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  • 1
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    A borna virus cDNA encoding a protein recognized by antibodies in humans with behavioral diseases (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-30
    Description: Borna disease virus (BDV) causes a rare neurological disease in horses and sheep. The virus has not been classified because neither an infectious particle nor a specific nucleic acid had been identified. To identify the genome of BDV, a subtractive complementary DNA expression library was constructed with polyadenylate-selected RNA from a BDV-infected MDCK cell line. A clone (B8) was isolated that specifically hybridized to RNA isolated from BDV-infected brain tissue and BDV-infected cell lines. This clone hybridized to four BDV-specific positive strand RNAs (10.5, 3.6, 2.1, and 0.85 kilobases) and one negative strand RNA (10.5 kilobases) in BDV-infected rat brain. Nucleotide sequence analysis of the clone suggested that it represented a full-length messenger RNA which contained several open reading frames. In vitro transcription and translation of the clone resulted in the synthesis of the 14- and 24-kilodalton BDV-specific proteins. The 24-kilodalton protein, when translated in vitro from the clone, was recognized by antibodies in the sera of patients (three of seven) with behavioral disorders. This BDV-specific clone will provide the means to isolate the other BDV-specific nucleic acids and to identify the virus responsible for Borna disease. In addition, the significance of BDV or a BDV-related virus as a human pathogen can now be more directly examined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉VandeWoude, S -- Richt, J A -- Zink, M C -- Rott, R -- Narayan, O -- Clements, J E -- RR00130/RR/NCRR NIH HHS/ -- RR07002/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1278-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Colorado State University, Lab Animal Resources, Fort Collins 80532.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2244211" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Viral/*blood ; Borna Disease/*microbiology ; Borna disease virus/*genetics/immunology ; Brain/microbiology ; Cloning, Molecular ; DNA/*genetics ; Fluorescent Antibody Technique ; Humans ; Immunoblotting ; Mental Disorders/*microbiology ; Molecular Sequence Data ; Molecular Weight ; Nucleic Acid Hybridization ; RNA, Messenger/analysis/genetics ; RNA, Viral/analysis/genetics ; Rats ; Transcription, Genetic ; Viral Proteins/*genetics/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Susceptibility of skeletal muscle to Coxsackie A2 virus infection: effects of botulinum toxin and denervation (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: Coxsackie A viruses can infect denervated but not innervated mature skeletal muscles. The role of synaptic transmission in preventing susceptibility to Coxsackievirus infection was studied by surgically denervating leg muscles of mice or injecting the muscles with botulinum toxin to block quantal release of acetylcholine. Control muscles were injected with heat-inactivated toxin. Subsequent injection of Coxsackie A2 virus resulted in extensive virus replication and tissue destruction in the denervated and botulinum toxin-treated muscles, while the control muscles showed only minimal changes. This suggests that the susceptibility of skeletal muscle to Coxsackievirus infection is regulated by synaptic transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andrew, C G -- Drachman, D B -- Pestronk, A -- Narayan, O -- 5 K07 NS 00531-02/NS/NINDS NIH HHS/ -- 5R01 HD04817/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):714-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320369" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Botulinum Toxins/*pharmacology ; Coxsackievirus Infections/*microbiology ; Enterovirus/*pathogenicity ; Mice ; *Muscle Denervation ; Muscles/drug effects/microbiology ; Muscular Diseases/*microbiology ; Sciatic Nerve/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Behavioral disease in rats caused by immunopathological responses to persistent borna virus in the brain (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-06-24
    Description: Borna virus replicated persistently in the brains of rats, causing frenzied and apathetic behavioral states in sequence but no mortality. The transient frenzied behavior was caused by an immune-mediated, cytolytic, encephalitic response that was unexpectedly self-limiting. Cessation of active pathological processes coincided with the onset of the passive phase of the disease. This study thus demonstrates suppression of virus-specific inflammation despite continuous viral replication and describes a new mechanism by which chronic encephalitis may become established.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Narayan, O -- Herzog, S -- Frese, K -- Scheefers, H -- Rott, R -- New York, N.Y. -- Science. 1983 Jun 24;220(4604):1401-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6602380" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; Borna Disease/immunology/*pathology/psychology ; Brain/pathology ; Humans ; Inflammation/pathology ; Limbic System/pathology ; Mice ; Motor Activity ; Rats ; Rats, Inbred Lew ; T-Lymphocytes/microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    cis- and trans-acting transcriptional regulation of visna virus (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-08-02
    Description: Visna virus is a pathogenic lentivirus of sheep that is related to human T-cell lymphotropic virus type III (HTLV-III), the probable etiologic agent of the acquired immune deficiency syndrome (AIDS). The transcriptional activity of visna virus promoter and enhancer sequences was studied by means of an assay based on the transient expression of the bacterial gene chloramphenicol acetyltransferase (CAT). The results suggest that the high level of expression of visna virus is due in part to cis-acting enhancer sequences that give the viral promoter a high level of transcriptional activity. In addition, the rate of transcription from the visna virus promoter situated in a plasmid expressing the CAT gene was much greater in infected than uninfected cells. This phenomenon of trans-acting transcriptional activation may involve either virally or cellularly encoded factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hess, J L -- Clements, J E -- Narayan, O -- NS-15721/NS/NINDS NIH HHS/ -- NS-16145/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Aug 2;229(4712):482-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990051" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Animals ; Base Sequence ; Cell Line ; Chloramphenicol O-Acetyltransferase ; Choroid Plexus ; Chromosome Mapping ; Enhancer Elements, Genetic ; *Genes, Regulator ; Goats ; Humans ; L Cells (Cell Line) ; Macrophages ; Mice ; Plasmids ; Promoter Regions, Genetic ; Sheep ; Synovial Membrane ; T-Lymphocytes ; *Transcription, Genetic ; Transfection ; Visna-maedi virus/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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