Borna disease virus antibodies and the deficit syndrome of schizophrenia

@article{Waltrip1997BornaDV,
  title={Borna disease virus antibodies and the deficit syndrome of schizophrenia},
  author={Royce W. Waltrip and Robert Williams Buchanan and William T. Carpenter and Brian Kirkpatrick and Ann Summerfelt and Alan Breier and Steven A. Rubin and Kathryn M. Carbone},
  journal={Schizophrenia Research},
  year={1997},
  volume={23},
  pages={253-257}
}
Borna disease virus and deficit schizophrenia
TLDR
BDV transcripts were not detected in samples from any of the 62 schizophrenic patients and these data do not support an etiologic association between BDV infection and the deficit form of schizophrenia.
Borna disease virus and psychiatry
High seroprevalence of Borna virus infection in schizophrenic patients, family members and mental health workers in Taiwan
TLDR
It is demonstrated that Chinese schizophrenic patients from Taiwan also have a higher seroprevalence of BDV-specific antibodies than controls than controls, providing support to the positive association between bdv and psychiatric disorders in this population.
Cerebrospinal fluid filtration in a case of schizophrenia related to “subclinical” Borna disease virus encephalitis
TLDR
This work hypothesized a therapeutic effect of cerebrospinal fluid fiitration (CSFF) in such case comparable to that in therapy resistant postinfectious Guillain-Barre syndrome (GBS).
Detection of Borna Disease Virus-Reactive Antibodies from Patients with Psychiatric Disorders and from Horses by Electrochemiluminescence Immunoassay
TLDR
A new electrochemiluminescence immunoassay for the antibody to BDV that uses two recombinant proteins of BDV, p40 and p24 (full length) was developed and concluded that BDV infection was associated in some way with psychiatric disorders.
Deficit schizophrenia: association with serum antibodies to cytomegalovirus.
TLDR
The association between deficit schizophrenia and cytomegalovirus antibody seropositivity provides further evidence for differences in etiopathophysiology between deficit and nondeficit schizophrenia.
Multi-factorial Etiology of Bipolar Disorder and Schizophrenia in Iran: No Evidence of Borna Disease Virus Genome
TLDR
Investigation of the prevalence of Borna disease virus among patients with schizophrenia and bipolar disorder indicated no evidence of BDV genome, and contact with cats is significantly more prevalent among Patients with mental illnesses, which might be due to infection with cats.
Borna disease virus and infection in humans.
TLDR
Serological and molecular data support the possibility of human infection with Borna disease virus and support the absence of a link between BDV infection and psychiatric disorders as well as excluding it as a human pathogen.
Encephalitis and Schizophrenia
TLDR
i) the established ability of viruses to cause psychosis; and ii) the burgeoning and controversial literature on Borna disease virus.
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References

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Borna disease virus and schizophrenia
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TLDR
First data on different viral genomic transcripts in such patients' cells as well as sequence data of transcripts are presented, pointing to a new human virus infection possibly threatening mental health.
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TLDR
This is the first demonstration that BDV can infect human brain tissue, possibly contributing to the pathophysiology of specific human neuropsychiatric disorders.
Tardive dyskinetic syndrome in rats infected with Borna disease virus
TLDR
A hyperkinetic movement disorder in rats experimentally infected with a neurotropic RNA virus, Borna disease virus, is observed that may provide important insights into the pathophysiology of TD.
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Borna virus replicated persistently in the brains of rats, causing frenzied and apathetic behavioral states in sequence but no mortality. The transient frenzied behavior was caused by an
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TLDR
Isolation of BDV from patients with major mood disorders at a time of acute depression strengthens the possibility that BDV infection is one of the environmental factors that contributes to recurrent depressive illnesses in man.
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TLDR
Findings support the utility of deficit symptoms for defining a more homogeneous subgroup of schizophrenia.
A neural substrate of hyperactivity in borna disease: changes in brain dopamine receptors.
Rats experimentally infected with the neurotropic RNA virus, Borna disease virus, have a hyperactive movement disorder. Because locomotor activity is modulated by the nucleus accumbens (N. Acc.)
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