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News in Brief

Molecular Psychiatry volume 5, pages 9–10 (2000)Cite this article

Although largely based on circumstantial evidence, viral infection has been posited as a risk factor for neuropsychiatric diseases such as schizophrenia. Severe childhood viral infections, borna disease virus (BDV) and maternal influenza or polio infection during gestation have all been associated with increased risk of psychosis. Evidence for BDV serum antibodies in patients with neuropsychiatric illness has been conflicting, and the hypothesis that this virus causes brain alterations relevant to psychosis lacks mechanistic detail. Three recent papers provide some answers to this viral puzzle. Hornig et al1 have developed a model for the neurodevelopmental damage caused by BDV through infecting neonatal rats. They found marked neurological and behavioural changes, including abnormal righting reflexes, growth delay, hyperactivity, inhibition of open field exploration, and stereotypy. The hippocampus and cerebellum showed significant disruption, cell loss and molecular evidence of abnormal apoptosis and pro-inflammatory cytokine gene expression. Unlike a previous analysis of bornavirus infection in rats which found similar cytokine effects,2 there was no mortality and the animals did not manifest typical BDV disease. Hornig et al postulate that the behavioural changes they see in infected rats are like autism despite the lack of evidence for BDV infection in that disorder.

So is there a human brain BDV infection phenotype? In the November issue of the Journal of Infectious Diseases, Czygan et al3 studied postmortem brains for evidence of infection. They found no evidence for BDV in 86 brains from subjects who had neuropsychiatric disease in life, but confirmed viral infection in three brains of psychiatric patients with prominent hippocampal pathology. The most parsimonious interpretation of these data is that persistent bornavirus infection is very rare in humans and leads to a form of hippocampal neurodegeneration. However since a significant number of people with neuropsychiatric disorders appear to be bornavirus seropositive, it is still possible that transient subclinical brain infection might have a significant consequence. This hypothesis will take some proving. The use of new, sensitive assays for BDV infection in large populations with psychiatric illness may be the best way forward,4 but temporal relationships between BDV infection and neuropsychiatric disease will need to be established.

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  1. D A Collier PhD
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Collier, D. News in Brief. Mol Psychiatry 5, 9–10 (2000). https://doi.org/10.1038/sj.mp.4000715

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