Antibodies to Borna Disease Virus in Infected Adult Rats: An Early Appearance of Anti-p10 Antibody and Recognition of Novel Virus-Specific Proteins in Infected Animal Brain Cells.

Watanabe, Makiko; Kobayashi, Takeshi; Tomonaga, Keizō; Ikuta, Kazuyoshi

doi:10.1292/jvms.62.775

Cited by 4 publications

(1 citation statement)

References 25 publications

(22 reference statements)

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“…Monolayers of representative OL cell clones, OL and OL/BDV, were collected after being washed and mixed with an equal volume of sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) sample buffer, as described previously (46). After cell lysis by sonication, followed by boiling, the proteins were separated by using a 12% gel and transferred to polyvinylidene difluoride membranes.…”

Section: Cells and Virusmentioning

confidence: 99%

Varied Persistent Life Cycles of Borna Disease Virus in a Human Oligodendroglioma Cell Line

Ibrahim

Watanabe

Palacios

et al. 2002

J Virol

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Borna disease virus (BDV) establishes a persistent infection inBorna disease virus (BDV) causes progressive meningoencephalomyelitis in horses and sheep, in addition to several other vertebrate species (4,26,41). BDV is a single nonsegmented, negative-stranded (NNS) RNA virus (7,11,14,42) that is unique among members of the order Mononegaverales, in that it uses the nucleus as a site for replication and transcription (10, 43). BDV is a highly neurotropic virus that persists in the central nervous system (CNS) of infected animals. In adult rats, BDV infection is associated with massive brain inflammation and extensive neuronal damage (33). Neonatal infection, by contrast, results in life-long persistence without encephalitis (2,3,8,16,33). However, infected rats of all ages express a variety of behavioral abnormalities. Therefore, BDV provides an important model for the investigation of the mechanisms and consequences of viral persistence in the CNS.Generally, the CNS is known to be unique in its response to viral infections. This may be because of the lack of specialized lymphatic drainage, potentially limiting and delaying viral antigen recognition, in addition to the lack of dendritic cells and the use of microglia for the initial recognition and presentation of viral antigens, as well as the lack of expression of major histocompatibility molecules by normal neurons and glial cells (36). Thus, these factors result in immune limitations, which could contribute to the fate of viral persistence in the CNS, in general and for BDV as well. In addition, persistent BDV infection in the CNS is due to its noncytolytic strategy for replication (25).Persistent infection with BDV has been established in a variety of neuronal and glial cell lines during which viral antigens are continuously detected (9). The choice of a cell line for the in vitro characterization of BDV appears to depend on the in vivo tropism of the virus, as well as on the functional importance and abundance of cells in the CNS such as neurons and glial cells (astrocytes and oligodendrocytes). The rat astrocytoma cell line (C6) is frequently used for such a purpose (9, 17), in addition to the neuronal cell lines SK-N-SH and SK-N-SHEP (9).The cell-specific variations in BDV replication in vitro have been studied. BDV persistence in the C6 cell line is characterized by high-level expression of BDV-specific proteins and RNA and low-level production of infectious virions (9). Such an expression is related in part to the secretion of several neurotrophic factors into the culture medium by the cells (9, 35). Although BDV is characterized by high genomic stability, a recent report demonstrated the possibility of isolating stable virus variants from a persistently infected C6 cell line (17).Although oligodendrocytes are a major cellular component of the white matter in the CNS and have a pivotal role in neuronal cell functions, they have not been well studied in terms of BDV characterization. Oligodendrocytes have been shown to support experimental and natural i...

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Section: Cells and Virusmentioning

confidence: 99%

Varied Persistent Life Cycles of Borna Disease Virus in a Human Oligodendroglioma Cell Line

Ibrahim

Watanabe

Palacios

et al. 2002

J Virol

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Translation Initiation of a Bicistronic mRNA of Borna Disease Virus: A 16-kDa Phosphoprotein Is Initiated at an Internal Start Codon

et al. 2000

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We examined translational initiation of a bicistronic 0.8-kb mRNA of Borna disease virus (BDV) using a cDNA clone of the mRNA. Upon transfection with the clone, COS-7 cells produced a 16-kDa protein (P'), in addition to the previously identified products of BDV, 24- (P) and 14.5-kDa proteins. The 16-kDa product was detected by anti-P monoclonal antibody and was shown to exist in BDV-infected cell lines as well as in infected animal brain cells. Transient expression analysis of mutated cDNA clones encoding the BDV 0.8-kb mRNA revealed that the 16-kDa protein was initiated at the second AUG codon on the same open reading frame of the P protein. The mutational analysis also demonstrated that the first AUG within the 0.8-kb mRNA is not optimal, although the signal contains a better Kozak's motif. These results demonstrated the presence of three functional AUG codons in the smallest mRNA of BDV and also suggested that a leaky scanning mechanism is involved in translational initiation at AUG codons downstream of the bicistronic mRNA of BDV. Furthermore, the 16-kDa protein was located in the BDV-specific nuclear foci and was found to associate with the other viral proteins in BDV-infected cells, demonstrating an important role of the novel identified BDV protein in viral replication.

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Neurological Diseases and Viral Dynamics in the Brains of Neonatally Borna Disease Virus-Infected Gerbils

et al. 2001

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Borna disease virus (BDV) is a noncytolytic, neurotropic RNA virus that causes a chronic neurological disease in a wide variety of animal species. To develop a better understanding of the correlation between neurological disorders caused by BDV infection and virus distribution in the brain, we investigated viral dynamics in the central nervous system (CNS) of neonatally BDV-infected gerbils during the late stage of infection. Despite the severe symptoms and aggressive proliferation of BDV in the infected gerbils, no apparent neuroanatomical abnormalities or neuronal cell loss was observed in the infected gerbil brain. Furthermore, no or only minimal infiltration was observed in the infected gerbil brain. By in situ hybridization and real-time PCR analyses, we demonstrated that the predominant area of expression of BDV mRNA, as well as the protein, was shifted in the brain in association with progression of disease. In nondiseased gerbils, the virus replication was predominantly detected in the cerebral cortex and hippocampus of the CNS. On the other hand, diseased animals showed a high level of expression in the lower brain stem and cerebellum, especially in Purkinje cell neurons. These observations suggested that significant replication of the virus in specific areas of the CNS is critical for development of the neurological disorders in BDV-infected neonatal gerbils.

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Antibodies to Borna Disease Virus in Infected Adult Rats: An Early Appearance of Anti-p10 Antibody and Recognition of Novel Virus-Specific Proteins in Infected Animal Brain Cells.

Cited by 4 publications

References 25 publications

Varied Persistent Life Cycles of Borna Disease Virus in a Human Oligodendroglioma Cell Line

Varied Persistent Life Cycles of Borna Disease Virus in a Human Oligodendroglioma Cell Line

Translation Initiation of a Bicistronic mRNA of Borna Disease Virus: A 16-kDa Phosphoprotein Is Initiated at an Internal Start Codon

Neurological Diseases and Viral Dynamics in the Brains of Neonatally Borna Disease Virus-Infected Gerbils

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