorations of the mechanisms wherein viruses can cause severe psychological sickness.

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Chapter 2 34 Table 3 Essential requirements for viral persistence . I. Avoidance of immunological surveillance A. Removal of recognition molecules from surface of infected cells 1. Alteration of viral protein expression, antiviral antibody response inducing capping "and modulation of viral gene expression 2. Alteration of MHC expression a. Direct viral effect on MHC expression b. Modulation of MHC expression by virally-induced cytokine production c. , neurons) B. Infection of thymus prior to or during immune system development (central tolerance or hyporesponsiveness) establishing persistent infection C.

During this latent period, the virus is occult and cannot generally be detected unless highly sensitive PCR techniques are used. Such techniques obviously require considerable knowledge about the viral genome, and prior to their development it was debated as to whether the virus was present in the circulation at all. Thus, the lesson for the viral hypothesis of schizophrenia is that the absence of detectable virus does not imply the absence of a smoldering virus-induced disease process. ii) Even in cases when opportunistic infections are apparently not present, HIV infection of the brain can cause complex neurobehavioral syndromes such as AIDS dementia.

The lag between the development of psychotic symptoms and the neurological manifestations of encephalitis varied from days to several weeks. The ultimate clinical course ranged from death (5 patients) to complete recovery (8 patients); about one fourth of the surviving patients had residual psychiatric symptoms. Psychosis can also occur as a sequela to a viral infection that actually never enters the brain. In this disease, which is been referred to by various names such as 'post infectious encephalomyelitis" and "acute disseminated encephalomylelitis", the peripheral infection triggers an inflammatory process in the central nervous system.

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