Borna Disease Virus (BDV) - Root of BiPolar?

Scientists are increasingly coming to recognize that bacteria and viruses that cause sore throats and other minor ailments may also unleash a host of mental and emotional illnesses, including anorexia, schizophrenia, obsessive-compulsive disorder and BIPOLAR AFFECTIVE. (66)

Borna disease virus (BDV) is a neurotropic, and virus that persistently infects various domestic animal species. Infection causes disturbances in behavior and cognitive functions, but can also lead to a fatal neurologic disease. Human infections seemed likely, since serum antibodies were detected in neuropsychiatry patients. Further proof came from our discovery that peripheral blood monocytes carry viral antigens. Viral markers seem to coincide with acute episodes of mood disorders, thus pointing to a new human virus infection possibly threatening mental health.(94.1)

Evidence suggests an association of BDV, or a related virus, with specific psychiatric diseases in humans. In an examination of a total of 60 patients from 5 wards of a hospital in Japan, the detection rate differed within each ward, ranging from 8% to > 50% (37% on the average). Of particular note was the finding that the human derived BDV sequences, which included deleted forms in about 23% of the positive samples, were slightly different from those derived from horse BDV. The detection of a high level of BDV in the PBMC of patients might help our understanding of the pathogenesis in the disease. (94.2)

Borna Disease virus (BDV) can persistently infect the central nervous system of a broad spectrum of animal species. The clinical course varies from slight behavioral disturbances to a fatal neurological syndrome. We presented the first data of a current follow-up study on 70 psychiatric patients who were tested three times each after hospitalization. In contrast to previously found low prevalence of antibody carriers by screening (2-4%), w now found 20% positives by follow-up testing. In randomly selected patients with different psychiatric diagnosis, the highest proportion of antibody carriers was detected among patients with major depression (more than 30%), compared to only 8% among patients with Dysthymia (neurotic depression). This led us to hypothesize that Bornavirus infection might contribute to some depressive illness. (94.3).

Borna virus is found naturally in many mammals and marsupials. Known to cause a wide array of neurological manifestations, many of which are fatal. Most animals exhibit no symptoms of disease and become carriers. Those that do develop symptoms first exhibit hyper-thermia (fever), anorexia, colic, and constipation. As the illness progresses, animals develop neurologic symptoms These illnesses last 1-3 weeks with an 80-100% death rate. Survivors often have periodic recurrences. Experimental infection of susceptible species including chickens and rodents, show they may become carriers, with no clinical symptoms.

It is believed that BDV gains entry into the CNS via neuroaaxonal migration through olfactory nerves or through intestinal nerve endings in the oralpharyngeal and intestinal regions (although I feel this is less likely as the virus is of enveloped genomic structure). Similar to the rabies virus it spreads throughout the CNS by intraaxonal transport and centrifugation into peripheral nerves. This could also explain why, like rabies, the mode of transmission is via saliva, nasal, and optical secretions (as seen in rabies cases borne through corneal transplant). Strangely, immuno-compromized animals do not appear to develop BDV encephalopathy, as do immuno-competent animals, leading to a hypothesis of a virus-induced cell- mediated immuno-pathology.

Attempts at immunization via inactivated virus preparations therefore failed to produce a protective immunity despite detectable levels of BDV specific antibodies. In fact, immunized animals developed the infection faster than the non-immunized controls. It would appear to me that these results indicate the possibility of the viral usage of antibodies as a masking mechanism to gain access to monocytes and the brain. Further study is necessary in order to determine the nature of this phenomenon.

When BDV was identified in one study 4% of 285 psychiatric patients had been infected with BDV, whereas none of the healthy controls was Borna-positive. Another study showed as many as 15 percent of psychiatric patients to be infected with Borna, while no more than 2 percent of people in the normal population were infected. A United States clinician, Ian Lipkin found 9 of 17 schizophrenics and 2 of 5 BIPOLAR AFFECTIVE patients to be Borna positive while none of his healthy controls were positive for it. At present, studies continue in an effort to determine the best treatment for potential BDV induced psychiatric cases, and possibly even a vaccine to protect the population. At present there is no cure for BDV, although amantadine can bring it into remission, relapses are likely.(98.1)

Some similarities between particular animal models of BDV infection and schizophrenia have been reported. The subtle signs of disease caused by infection in neonatal rats (e.g., learning deficiencies, hyperactivity with CNS abnormalities including cerebellar disorganization and loss of certain types of cells are consistent with a longstanding hypothesis that schizophrenia reflects an early brain insult (e.g., infection) resulting in abnormal brain development and prompted investigation of the role of BDV infection in the pathogenesis of schizophrenia (55.1).

Borna disease virus (BDV) has been associated with severe psychiatric disorders. The association is mainly based on the findings that patients with schizophrenia and depression have a higher seroprevalence rate of BDV-specific antibodies than controls. ), providing support to the positive association between BDV and psychiatric disorders in our population. Because of the contagious nature of viral infection, we further examined patients’ family members and mental health workers, who have close contact with patients. We found that both groups also have a higher seroprevalence of BDV-specific antibodies, 12.1% and 9.8%, respectively, than controls. This finding provides some evidence for a possible human-to-human transmission of Borna disease virus. Our finding needs further independent verification (65.2)

Currently medical science is discovering many formerly alleged ‘non infectious’ diseases, such as ulcers, heart disease certain cancers and now BPADand schizophrenia, and others may have a causative factor of pathogens, Although the rate of transmission is low, many of these diseases tend to run in families or among close contacts. Could these also be, at least in part, transmitted from person to person? Is it contagious? Can a vaccine against it be developed. Many researchers are currently looking into these possibilities. One route being investigated is the use of an anti Parkinson’s disease. It also goes without saying that any pathogen may , due to fever or direct influence, cause irreversible damage to brain cells or nerve complexes in the brain and elsewhere. (2)

Bode’s and a German team’s most recent discovery was serendipitous. The researchers had given a 67-year-old Parkinson’s victim amantadine sulfate, a standard drug against the disease. The woman also had been diagnosed with bipolar depression and was infected with Borna virus. To the researchers’ delight, the drug purged both the virus and symptoms of depression; the patient has been free of depression for 10 months. In a second case, a 30-year-old woman prone to bipolar depression since age 13 reported a dramatic improvement in her mood 9 days after starting an amantadine sulfate regimen. Within 2 weeks, all traces of Borna viral protein and DNA had disappeared from her blood. (35.1)

All Sources for this article can be found at: http://www.lorenbennett.org/sources.htm#6


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