Identification and characterization of a new intron in Borna disease virus

Cubitt, Beatrice; Ly, Calvin; Torre, Juan Carlos de la

doi:10.1099/0022-1317-82-3-641

Cited by 25 publications

(17 citation statements)

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“…One ORF predicts a polypeptide that corresponds to the first 58 aa of G fused to a new C terminus of 20 aa, whereas the other ORF predicts a protein corresponding to a variant BDV L protein (p190) with 153 aa added to the N terminus. Intron III is generated by alternative 3 splice site choice and covers nucleotides 2410-4559 of the BDV genome [23,24]. Alternative splicing of introns II and III is regulated by the use of an alternative transcription termination/polyadenylation signal (GE6) and a cis-acting exon-splicing suppressor element located within the L gene [24].…”

Section: The Bdv Life Cyclementioning

confidence: 99%

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Bornavirus and the Brain

Torre

2002

J INFECT DIS

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Borna disease virus (BDV) causes central nervous system (CNS) disease that is frequently manifested by behavioral abnormalities. BDV is a nonsegmented, negative, single-stranded RNA virus. On the basis of its unique genetic and biologic features, BDV is the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales. Therefore, the investigation of the molecular and cell biology of BDV may provide new insights about virus-cell interactions in the CNS. BDV is an important model system for the investigation of viral persistence in the CNS. Serologic and molecular epidemiologic studies suggest that BDV can infect humans. Despite controversy about potential association with human neuropsychiatric illnesses, BDV affords an intriguing model for the study of these illnesses. Neonatal BDV-infected rats display neurodevelopmental, physiologic, and neurobehavioral abnormalities that closely parallel some of the main features associated with several human mental disorders.

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Section: The Bdv Life Cyclementioning

confidence: 99%

“…Virus-derived BDV mRNAs are spliced with significantly lower efficiency compared with the same plasmid-derived mRNAs [23,24,26]. This could prevent BDV-induced disturbances in the regulation of the cellular RNA processing machinery, thus facilitating viral persistence without compromising cell viability.…”

Section: The Bdv Life Cyclementioning

confidence: 99%

Bornavirus and the Brain

Torre

2002

J INFECT DIS

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“…BDV has the property, unique among known animal negative-stranded RNA viruses, of a nuclear site for the replication and transcription of its genome (Briese et al, 1992;. In addition, BDV uses a remarkable diversity of strategies, including RNA splicing, to regulate its genome expression (Cubitt et al, 2001;de la Torre, 1994;Schneemann et al, 1995; Tomonaga et al, 2000). Based on its distinct genetic and biological features among known negative-stranded RNA viruses, BDV is considered to be the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales.…”

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A reverse genetics system for Borna disease virus

Perez

Sánchez

Cubitt

et al. 2003

Journal of General Virology

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Borna disease virus (BDV) is an enveloped virus. Its non-segmented, negative-stranded RNA genome has the coding capability for six main polypeptides and has an organization characteristic of members of the order Mononegavirales. However, based on its unique genetics and biological features, BDV is considered to be the prototypic member of a new virus family, Bornaviridae. Here, the establishment of a reverse genetics system for BDV is described. Intracellular synthesis of a BDV RNA analogue or minigenome (MG) from a plasmid was driven by RNA polymerase I. Co-transfection with plasmids expressing the BDV polymerase (L), nucleoprotein (N) and phosphoprotein (P) under the control of RNA polymerase II allowed for BDV MG replication and expression. This process depended on a delicate N : P ratio, whereas the L : P ratio was less critical. Two isoforms of N, Np40 and Np38, are present in BDV-infected cells but only Np40 was strictly required for virus polymerase activity. BDV p10 polypeptide encoded by the P gene exhibited a strong inhibitory effect on BDV MG expression.Borna disease virus (BDV) causes CNS disease that is frequently manifested by behavioural abnormalities (Ikuta et al., 2002;Pletnikov et al., 2002;Rott & Becht, 1995). Evidence indicates that the natural host range of BDV, as well as its prevalence and geographical distribution, are very broad (Hatalski et al., 1997;Ikuta et al., 2002;Richt et al., 1997;Richt & Rott, 2001;Rott & Becht, 1995; Staeheli et al., 2000). Moreover, serological data and molecular epidemiological studies indicate that BDV can infect humans and might be associated with certain neuropsychiatric disorders (Billich et al., 2002;Carbone, 2001;Planz et al., 2002;Richt et al., 1997;Richt & Rott, 2001;Rott & Becht, 1995; Staeheli et al., 2000). Both virus and host factors contribute to a variable period of incubation, as well as significant heterogeneity, in the symptoms and pathology associated with BDV infection (Gonzalez-Dunia et al., 1997;Hatalski et al., 1997;Ikuta et al., 2002;Richt et al., 1997;Rott & Becht, 1995; Staeheli et al., 2000).BDV is an enveloped virus with a non-segmented, negativestranded RNA genome. Its genome is about 8?9 kb long, the smallest among known negative-stranded RNA viruses, and has an organization similar to that of other mononegaviruses (de la Torre, 1994;Schneemann et al., 1995). Six major ORFs are found in the BDV genome sequence (de la Torre, 1994;Schneemann et al., 1995). Based on their positions in the viral genome (39-N-p10/P-M-G-L-59), together with their biochemical and sequence features, these polypeptides are the counterparts of the nucleoprotein (N), phosphoprotein (P), transcriptional activator, matrix (M) protein, surface glycoprotein (G) and polymerase (L), respectively, found in other negative-stranded RNA viruses (Tordo et al., 1992). BDV has the property, unique among known animal negative-stranded RNA viruses, of a nuclear site for the replication and transcription of its genome (Briese et al., 1992;. In addition, BDV uses a remark...

