Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Borna Disease”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1977

The cerebrospinal fluid of rabbits infected with Borna disease virus.

Rabbits were inoculated intracerebrally with Borna disease virus infected brain suspension or tissue culture extracts. In 30 per cent of the diseased animals infectious virus was present in the cerebrospinal fluid (CSF). The CSF had increased numbers of lymphocytes and an elevation of the protein concentration, mainly due to an increase in gamma-globulins, was measured. The gamma-globulins were of oligoclonal character and reacted with a borna disease virus specific antigen of infected brains or tissue culture cells. The antibody titers in the CSF were of similar level to those in the serum. In comparison, those of the CSF of naturally infected horses always exceeded the serum titers. Injection of tracer substances revealed that no drastic damage to the blood-brain barrier was caused during the disease. The results suggest that antibodies detected in the CSF are locally produced. The significance of these findings for the pathogenesis of Borna disease is discussed.

Albumins↗
PubMed1978

Behavior alterations in tree shrews (Tupaia glis, Diard 1820) induced by Borna disease virus.

Intracerebral injection of Borna disease virus in tree shrews led to a persistent infection that sometimes resulted in clinical symptoms and/or specific alterations in the animals' behavior. Whereas infective virus in the brain and in the serum antibodies were always present after infection, only some of the animals showed signs of clinical disease and behavior changes. Animals kept in pairs showed especially obvious behavior alterations expressed as an exaggeration of all the components of normal social behavior. The division of the roles between males and females was seriously disturbed. The breeding behavior of females was especially impaired, although no stress factors were given and the animals were obviously in good physical condition. Some females that were maintained solitarily showed considerably exaggerated spontaneous locomotor activities (hyperactivity) 4 weeks after infection, followed by a phase of clinical neurologic symptoms (decline phase), spatial and temporal disorientation, and alterations in comfort behavior. Following a slow recovery the animals remained unusually docile and were much less timid than before infection. A recurrence of the clinical illness is possible, as shown by the occurrence of a second decline phase. All the behavior alterations can be interpreted as a disturbance in the balance of approach and avoidance. In paired animals this imbalance results in interference with normal sociosexual behavior. These alterations indicate that BD preferentially involves the limbic system, an interpretation supported by the results of neuropathologic investigations.

Animals↗
PubMed1979

Spread of infectious virus along the optic nerve into the retina in Borna disease virus-infected rabbits.

Selective damage of the optic nerve of 14 rabbits without interfering with the choroidal blood flow which supplies the retina and without altering the autonomic nerve supply was successfully achieved by Xenon coagulation. This procedure interrupted the axonal pathway between the brain and the eye. After experimental infection with Borna disease virus the typical disease could be induced. The pathognomonic retinopathy as well as characteristic perivascular choroidal infiltrates, however, did not appear in eyes with coagulated nerve heads. In general virus-specific antigen or infectious virus were not present in the retinas of such damaged eyes. These results permit the conclusion that the ocular expression of Borna disease is a consequence of virus transport via the optic nerve.

Animals↗
PubMed1979

Multifocal retinopathy in Borna disease virus infected rabbits.

Experimental infection of rabbits with Borna disease virus led in all cases to a multifocal retinopathy that paralleled the clinical neurologic symptoms. The retinal changes always became evident first in the lower anterior quadrant of the eye. Infectious virus and antigen were detected in altered and unaltered regions of the retina. Individual chorioretinal lesions showed destruction of the pigment epithelium and the photoreceptors and perivascular inflammation close to small choroidal veins. Because of maximal antigen accumulation and the focal destruction of the retinal pigment epithelium we consider this cell layer to be the initially damaged structure.

Animals↗
PubMed1977

Demonstration of specific antibodies in the central nervous system of horses naturally infected with Borna disease virus.

From 18 horses with clinical symptoms of an affection of the central nervous system and with histopathologic alterations in the brain, four were demonstrated to have Bornavirus-specific antibodies. The antibodies are monospecific, recognizing identical antigens from infected brains of different animal species as well as from persistently infected tissue culture cells. Discrete immunoglobulin species (oligoclonal IgG) can be demonstrated in concentrated horse cerebrospinal fluid; they carry Bornavirus antibody specificity. Their presence, together with the higher antibody titers in the cerebrospinal fluid as compared to those in the serum, indicate that in these natural Bornavirus infections local antibody production occurred in the central nervous system.

Animals↗
PubMed1975

[Demonstration of antigen and production of interferon in rabbits infected with borna virus (author's transl)].

Examinations were carried out on the occurrence of active virus, antigen and antibodies in the brain blood, or resp. of rabbits which were infected intracerebrally with the virus of Borna disease as a model of slow viruses. The techniques of the complement fixation and the immunofluorescence were used. Furthermore, an attempt was made to demonstrate interferon in the blood serum of the infected rabbits. Virulent Boran virus was observed two days after the infection and complement fixing antigen from the 10th day on. The immunofluorescence technique gave positive results in the nucleus of ganglion cells eight days after infection. The production of interferon in the sera could not be demonstrated. The brains tested 2, 4, 8, and 20 days after infection were also negative.

