Disease relevance of Immunodeficiency Virus, Feline

• The S3 and S3' subsite binding specificities of HIV and feline immunodeficiency virus proteases (FIV) proteases (PRs) have been explored by using C2-symmetric competitive inhibitors [1].
• Common antigenic determinants appeared to be shared by FIV, caprine arthritis encephalitis virus, and visna virus as shown by serological cross-reactivity of rabbit antibodies to caprine arthritis encephalitis virus and visna virus with the putative FIV core protein p28 [2].
• The GP64 glycoprotein from baculovirus Autographa californica multinuclear polyhedrosis virus pseudo-typed FIV efficiently and showed excellent hepatocyte tropism [3].
• We investigated the efficacy of feline immunodeficiency virus (FIV)-based vectors in targeting hepatocytes and correcting FVIII deficiency in a hemophilia A mouse model [3].
• In the pull-down assay LEDGF/p75 interacted with HIV-1, HIV-2, and feline immunodeficiency virus IN, but not with the IN of human T-cell lymphotropic virus type 2, Moloney murine leukemia virus, or Rous sarcoma virus [4].

High impact information on Immunodeficiency Virus, Feline

• Although long terminal repeat (LTR)-directed FIV expression was found to be negligible in human cells, promoter substitution enabled an env-deleted, three-plasmid, human cell-FIV lentiviral vector system to express high levels of FIV proteins and FIV vectors in human cells, thus bypassing the hazards of feline vector producer cells [5].
• Here, we demonstrate that the 43-kDa molecule is CD134, a receptor for FIV recently identified independently [Shimojima, M., et al. (2004) Science 303, 1192-1195] [6].
• The major surface glycoprotein of feline immunodeficiency virus (FIV) specifically binds to a 43-kDa glycoprotein expressed on the surface of a subset of T cells in peripheral blood mononuclear cells and IL-2-dependent T cell lines [6].
• Altogether, our results substantiate that CD134 acts as a primary binding receptor for FIV and explain the specific targeting and depletion of the CD4+ T cell population observed during the course of infection independent of the use of CD4 as a binding receptor/coreceptor [6].
• Effects of feline immunodeficiency virus on astrocyte glutamate uptake: implications for lentivirus-induced central nervous system diseases [7].

Chemical compound and disease context of Immunodeficiency Virus, Feline

• This novel NES does not contain multiple leucine residues unlike other CRM1-interacting NES, is conserved in GAPDH from multiple species, and has sequence similarities to the export signal found in feline immunodeficiency virus Rev protein [8].
• The visible absorption spectrum, EPR signal, and acid phosphatase activity of Uf in FIII are almost identical to those of FIV Uf after the latter has been reduced by 2-mercaptoethanol [9].
• 9-(2-Phosphonylmethoxyethyl)adenine (PMEA) is a potent and selective inhibitor of the in vitro replication of a number of retroviruses, including HIV-1 and HIV-2, simian immunodeficiency virus (SIV), simian AIDS-related virus (SRV), feline immunodeficiency virus (FIV) and Moloney murine sarcoma virus (MSV) [10].
• The cat/feline immunodeficiency virus model for transmucosal transmission of AIDS: nonoxynol-9 contraceptive jelly blocks transmission by an infected cell inoculum [11].
• Extremely low frequencies of CpG dinucleotides are found in the genomes of the lentivirus subfamily of retroviruses, including the human, simian and feline immunodeficiency viruses (HIV1, HIV2, SIV, and FIV, respectively), equine infectious anemia virus (EIAV), and the ovine lentivirus, Visna [12].

Biological context of Immunodeficiency Virus, Feline

• We generated a GP64-pseudotyped FIV vector encoding the B domain-deleted human FVIII coding region driven by the liver-specific promoter, with 2 beneficial point mutations in the A1 domain [3].
• The development of an antibody response to FIV gag-encoded proteins and detection of virus-specific sequences in sera, blood-derived cells, and necropsied tissue accompanied these changes [13].
• OBJECTIVE: To evaluate the efficacy of a genetic vaccination protocol based on minimalistic, immunogenic defined gene expression (MIDGE) vectors coding for domains of the feline immunodeficiency virus (FIV) env gene and feline IL-12 [14].
• CONCLUSION: Genetic vaccination using a MIDGE-based construct for the expression of the surface-transmembrane protein domain of FIV env and feline IL-12 DNA led to protection against homologous virus challenge in three out of four vaccinated cats [14].
• DNA extracted from TNF-alpha-treated CRFK cells infected with FIV showed a ladder of nucleosomal DNA, indicating that this cytocidal effect by TNF-alpha was due to programmed cell death, or apoptosis [15].

Anatomical context of Immunodeficiency Virus, Feline

• RESULTS: Three days after isolation, 85% of cultured KC were able to internalize red blood cells; 45% were CD4-positive and 65% expressed a 24 kD protein thought to be a receptor for FIV (CD9) [16].
• OBJECTIVE: To study the effects of HIV-1 and feline immunodeficiency virus (FIV) on neural stem cell viability, together with the neurotrophic properties of growth hormone (GH) in models of pediatric neuroAIDS [17].
• The processing and transport of the envelope glycoprotein complex of feline immunodeficiency virus (FIV) in the persistently infected Crandell feline kidney (CRFK) cell line were investigated [18].
• Lymphocytes were restimulated in vitro with paraformaldehyde-fixed, autologous lymphoblasts which had been infected with recombinant vaccinia viruses expressing FIV GAG or ENV proteins [19].
• Synthetic peptides have been used to map linear B-cell epitopes of the third variable (V3) region of the feline immunodeficiency virus (FIV) external membrane glycoprotein gp120 [20].

Gene context of Immunodeficiency Virus, Feline

• The data suggest that infection of feline cells with FIV can be mediated by CXCR4 and that, depending on the assay conditions, infection can be either inhibited or enhanced by SDF-1alpha [21].
• These findings provide direct evidence for a sequential interaction of FIV Env with CD134 and CXCR4 and reveal the presence of a cryptic epitope in V3 that is masked in the mature envelope oligomers [22].
• Antibodies binding the CCR3 chemokine receptor maximally inhibited infection of human PBMC by both FIV strains compared to antibodies to CXCR4 or CCR5 [23].
• The feline CXCR4 has been shown to facilitate fusion by FIV [44] and we suggest that the feline CCR5 receptor mediates infection of feline cells by M-tropic strains of FIV [24].
• These results suggest that the inhibitory effect of IL-12 on both virus replication and apoptosis has potential implications for the design of immunotherapy strategies using IL-12 in FIV infection [25].

Analytical, diagnostic and therapeutic context of Immunodeficiency Virus, Feline

• Protection against FIV challenge infection by genetic vaccination using minimalistic DNA constructs for FIV env gene and feline IL-12 expression [14].
• Functional assays included virus neutralization performed with two different cell substrates, complement- and antibody-dependent virolysis, blocking of reverse transcriptase, and an assay that measured the ability of sera to prevent FIV growth in cocultures of infected and uninfected cells [26].
• We cloned and expressed the integrase gene of feline immunodeficiency virus (FIV) in Escherichia coli as a fusion to the malE gene and purified the IN fusion protein by affinity chromatography [27].
• Southern blot detection of amplified gag gene sequences and limiting-cell-dilution polymerase chain reaction analysis indicated that Ig+ cells carried a higher FIV provirus burden in chronically (> or = 1-year) infected cats than either CD4+ or CD8+ cells [28].
• Epitope mapping of the V3 domain of feline immunodeficiency virus envelope glycoprotein by monoclonal antibodies [29].

References