Disease relevance of Visna

• An open reading frame whose 5' end overlaps with the pol gene, but is unrelated to the env gene, has been observed in HTLV-III/LAV and visna virus, both cytopathic mammalian retroviruses [1].
• Despite close homology between genetic sequences of HIV-I and -II, these two viruses seem to have as much biological disparity from each other as does visna virus from caprine arthritis-encephalitis virus [2].
• The transcriptional activity of the CAEV and visna virus LTRs was measured by a chloramphenicol acetyltransferase assay, and the activity of the visna virus LTR was generally higher in a variety of uninfected cell types [3].
• Here, we demonstrate that the known functional organization of the human immunodeficiency virus type 1 Rev trans activator is shared by the distantly related visna virus Rev protein [4].
• Genetic variation among lentiviruses: homology between visna virus and caprine arthritis-encephalitis virus is confined to the 5' gag-pol region and a small portion of the env gene [5].

High impact information on Visna

• We conclude that mutation in the glycoprotein gene rather than recombination is more probably responsible for antigenic variation, and speculate on the special aspects of visna virus replication relevant to this phenomenon [6].
• Visna and myelin basic protein [7].
• The acyclic nucleoside phosphonate analog 9-(2-phosphonylmethoxyethyl)adenine (PMEA) was recently found to be effective as an inhibitor of visna virus replication and cytopathic effect in sheep choroid plexus cultures [8].
• Inhibitory effect of 9-(2-phosphonylmethoxyethyl)adenine on visna virus infection in lambs: a model for in vivo testing of candidate anti-human immunodeficiency virus drugs [8].
• Transactivation by Rev-V was shown to require a cis-acting target sequence that coincides with a predicted RNA secondary structure located within the visna virus env gene [9].

Chemical compound and disease context of Visna

• Lentivirus-host interactions: lessons from visna and caprine arthritis-encephalitis viruses [2].
• Phosphonoformate inhibition of visna virus replication [10].
• Complexity and polyadenylic acid content of visna virus 60-70S RNA [11].
• In transient-transfection assays using visna virus LTR-CAT as a reporter construct, the activity of this leucine mutant was dramatically reduced [12].
• Characterization of visna virus envelope neuraminic acid [13].

Biological context of Visna

• The visna virus genome encodes a small regulatory protein, Tat, which is necessary for efficient viral replication and enhanced viral transcription [14].
• The visna virus Tat protein is required for efficient viral transcription from the visna virus long terminal repeat (LTR) [15].
• Analysis of the potential RNA folding pattern of the visna virus env gene shows that this hypervariable site falls within a region with little potential for intramolecular base pairing [16].
• Functional murine leukemia virus vectors pseudotyped with the visna virus envelope show expanded visna virus cell tropism [17].
• Visna virus encodes an analogous Tat protein that greatly increases gene expression directed by the visna viral LTR [18].

Anatomical context of Visna

• Adenoviral vectors expressing the 216 bp TNF alpha antisense fragment, controlled by the CMV promoter or the Visna LTR, were both effective at suppressing LPS-induced TNF alpha secretion by primary human macrophages [19].
• Of the ddN derivatives, 2',3'-dideoxycytidine (ddCyd) proved to be the most inhibitory to visna virus-induced syncytium formation (50% effective concentration, 0.02 microM) [20].
• The new antiviral substance phosphonoformate (PFA) has been tested in a cell-free system for its effect on reverse transcriptases from an avian retrovirus (avian myeloblastosis virus, AMV) and from mammalian retroviruses (Rauscher leukaemia virus, RMuLV; bovine leukaemia virus; baboon endogenous virus; simian sarcoma virus; visna virus) [21].
• Cultured cells transfected with a full-length clone of visna DNA produce infectious virus but visna DNA with mutations in rev does not [22].
• Furthermore, the absence of this AP-4 sequence dramatically decreased the additive effect observed when U937 cells were both treated by phorbol ester and expressed the tat gene product, suggesting a high interdependence of the AP-1 and AP-4 sequences for the regulation of the transcription driven by the visna LTR [23].

Gene context of Visna

• The visna virus Tat protein was also able to interact with covalently cross-linked Fos and Jun dimers [15].
• 7. The CMV promoter and the Visna LTR were the most strongly expressed and were therefore used to drive the expression of TNF alpha antisense fragments [19].
• After purification recombinant ovine IL-2 was functionally active as shown by its ability to support the proliferation of Con A-activated T cells and was capable of generating maedi visna virus-specific cytotoxic T cells from primed precursor cells [24].
• Targeting of the visna virus tat protein to AP-1 sites: interactions with the bZIP domains of fos and jun in vitro and in vivo [15].
• Subcellular localization of rev-gene product in visna virus-infected cells [25].

Analytical, diagnostic and therapeutic context of Visna

• The proteins of visna are separated into nine major peaks by agarose gel chromatography in 6 M guanidine hydrochloride (GuHCl) [26].
• We used the MAbs and polyclonal immune sera directed against visna virus, gp135, or p27 in enzyme-linked immunosorbent assays to compare visna virus (strain 1514) with antigenic mutants (LV1-1 to LV1-6) previously isolated from a single sheep persistently infected with plaque-purified strain 1514 [27].
• Indirect immunofluorescence staining of infected cells confirmed the cytoplasmic location of visna Rev protein and could reveal in some stained cells a higher concentration of Rev at the cellular plasma membrane [25].
• In contrast, several 2',3'-dideoxynucleosides and acyclic nucleoside phosphonate analogues, which inhibit reverse transcription, were found to be very effective inhibitors of visna virus replication and viral CPE in cell culture [28].

References