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Integrated viral genes as potential pathogens in the functional psychoses
1Division of Psychiatry, Clinical Research Centre, Harrow, Middlesex, U.K.
Journal of Psychiatric Research
|January 1, 1987
Summary
The retrovirus-transposon hypothesis suggests psychosis arises from pathogenic genetic sequences (virogenes). These sequences can be inherited or acquired, potentially explaining the spectrum of psychotic disorders.
Area of Science:
- Neuroscience
- Genetics
- Psychiatry
Background:
- The retrovirus-transposon hypothesis proposes that psychosis results from pathogenic genetic sequences (virogenes).
- These virogenes may be inherited or acquired through genetic rearrangements like transposition or tandem repeat generation.
- Psychotic disorders are viewed as a continuum from unipolar to schizophrenia, with severity correlating to genetic rearrangements.
Purpose of the Study:
- To explore the retrovirus-transposon hypothesis of psychosis.
- To elucidate the genetic mechanisms underlying the spectrum of psychotic disorders.
- To investigate the role of genetic rearrangements in the development of psychosis.
Main Methods:
- Theoretical review of the retrovirus-transposon hypothesis.
- Analysis of genetic mechanisms potentially involved in psychosis.
- Examination of the proposed link between genetic rearrangements and the psychosis continuum.
Main Results:
- Psychosis is hypothesized to originate from pathogenic sequences (virogenes) within the genome.
- Genetic rearrangements, such as transposition, are proposed mechanisms for acquiring or activating these virogenes.
- The severity of psychosis may correlate with the extent of these genetic alterations.
- The genetic locus involved is suggested to relate to cerebral lateralization genes.
Conclusions:
- The retrovirus-transposon hypothesis offers a framework for understanding psychosis as a genetic disorder.
- Genetic rearrangements and their interaction with specific genomic loci may drive the spectrum of psychotic disorders.
- Potential growth-enhancing effects of pathogen-gene interactions might explain the evolutionary persistence of these genetic "hot-spots".