Borna-be-wild: Recent Findings
1. Brain potential amplitude varies as a function of Borna
disease virus-specific immune complexes in
A recent pilot study examined event related potentials in the brain of
obsessive compulsive disorder patients and control subjects. The
results imply a relationship between borna-disease virus activity (as
represented by borna disease virus immune complexes) and attention
deficits. This study suggests that the hyperactivity of brainwaves in
the secondary visual areas and anterior cingulate gyrus are modulated
by borna disease virus infection. The neurological mechanism for this
association is thought to be a result of direct interactions of the
borna disease virus with inhibitory neurotransmitters in the brain.
Dietrich, et al. "Brain potential amplitude varies as a function of
Borna disease virus-specific immune complexes in obsessive-compulsive
disorder." Molecular Psychiatry (2005) 10, 515.
2. What is the exact mechanism for
That is, how is bornavirus bornagain?
Genome trimming: A unique strategy for replication
control employed by Borna disease virus.
Although the exact means of Bornavirus replication are still unknown,
scientists are making great advances to uncover just how bornavirus
replication produces bornavirus virions that are born-again and again
and again. A recent article by Schneider et al. suggests that Borna
disease virus uses a unique mechanism of genome trimming to control
replication. The researchers suggest that this means of replication is
what allows for noncytolytic virus persistence in neurons and
astrocytes. This mechanism of active genome trimming at the 5' termini
involves deletion of the viral genome, which limits viral gene
expression. However, scientists propose that this replication mechanism
is beneficial to the virus because it allows for persistence without
inducing cytolytic effects.
Schneider, et al. "Genome trimming: A unique strategy for replication
control employed by Borna disease virus." PNAS. March 1, 2005. Vol 102.
No 9. 3441-3446.
Rosario, et al. "Functional Characterization of the Genomic Promoter of
Borna Disease Virus (BDV): Implications of 3'-Terminal Sequence
Heterogeneity for BDV Peristence." Journal of Virology, May 2005, p.
6544-6550, Vol 79, No. 10.
3. Born to Persist: Recent updates on
Borna disease virus persistence
The negative regulator of Borna disease virus polymerase is a
Further research regarding the mechanisms by which borna disease virus
successively persists in hosts provides evidence for negative
regulation of viral polymerase by viral protein X. Schwardt, et al.
suggest that viral protein X is only incorporated into viral particles
in late infection, allowing for sufficient viral replication early in
the course of infection. Schwardt et al.'s results suggest that X is a
non-structural protein that is present in persistently infected cells
and may allow for viral persistence through inhibitory interactions
with the viral polymerase. Their conclusions were based on finding that
viral protein X is absent from viral particles, but present in purified
borna disease virus stock.
Schwardt, et al. "The negative regulator of Borna disease virus
polymerase is a non-structural protein." J Gen Virol 86 (2005):
Schneider, U. (2005). "Novel insights into the regulation of the viral
polymerase complex of neurotropic Borna disease virus." Virus Res
4. Borna-pathology: Potential
mechanisms for pathogenesis
The neuropathological mechanism for borna disease virus is the current
topic of debate. A recent article involved examination of
virion-infected neurons of the hippocampus in mice. Hans, et
research provided more evidence for noncytolytic persistent infection
of borna disease virus. Moreover, Hans et al. showed that borna disease
virus infection blocked the BDNF-induced ERK 1/2 phosphorylation and
disrupted BDNF-induced expression of synaptic vesicle proteins. Borna
disease virus infection was thus shown to impair synaptogenesis and
damage neuronal connectivity through hampering neurotrophin-regulated
neuroplasticity. The results of Hans et al. suggest a possible
mechanism for the association between borna disease virus infection and
Hans A, Bajramovic JJ, Syan S, Perret E, Dunia I, Brahic M,
Persistent, noncytolytic infection of neurons by Borna disease virus
interferes with ERK 1/2 signaling and abrogates BDNF-induced
synaptogenesis. FASEB J. 2004 May;18(7):863-5.
Does Borna Nurture Nature?
"Neuron-glia interactions clarify genetic-environmental links in mental
Further research on genetically engineered mice suggests a role for
glial infected with borna disease virus in the neuropathogenesis of
psychiatric disorders. However, this research is in mice., and its
relevance to humans remains to be determined.
Sawa A, Pletnikov MV, Kamiya A "Neuron-glia interactions clarify
genetic-environmental links in mental
illness." Trends Neurosci. 2004 Jun;27(6):294-7.
5. Borna-sanity: More evidence
supporting a role for Borna disease virus in human behavioral disorders
For years, scientists have examined the potential role of borna disease
virus infection in human neurological and psychiatric illnesses.
However, the association between morbidity and borna disease virus
seroprevalence remains a topic of debate.
A recent cross-sectional retrospective cohort experiment was conducted
in UK farming communities to determine the epidemiological significance
of Borna Disease virus. Through analyzing the seroprevalence of borna
disease virus in farm communities (that contained borna disease virus
infected horses and sheeps), Thomas et al. found that the
seroprevalence of borna disease virus infection in these farm
communities was not statistically significant in comparison with farm
communities that did not have animals infected with borna disease
virus. Furthermore, no significant correlation was found in these
cohorts between borna disease virus seroprevalence and psychiatric
However, although there is evidence that does not support a significant
role for Borna Disease virus and human psychiatric disorders, a recent
systemic review indicates that there is enough evidence that humans are
exposed to the virus to substantiate further investigations on whether
or not it plays a role in behavioral disorders. Chalmers, et
review found 75 papers published before Janurary 2000 regarding 44
different cases of the seroprevalence of borna disease virus in humans,
of which five were case studies. Overall, they found that
seroprevalence of the virus ranged from 0-48%, which is to broad a
range for analysis using standard statistical methods. Chalmers et al
concluded that further epidemiological research is necessary to
determine the significance of borna disease virus in human populations.
Chalmers, R. M., D. R. Thomas, et al. (2005). "Borna disease
virus and the evidence for human pathogenicity: a systematic review."
Qjm 98(4): 255-74.