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BORNA VIRUS
By Sean Henahan, Access Excellence
BERLIN (3/26/95)
Do domestic animals transmit a virus to humans that
causes psychiatric disorders? An increasing body of research
suggests this may indeed be the case.
The suspect virus, Borna disease virus (BDV), was first
described a century ago. Named after the region in eastern
Germany where it was first described, the virus can cause a fatal
encephalitis in horses, cattle and sheep. BDV is a
single-stranded RNA virus that established a persistent infection
without directly damaging host cells.
Borna disease can also cause neurological symptoms in
domestic animals, which is where it gets its nickname, 'crazy
virus'. The neurological symptoms resemble those seen in humans
with manic depression. (N.B. this is entirely separate from
'madcow disease'.)
It was these neurological symptoms that led researchers to
study BDV more closely. Early research indicated that the virus
has a tropism for a specific group of neurons in the limbic
system, the part of the brain associated with moods and emotions.
This in turn led to attempts to isolate the virus from humans
with various psychiatric disorders.
About ten years ago, researchers did studies in a population
of patients with schizophrenia and other psychiatric disorders
and found higher levels of BDV antibodies in the blood of
patients compared with controls. In that study, 20% of 70
psychiatric patients showed the presence of BDV antibodies. The
highest percentage, 30%, was seen among patients with major
depression, while the lowest rate, eight percent, was seen in
patients with neurotic depression, a less severe disorder. BDV
antibodies have been isolated in about two percent of normal
populations.
Next, a German team used fluorescence activated cell sorting
analysis of peripheral blood monocyctes to isolate BDV
antigen-containing monocytes in patients during acute episodes of
disease. Interestingly, these patients had no detectable anti-BDV
antibodies.
In their most recent study, the same researchers report
isolating BDV genetic material in patients with depression and
panic disorders. The patients were drawn from a study group of
139 patients with acute or chronic psychiatric disease. The team
isolated peripheral blood monocytes from two patients with
chronic psychiatric disease (obsessive-compulsive disorder,
organic mood disorder) and four with acute illness (major
depression, panic disorder) and then looked for BDV antigen
positivity and BDV DNA sequences.
The two chronic patients appeared to express viral activity
continuously on repeated testing over a seven month period. The
findings in the acute cases were less consistent. In two of the
patients, the presence of the viral markers coincided with
symptomatic episodes. The two other patients with acute disease
did not show viral activity at first, but some weeks later BDV
antigen was isolated . As viral activity declined, so too did the
patients' symptoms.
"The presence of viral markers seems to coincide with acute
disease episodes and to disappear during the patients' recovery
or at least during decreases in symptoms. In contrast, a more or
less continuous level of viral activity is seen in chronically
infected patients," said Dr. Liv Bode, Koch Institute, Berlin,
Germany.
The researchers hypothesize that BDV infection may
contribute to depressive illness by altering neuronal cells in
the limbic system. The leading hypothesis is that BDV, as it
inserts itself into neurons, may compromise the function of those
cells by binding to neurotransmitter receptors.
"This is the first definite proof of human infection with
the animal virus or a related human BDV strain. Although
definitive proof of active virus in these patients must await
isolation of the virus, the demonstration of BDV DNA is exciting
and important evidence supporting the ability of BDV to give rise
to human neuropsychiatric disease," said Dr. Bode.
The cause of most of the common psychiatric disorders,
including depression, manic depression, anxiety and
schizophrenia, remains a mystery. In some cases, symptoms appear
suddenly and follows a catastrophic course, while in other cases
the disease may be intermittent. Despite a large amount of
research, and a lot of familial association evidence, the search
for causative genes has produced mixed results. This has helped
fuel the search for other factors, such as viral infection.
One group of investigators at the National Institute of
Mental Health is pursuing the hypothesis that schizophrenia
might be caused by pestiviruses transmitted from household pets
to pregnant women or young children. Another group of researchers
at the University of Southern California is looking for a link
between chronic fatigue syndrome and 'stealth viruses', i.e.
viruses that have been incorporated into the host DNA and are no
longer recognized by the immune system. These viruses cannot be
detected by standard immunological methods or standard culture
techniques. However, they can be detected with PCR based
techniques, matching DNA sequences with known viral DNA.
Dr. Bode's research appeared in Nature Medicine, V.1, No.3,
3/95.
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