Disease relevance of Arthritis-Encephalitis Virus, Caprine

• We previously reported that infection of goats with caprine arthritis encephalitis virus (CAEV) tat- proviral DNA or virus results in persistent infection, since the animals seroconverted and direct virus isolation from cultures of blood-derived macrophages was positive [1].
• The virion-associated dUTPase activities of caprine arthritis-encephalitis virus (CAEV) and visna virus were determined by using an assay which measure the actual ability of the dUTPase to prevent the dUTP misincorporations into cDNA during reverse transcription [2].
• These findings suggest that MS is not related to infection by human retroviruses with antigenic similarity to HTLV-I, HIV-1, or CAEV [3].
• We also show that, unlike the human immunodeficiency virus (HIV) Tat protein, MVV Tat was not secreted into the medium by transfected human or caprine cells in the absence of cell lysis but that, like the primate accessory protein Vpr, MVV and CAEV Tat proteins were incorporated into viral particles [4].
• Furthermore, infection with CAEV led to an altered pattern of cytokine expression in response to lipopolysaccharide (LPS), heat-killed Listeria monocytogenes plus gamma interferon, or fixed cells of Staphylococcus aureus Cowan I [5].

High impact information on Arthritis-Encephalitis Virus, Caprine

• Replication-defective CAEV proviral constructs lacking the env, tat, and vif genes and carrying the neomycin phosphotransferase gene in the vif-tat region were developed for the infectivity assays [6].
• The complete surface glycoprotein (SU) nucleotide sequences of three French isolates of caprine arthritis-encephalitis virus (CAEV) were determined and compared with those of previously described isolates: three American isolates and one French isolate [7].
• Binding of the nuclear factor to the GAS element in the CAEV LTR is inhibited by antibody directed against STAT1 (p91/84) [8].
• When macrophages were infected with a CAEV clone lacking the trans-acting nuclear regulatory gene tat, IL-8 and MCP-1 were also increased [5].
• Consistent with the binding data, the same mutations in the GAS element eliminate responsiveness to IFN-gamma in the context of both a functional CAEV LTR and a heterologous promoter [8].

Chemical compound and disease context of Arthritis-Encephalitis Virus, Caprine

• We describe the morphological features of CAEV replicating in cultured caprine cells [9].
• All of these rev transcripts, including cDNA g1, increased the level of chloramphenicol acetyltransferase expression when cotransfected with a reporter plasmid containing the CAEV Rev-response element-spanning region downstream of the cat coding sequences [10].
• The CAEV LTR is not significantly homologous with the HTLV-III LTR; however, like HTLV-III, visna virus, and equine infectious anemia virus, CAEV uses tRNA lysine as a primer for reverse transcription [11].
• Mutation of isoleucine-166 to alanine in the putative loop B of gp135 increased the affinity of soluble gp135 for the CAEV receptor(s) and goat monoclonal antibody (Mab) F7-299 which recognizes an epitope overlapping the gp135 RBS [12].
• Failure of non-neutralizing sera to inactivate CAEV may be due in part to low avidity of the antibodies for the virus particles which contain sialic acids on their envelopes, because desialylation of the particles made them neutralizable [13].

Biological context of Arthritis-Encephalitis Virus, Caprine

• We showed that the CAEV molecular clone from the Cork isolate was dUTPase defective as a result of a single amino acid substitution [2].
• Also, sera from CAEV-infected goats specifically immunoprecipitates an in vitro-translated product from the full-length Rev cDNA clone as well as that from the unique second open reading frame of Rev-C which shows that the Rev-C protein is expressed during natural CAEV infection of animals [14].
• The ovine maedi-visna (MVV) and caprine arthritis-encephalitis (CAEV) small ruminant lentiviruses (SRLV) exhibit differential species tropism and cytopathic effects in vitro [15].
• To initiate in vitro studies into the pathogenesis of encephalomyelitis caused by CAEV, we characterized primary cultures of caprine microglia, determined their susceptibility to virus infection, and examined the effect of virus infection on class I and class II major histocompatibility complex antigen expression [16].
• Goats receiving prime-boost vaccination with CAEV env plasmids and SU-FIA became infected but suppressed postchallenge virus replication, provirus loads in lymph node, and development of arthritis for at least 84 weeks [17].

Anatomical context of Arthritis-Encephalitis Virus, Caprine

• The STAT-1 signaling pathway provides at least one mechanism for activation of the CAEV LTR by IFN-gamma in monocytes [8].
• Moreover, we were able to isolate tat mutant CAEV from blood-derived macrophages that was still able to infect synovial membrane cells in vitro [18].
• Sequential isolates of caprine arthritis-encephalitis lentivirus (CAEV) were obtained from clinically arthritic carpal joints of three Saanen goats between 36.4 and 44.9 months after infection with biologically cloned CAEV isolate 63 [19].
• The aim of this study was to investigate whether cells of early goat embryos isolated from in vivo-fertilized goats interact with the caprine arthritis-encephalitis virus (CAEV) in vitro and whether the embryonic zona pellucida (ZP) protects early embryo cells from CAEV infection [20].
• Increased production of IL-16 in CAEV infection may partly be responsible for increased lymphoid cell infiltrations observed in arthritic joints and other tissues of CAEV-infected goats [21].

Gene context of Arthritis-Encephalitis Virus, Caprine

• The most striking difference in the organization of CAEV is in the env gene [22].
• Using an infectious molecular clone of CAEV the role of the tat ORF in viral replication was examined [23].
• A cDNA clone was isolated from CAEV infected cells and shown to encode the 18-kDa Rev protein of CAEV [24].
• Moreover, serum catalase activity increased with increase in the time after infection with CAEV [25].
• It is assumed that such interactions might modulate the physiological functions of Notch2 and epithelin/granulin, thereby affecting various pathologies associated with CAEV [26].

Analytical, diagnostic and therapeutic context of Arthritis-Encephalitis Virus, Caprine

• In-vivo expression of IFN-gamma cDNA promoted by the CAEV LTR was confirmed by the intramuscular (IM) injection of Balb/C mice with plasmid followed by Western blot analysis of mouse serum against purified rCaIFN-gamma produced in E. coli [27].

References