Adaptation of Borna Disease Virus to the Mouse

Kao, Moujahed; Ludwig, Hanns; Gosztonyi, Georg

doi:10.1099/0022-1317-65-10-1845

Cited by 67 publications

(46 citation statements)

References 14 publications

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“…It is remarkable that in the upper region of the gels two components, most likely of cellular origin, bind to gamma globulins from normal rat and rabbit serum, but have no affinity for mouse serum, although mice are susceptible to BD virus infection without becoming clinically ill (Kao et al, 1984). This lack of non-specific adsorption of cellular material by mouse Ig was also found when a monoclonal antibody was used for the preparation of an immunoaffinity column.…”

Section: Discussionmentioning

confidence: 82%

Purification and Properties of an Intranuclear Virus-specific Antigen from Tissue Infected with Borna Disease Virus

Haas

Becht

Rott

1986

Journal of General Virology

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SUMMARYA virus-specific antigen was extracted from brains of rats and from MDCK cells infected with Borna disease (BD) virus and purified to homogeneity by immunoaffinity chromatography and HPLC. The antigen consists of two components which are almost equal in size (38000 tool. wt.), and it forms aggregates in its native form. The virus specificity of the two antigenic entities was confirmed by immunoblots with convalescent serum and monoclonal antibodies. Immunofluorescent staining with monoclonal antibodies and a hyperimmune serum prepared against the purified antigen showed the intranuclear fluorescence typical for BD virus-infected cells.

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Section: Discussionmentioning

confidence: 82%

Purification and Properties of an Intranuclear Virus-specific Antigen from Tissue Infected with Borna Disease Virus

Haas

Becht

Rott

1986

Journal of General Virology

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“…These findings in BH rats resemble those found in neonatally inoculated LEW rats and in infection of mice. The failure for the development of the disease in neonatally infected rats has been demonstrated to be due to immunological immaturity (Narayan et al, 1983b), whereas the clinically inapparent course of infection in mice (Kao et al, 1984) as well as that of BH rats cannot be explained on this basis.…”

Section: Discussionmentioning

confidence: 99%

“…The clinical manifestations depend upon the host species and the virus strain used for infection. Mice and hamsters were found to be resistant to disease, despite high levels of virus persisting in the brain of the infected animals (Anzil et al, 1973;Kao et al, 1984). Lewis (LEW) rats are highly susceptible to disease, and lesions in the central nervous system (CNS) are caused by a virus-induced T cell-mediated immunopathological reaction (Narayan et al, 1983a, b) in which CD4 ÷ cells play a major role (Richtet al, 1989(Richtet al, , 1990.…”

Section: Introductionmentioning

confidence: 99%

Studies on the genetic control of resistance of black hooded rats to Borna disease

Herzog

Frese

Rott

1991

Journal of General Virology

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In contrast to Lewis (LEW) and Wistar rats, black hooded (BH) rats inoculated with Borna disease (BD) virus developed neither encephalitis nor clinical disease despite persistent replication of the virus in the central nervous system. In comparison to LEW rats, production of virus-specific antibodies was significantly delayed in BD-resistant BH rats, even though identical titres were finally reached. The different susceptibility in LEW and BH rats was studied further by investigating responses of F~ hybrid animals. Although these rats developed encephalitis, they did not become sick. The differences in host responses for BD virus were found to be genetically determined but were independent of class I or class II major histocompatibility complex gene products or to genes responsible for lymphocyte differentiation.

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“…Both animal strain-and age-specific host contributions to BD outcomes have also been reported in mice. For example, rodent-adapted BDV variants, but not rabbit-adapted variants or horse isolates, are able to replicate in mice (28), and a mouse-adapted BDV variant causes encephalitis and mild behavioral disease (i.e., hyperactivity) in adult MRL/ϩ mice but not in SJL mice (43). Infection of neonatal MRL mice with a rat-adapted BDV variant produces significant neurological disease linked to cytotoxic-T-cell-mediated immune responses restricted to H-2 k of major histocompatibility complex class I (20,22).…”

mentioning

confidence: 99%

Enhanced Neurovirulence of Borna Disease Virus Variants Associated with Nucleotide Changes in the Glycoprotein and L Polymerase Genes

Nishino

Kobasa

Rubin

et al. 2002

J Virol

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Borna disease virus (BDV) infection produces a variety of clinical diseases, from behavioral illnesses to classical fatal encephalitis (i.e., Borna disease [BD]). Since the genomes of most BDV isolates differ by less than 5%, host factors are believed responsible for much of the reported variability in disease expression. The contribution of BDV genomic differences to variation in BD expression is largely unexplored. Here we compared the clinical outcomes of rats infected with one of two related BDV variants, CRP3 or CRNP5. Compared to rats inoculated with CRP3, adult and newborn Lewis rats inoculated with CRNP5 had more severe and rapidly fatal neurological disease, with increased damage to the hippocampal pyramidal neurons and rapid infection of brain stem neurons. To identify possible virus-specific contributions to the observed variability in disease outcome, the genomes of CRP3 and CRNP5 were sequenced. Compared to CRP3, there were four nucleotide changes in the CRNP5 variant, two each in the G protein and in the L polymerase, resulting in four amino acid changes. These results suggest that small numbers of genomic differences between BDV variants in the G protein and/or L polymerase can contribute to the variability in BD outcomes.Borna disease virus (BDV) is a nonsegmented negativestrand RNA virus (6) belonging to the family Bornaviridae (13,46). BDV infection in experimental animals has been used to study the pathogenesis of virus-induced central nervous system damage and as a model for specific human diseases, e.g., autism (37). BDV encodes at least six open reading frames (ORFs) in three transcription units: nucleoprotein p40 (N), p10 (X), phosphoprotein p24 (P), matrix protein gp18 (M), membrane glycoprotein gp94 (G), and an RNA-dependent RNA polymerase p190 (L polymerase) (6, 13, 57). Virus replication and transcription take place in the nucleus, a characteristic of Bornaviridae that is unique in the order Mononegavirales (5,8,12,13,46). BDV naturally infects a wide range of warm-blooded hosts (41). In horses and sheep, BDV causes classical Borna disease (BD), a fatal mononuclear inflammatory encephalomyelitis with severe signs of neurological disease (as reviewed in reference 41). Classical BD is in large part due to immunopathogenic damage to the nervous system by blood-borne inflammatory cells (49). However, responses to BDV infection vary according to differences in host-specific factors, e.g., species, animal strain, or age of the host at the time of infection (2, 24, 33, 48). For example, BDV-infected adult Lewis rats develop a highly immunopathogenic central nervous system disease characterized by acute, often fatal encephalitis with clinical signs of hyperactivity, aggression, and ataxia, followed by a chronic phase with resolving encephalitis and depressed behavior (19,41). In contrast, Lewis rats infected as neonates or as immunosuppressed adults do not develop significant inflammatory infiltrates in the brain and may develop behavioral signs of disease without becoming overtly ill (24,33,4...

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Adaptation of Borna Disease Virus to the Mouse

Cited by 67 publications

References 14 publications

Purification and Properties of an Intranuclear Virus-specific Antigen from Tissue Infected with Borna Disease Virus

Purification and Properties of an Intranuclear Virus-specific Antigen from Tissue Infected with Borna Disease Virus

Studies on the genetic control of resistance of black hooded rats to Borna disease

Enhanced Neurovirulence of Borna Disease Virus Variants Associated with Nucleotide Changes in the Glycoprotein and L Polymerase Genes

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