Bornavirus immunopathogenesis in rodents: models for human neurological diseases

Briese, Thomas; Hornig, Mady; Lipkin, W. Ian

doi:10.3109/13550289909021289

Cited by 37 publications

(19 citation statements)

References 71 publications

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“…Nonetheless, given what is known about BDV pathogenesis with other strains in other hosts (11), the bornaviruses identifi ed in these birds must be considered a biologically plausible candidate causative agent. Infection, lymphocyte infi ltration, and dysfunction of the central, peripheral, and autonomic nervous system are common to PDD as well as to classical Borna disease in natural disease and experimental models (2,12,13). Proteins and antisera we have used for 2 decades for BDV diagnostics failed to detect this virus in our PCR-positive birds.…”

Section: Discussionmentioning

confidence: 87%

Novel Borna Virus in Psittacine Birds with Proventricular Dilatation Disease

Honkavuori¹,

Shivaprasad²,

Williams³

et al. 2008

Emerg. Infect. Dis.

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199

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Section: Discussionmentioning

confidence: 87%

Novel Borna Virus in Psittacine Birds with Proventricular Dilatation Disease

Honkavuori¹,

Shivaprasad²,

Williams³

et al. 2008

Emerg. Infect. Dis.

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207

199

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“…Natural and experimental infections with BDV usually result in immune-system-mediated neurological disease and behavioral abnormalities (5,13,14,34). Sequence comparisons between old and recent BDV isolates of diseased animals from regions of endemicity in Central Europe revealed viral genome conservation of greater than 95%, in spite of the fact that some of these viruses were passaged many times in experimental animals or in cell culture (3, 28).…”

mentioning

confidence: 99%

Sequence Variability of Borna Disease Virus: Resistance to Superinfection May Contribute to High Genome Stability in Persistently Infected Cells

Formella

Jehle

Sauder

et al. 2000

J Virol

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The RNA genome of Borna disease virus (BDV) shows extraordinary stability in persistently infected cell cultures. We performed bottleneck experiments in which virus populations from single infected cells were allowed to spread through cultures of uninfected cells and in which RNase protection assays were used to identify virus variants with mutations in a 535-nucleotide fragment of the M-G open reading frames. In one of the cell cultures, the major virus species (designated 2/1) was a variant with two point mutations in the G open reading frame. When fresh cells were infected with a low dose of a virus stock prepared from 2/1-containing cells, only a minority of the resulting persistently infected cultures contained detectable levels of the variant, whereas the others all seemed to contain wild-type virus. The BDV variant 2/1 remained stable in the various persistently infected cell cultures, indicating that the cells were resistant to superinfection by wild-type virus. Indeed, cells persistently infected with prototype BDV He/80 were also found to resist superinfection with strain V and vice versa. Our screen for mutations in the viral M and G genes of different rat-derived BDV virus stocks revealed that only one of four stocks believed to contain He/80 harbored virus with the original sequence. Two stocks mainly contained a novel virus variant with about 3% sequence divergence, whereas the fourth stock contained a mixture of both viruses. When the mixture was inoculated into the brains of newborn mice, the novel variant was preferentially amplified. These results provide evidence that the BDV genome is mutating more frequently than estimated from its invariant appearance in persistently infected cell cultures and that resistance to superinfection might strongly select against novel variants.Genome replication of RNA viruses is error prone, because RNA-dependent RNA polymerases lack proofreading activity (10, 18). Nevertheless, field isolates of certain RNA viruses exhibit a high degree of genetic stability over many decades (10). The selective forces which restrict virus variability are presumably complex and nonuniform. In most cases, the mechanisms of restriction are largely unknown.Borna disease virus (BDV) is a newly classified nonsegmented negative-strand RNA virus that can persistently infect the central nervous systems of a broad range of warm-blooded animals and possibly humans without destruction of its host cells (11,13,21,29). Natural and experimental infections with BDV usually result in immune-system-mediated neurological disease and behavioral abnormalities (5,13,14,34). Sequence comparisons between old and recent BDV isolates of diseased animals from regions of endemicity in Central Europe revealed viral genome conservation of greater than 95%, in spite of the fact that some of these viruses were passaged many times in experimental animals or in cell culture (3, 28). Recent evidence indicates that BDV strains from outside the classical regions of endemicity (e.g., Japan, Sweden, and the United S...

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“…Experimental infection of animals with BDV may result in symptoms such as aggression, hyperactivity and behavioural disturbances, apathy or motor symptoms that resemble the core features of human psychiatric disorders such as depression and schizophrenia. [70] 3.1. Unique features of BDV along with its incredible pathogenic flexibility and many evidences implicating its increasing strength of association definitely point towards its causative role in human BDV infections.…”

Section: Resultsmentioning

confidence: 99%

Role of Borna Disease Virus in Neuropsychiatric Illnesses: Are We Inching Closer?

Thakur

Sarma

Sharma

2009

Indian Journal of Medical Microbiology

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The biological cause of psychiatric illnesses continues to be under intense scrutiny. Among the various neurotropic viruses, Borna disease virus (BDV) is another virus that preferentially targets the neurons of the limbic system and has been shown to be associated with behavioural abnormalities. Presence of various BDV markers, including viral RNA, in patients with affective and mood disorders have triggered ongoing debate worldwide regarding its aetiopathogenic relationship. This article analyses its current state of knowledge and recent advances in diagnosis in order to prove or refute the association of BDV in causation of human neuropsychiatric disorders. This emerging viral causative association of behavioural disorders, which seems to be inching closer, has implication not only for a paradigm shift in the treatment and management of neuropsychiatric illnesses but also has an important impact on the public health systems.

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Bornavirus immunopathogenesis in rodents: models for human neurological diseases

Cited by 37 publications

References 71 publications

Novel Borna Virus in Psittacine Birds with Proventricular Dilatation Disease

Novel Borna Virus in Psittacine Birds with Proventricular Dilatation Disease

Sequence Variability of Borna Disease Virus: Resistance to Superinfection May Contribute to High Genome Stability in Persistently Infected Cells

Role of Borna Disease Virus in Neuropsychiatric Illnesses: Are We Inching Closer?

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