Animals↗
PubMed2025

Interferon and TLR genes, but not endogenous bornavirus-like elements, limit BoDV1 replication after intracerebral infection.

Borna disease virus 1 (BoDV1) is a disease-causing agent in some livestock and, as has recently been shown, in humans. What constitutes a protective immune response to BoDV1 is unclear. Previous studies found that endogenous bornavirus-like nucleoprotein elements (EBLNs) present in mammalian genomes produce piRNAs antisense to BoDV1 nucleoprotein mRNAs. As a known function of piRNAs is to restrict transposons via RNA interference, it has been hypothesized that EBLN-derived piRNAs may restrict BoDV1. Here we used EBLN knockout (KO) and other KO mice to test genetic factors potentially involved in antiviral immunity to BoDV1. In previous reports, BoDV1 replication was higher in mice deficient in interferon gamma, and we confirmed a role for this cytokine in BoDV1 restriction at 12 weeks post infection using mice lacking its receptor. We show that BoDV1 replicates to higher levels in the brain of mice without Toll-like receptor 7 (TLR7), suggesting a role for this innate immune receptor in BoDV1 immunity. In contrast, mice lacking piRNA-producing EBLNs were no more susceptible to BoDV1 infection than wild-type under the infection conditions used here. We thus expand the genetic evidence implicating specific conventional immune pathways in BoDV1 control and conclude that EBLN-derived piRNA-guided antiviral silencing, if it occurs, is relatively less impactful in intracerebral infection of neonates.

Animals↗
PubMed1979

In vitro studies on Borna virus. II. Properties of the virus.

Successful cultivation and titration of Borna disease virus in cell cultures enabled detailed studies of the virus properties. Borna virus is labile towards treatment with heat, pH 3.0 and lipid solvents. It is relatively stable at low temperatures and in frozen state. It is easily inactivated by ultraviolet light as e.g. vesicular stomatitis virus. After ultrafiltration studies, the size of the infectious virus unit is between 80 and 100 nm. Its buoyant density in cesium chloride is 1.165 g per ml. The one step multiplication curve shows that Borna virus has a replication cycle of about 2 days in BSC 1 cells. In growth experiments using antimetabilites it behaves like certain RNA containing viruses. As its multiplication is not inhibited by bromo- and iododeoxyuridine and actinomycin D, no DNA step seems to be involved in virus synthesis. Regarding these properties and the intracellular antigen distribution as shown by fluorescent antibodies, it is not possible to attribute Borna virus to any of the established virus groups.

Antimetabolites↗
PubMed1976

Equine viral encephalitis.

The most important neurotropic viral infections of the horse are the arthropod-borne encephalitides. These include Venezuelan encephalitis (VE), eastern encephalitis (EE) and western encephalitis (WE), which are found in the Americas, and Japanese B encephalitis which occurs in the Far East. All the viruses cause encephalitis in man. Between 1969 and 1972 an epidemic of VE occurred in Central America. In 1971 the disease was reported in Texas, where it was brought under control by the vaccination of susceptible horses with an attenuated live virus vaccine and by the reduction of the mosquito population with insecticides sprayed from aircraft. A high titre viraemia occurs with VE virus in the horse and epidemics are maintained by a mosquito/horse cycle; infection of man and other species is incidental. EE and WE have been recognised as separate diseases since 1933 and in the U.S.A. horses are protected by routine vaccination. Epidemics of these diseases are routine vaccination. Epidemics of these diseases are now uncommon. In contrast with VE, both EE and WE viruses are maintained by a bird/mosquito cycle. The viraemia in the horse is generally considered insufficient to infect mosquito vectors; the horse is a "dead end host". Several species of mosquito can act as vectors of VE, WE and EE. The extension of other arthropod-borne diseases to areas originally outside their geographical distribution (e.g. bluetongue in sheep) serves to illustrate the potential of VE, WE and EE to cause disease on other continents.

Animals↗
PubMed1978

In vitro studies on Borna virus. I. The use of cell cultures for the demonstration, titration and production of Borna virus.

Borna virus produces non-lytic infections in a wide spectrum of primary cell cultures and cell lines. The sensitivity and virus yields vary with the different cell systems. Accurate virus titrations can be performed in the RK 13 cell line by counting immunoflourescent microfoci between the 5th and 10th day after infection. Since the virus is not released from the cells and does not spread via the culture medium, the use of a semisolid overlay in unnecessary in virus titrations. The cell line most productive for Borna virus is the CV 1 line. The conditions for optimum virus production include a prolonged cultivation period of at least two weeks with regular changes of medium, and an incubation temperature of 35 degrees C. Harvest of the virus requires thorough disruption of the infected cells, preferably by ultrasonication, since Borna virus seems to be closely associated with cellular structures.

Borna disease virus↗