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“…BDV has the property, unique among known animal nonsegmented, negative-strand RNA viruses, of a nuclear site for the replication and transcription of its genome (3,9). Moreover, BDV uses a remarkable diversity of strategies, including RNA splicing, for the regulation of its genome expression (10,12,40,41,45). Based on its distinct features among known mononegaviruses, BDV is considered the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales.…”

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Functional Characterization of the Genomic Promoter of Borna Disease Virus (BDV): Implications of 3′-Terminal Sequence Heterogeneity for BDV Persistence

Rosario

Perez

Torre

2005

J Virol

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Borna disease virus (BDV) is an enveloped virus with a genome organization characteristic of Mononegavirales. However, based on its unique features, BDV is considered the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales. We have described the establishment of a reverse genetics system for the rescue of BDV RNA analogues, or minigenomes, that is based on the use of polymerase I/polymerase II. Using this BDV minigenome rescue system, we have examined the functional implications of the reported sequence heterogeneity found at the 5 and 3 termini of the BDV genome and also defined the minimal BDV genomic promoter within the 3-terminal 25 nucleotides. Our results suggest that the accumulation of RNA genome species containing truncations of one to three nucleotides at their 3 termini may contribute to modulate BDV RNA replication and gene expression during long-term persistence.Borna disease virus (BDV) causes central nervous system disease in a variety of vertebrate species, which is frequently manifested by behavioral abnormalities (20,33,37). However, both viral and host factors can influence symptoms and pathology associated with BDV infection (18-20, 35, 37, 43). Serologic and molecular epidemiological data indicate that the natural host range of BDV as well as its prevalence and geographic distribution are very broad (19,20,(35)(36)(37)43). Moreover, there is evidence that BDV can infect humans, being possibly associated with certain neuropsychiatric disorders (2,5,31,(35)(36)(37)43).BDV is an enveloped virus with a nonsegmented, negativestrand RNA genome. Its genome (ca. 8.9 kb), the smallest among known nonsegmented, negative-strand RNA viruses, has an organization similar to that of other mononegaviruses (12,40). Six major open reading frames are found in the BDV genome sequence (3Ј-N-p10/P-M-G-L-5Ј) (12,40). BDV has the property, unique among known animal nonsegmented, negative-strand RNA viruses, of a nuclear site for the replication and transcription of its genome (3, 9). Moreover, BDV uses a remarkable diversity of strategies, including RNA splicing, for the regulation of its genome expression (10,12,40,41,45). Based on its distinct features among known mononegaviruses, BDV is considered the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales.We have established an RNA polymerase I/polymerase II system for intracellular reconstitution of BDV RNA replication and transcription (30). In this system, a BDV RNA analog, or minigenome, is intracellularly synthesized by the cellular RNA polymerase I. This BDV minigenome RNA contains the BDV 5Ј and 3Ј untranslated regions cis-acting sequences required for RNA synthesis mediated by the BDV polymerase (30,39,40,42). Encapsidation of the polymerase I-derived BDV minigenome RNA by plasmid-supplied BDV N and P generates a template that is recognized by the intracellularly reconstituted BDV polymerase to direct synthesis of fulllength antiminigenome RNA (replicate) and a subgenomic mRNA (transcri...

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Identification and characterization of a new intron in Borna disease virus

Cited by 25 publications

References 32 publications

Bornavirus and the Brain

Bornavirus and the Brain

A reverse genetics system for Borna disease virus

Functional Characterization of the Genomic Promoter of Borna Disease Virus (BDV): Implications of 3′-Terminal Sequence Heterogeneity for BDV Persistence

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