Important note: Information in this article was accurate in 1990. The state of the art may have changed since the publication date.
GENETIC REGULATION OF VISNA VIRUS: STUDIES OF VIRAL TRANSCRIPTION AND OF A VIRAL TRANS-ACTIVATING PROTEIN
Diss Abstr Int [B]; 50(1):62 1989. Unique Identifier : AIDSLINE ICDB/90658123 Davis JL; Johns Hopkins Univ.
Abstract:
The unique pathogenesis of lentiviral infections in humans and ruminant animals may be explained, in part, by the complex mechanisms regulating transcription and translation of their viral genes. The studies described here address two central issues of visna virus gene regulation: (1) transcription of viral genes in infected cells and (2) the nature of viral encoded trans-regulatory proteins. Northern blot analysis employing gene-specific subgenomic probes revealed a complex pattern of six viral transcripts synthesized by infected cells. In addition to genomic sized RNA (9.4 kb) and singly spliced transcripts encoding structural proteins (5.0 and a doublet at 4.3 kb), small, multiply spliced mRNAs of 1.5 and 1.8 kb were found which contain sequences from the 5' region of the genome, the S region (between pol and env) and the 3' env region. This complex splicing pattern for visna virus is different from other retroviruses, yet is remarkably similar to HIV. This suggests that complex splicing is a common feature of lentivirus gene expression. The 1.8 and 1.5 kb transcripts were postulated to code for viral regulatory proteins. A cDNA library was constructed with poly(A)+ RNA from infected cells to investigate the protein(s) synthesized by the small transcripts. A detailed analysis of one clone corresponding to the 1.8-kb mRNA was performed. This clone encodes two proteins of 10 kD and 21.5 kD, respectively, as determined by in vitro transcription and translation experiments. The results of transient expression and cotransfection assays demonstrated that expression of the cDNA insert transactivates the visna virus promoter. Experiments employing constructs in which the coding sequences for either the 10-kD protein or the 21.5-kD protein had been mutated revealed that the 10-kD species is responsible for transactivation. This protein has been given the name vistat since it is functionally and genetically similar to the HIV tat protein. The effect of vistat upon the visna virus promoter is specific; it stimulates only its own and closely related promoters. A function for the second 21.5 kD protein has not been defined, but it may be analogous to another regulatory protein of HIV, the art/trs protein. (Full text available from University Microfilms International, Ann Arbor, MI, as Order No. AAD89-08097)
Keywords: Animal Cell Line, Transformed *Gene Expression Regulation, Viral Gene Library Gene Products, rev/GENETICS Human Trans-Activators/*GENETICS *Transcription, Genetic Visna-Maedi Virus/*GENETICS THESIS 900228
M9020581
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Important note: Information in this article was accurate in 1990. The state of the art may have changed since the publication date.
