Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The CD46 lymphocyte surface antigen of man (until recently called HuLy-m5), and defined by the E4.3 monoclonal antibody (MoAb), shares cross-reactive antigenic epitopes with the envelope gp70 glycoproteins of gibbon ape leukaemia virus (GaLV) and Mason Pfizer monkey virus (MPMV) primate retroviruses. It is now shown that the cross-reactive antigenic epitope shared by these three molecules is determined solely by the protein portion of these glycoproteins, and that the N-linked and O-linked carbohydrate moieties of these glycoproteins do not directly or sterically contribute to the antigenic cross-reactivity. When CD46 molecules (mol.wt = 66 and 56 kDa) from human thymocytes were stripped of sialic acid with neuraminidase, or stripped of N-linked carbohydrate with endoglycosidase F, the E4.3 MoAb was still able to bind and immunoprecipitate the protein core of CD46 (mol.wt = 56 and 44 kDa). Similarly, polyclonal antisera to GaLV and MPMV precipitated deglycosylated CD46, although at a reduced efficiency. The cross-reacting E4.3 MoAb, anti-GaLV and anti-MPMV antisera also immunoprecipitated HuLy-m5 primary translation protein lacking N- or O-linked carbohydrate from the in vitro translation products of human thymocyte mRNA. Thus, the antigenic cross-reactivity of CD46 molecules with GaLV gp70 and MPMV gp70 is both specific and due to protein structure rather than to carbohydrate; the findings suggest that retroviruses may have acquired a functional epitope from human CD46 or that an endogenous retroviral sequence of human may partially or completely encode the CD46 antigen.
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PMID:The human non-lineage antigen CD46 (HuLy-m5) and primate retroviral gp70 molecules share protein-defined antigenic determinants. 248 50

We have demonstrated that the gibbon ape leukemia virus (GALV) enhancer AP-1 element and the simian virus 40 AP-1 enhancer element bind different factors in HeLa nuclear extracts. A 39-kilodalton HeLa nuclear protein and the c-fos protein bind to the GALV element. Antibodies to c-fos abolish binding to the GALV AP-1 site. In contrast, anti-c-fos immunoglobulin fails to inhibit formation of the simian virus 40-specific complex from extracts of HeLa cells. Thus, AP-1-binding complexes are subject to compositional variation at different binding sites.
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PMID:Distinct factors bind the AP-1 consensus sites in gibbon ape leukemia virus and simian virus 40 enhancers. 253 54

Using in vitro protein binding and in vivo functional studies, we have identified novel regulatory sequences near the 5' end of murine leukemia virus (MuLV) long terminal repeats (LTRs). These sequences are highly conserved in all MuLV LTRs as well as in feline leukemia virus and gibbon ape leukemia virus LTRs. In this upstream conserved region (UCR), gel retardation assays detected two overlapping but distinct binding sites (UCR-U and UCR-L) for nuclear proteins (UCRF-U and UCRF-L). Three lines of evidence suggest a negative regulatory role for the UCR in viral transcription: (i) an inverse correlation was found between MuLV transcripts and nuclear proteins binding the UCR in the spleens of five different mouse strains; (ii) in vivo treatment of NFS mice with lipopolysaccharide resulted in the induction of splenic viral transcripts and the concomitant disappearance of UCR-binding proteins; and (iii) in mouse L cells transfected with an MuLV LTR linked to the chloramphenicol acetyltransferase (CAT) gene, cotransfected UCR oligonucleotides increased CAT expression, presumably by competing for inhibitory trans-acting factors.
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PMID:Negative control region at the 5' end of murine leukemia virus long terminal repeats. 254 Apr 25

Animal models of AIDS are essential for understanding the pathogenesis of retrovirus-induced immune deficiency and encephalopathy and for development and testing of new therapies and vaccines. AIDS and related disorders are etiologically linked to members of the lentivirus subfamily of retroviruses; these lymphocytopathic lentiviruses are designated human immuno-deficiency virus type 1 (HIV-1) and human immuno-deficiency virus type 2 (HIV-2). The only animals susceptible to experimental HIV-1 infection are the chimpanzee, gibbon ape, and rabbit but AIDS-like disease has not yet been reported in these species. Macaques can be persistently infected with some strains of HIV-2 but no AIDS-like disease has resulted. It is not yet clear how suitable HIV-infected SCID-hu mice will be as a model for AIDS. Several subfamilies of naturally occurring cytopathic retroviruses cause immune suppression, including fatal immunodeficiency syndromes in chickens, mice, cats, and monkeys. Domestic cats suffer immunosuppression from both an onco-virus, feline leukemia virus, and a member of the lentivirus subfamily, feline immunodeficiency virus (FIV). Asian macaques are susceptible to fatal simian AIDS from a type D retrovirus, indigenous in macaques, and from a lentivirus, simian immunodeficiency virus (SIV), which is indigenous to healthy African monkeys. SIV is the animal lentivirus most closely related to HIV. Of these animal models, the lentivirus infections of cats (FIV) and macaques (SIV) appear to bear the closest similarity in their pathogenesis to HIV infection and AIDS. This review will summarize these various animal model systems for AIDS and illustrate their usefulness for antiviral therapy and vaccinology.
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PMID:Animal models of AIDS. 255 12

At least two subunits contributed to the formation in vitro of a specific complex binding to the AP1 consensus sequence (TGAGTCA) in the gibbon ape leukemia virus (GALV) enhancer in MLA144 cells. This complex can be dissociated on a monomeric GALV oligonucleotide affinity column. One protein, termed the core protein, was retained on the oligonucleotide affinity column. The second protein flowed through the oligonucleotide affinity column and, when alone, did not bind to DNA; however, when present with the core protein, it bound strongly and very specifically to the GALV sequence. MLA144 cells contained only trace amounts of c-fos and c-jun by immunoblot analysis, suggesting that the proteins specifically binding to the GALV AP1 site were distinct from c-fos and c-jun. In addition to the major complex that recognized the GALV element, MLA144 cells contained a minor complex that is chromatographically different from and antigenically related to c-fos. The factor in the flowthrough complemented a human T-cell nuclear extract (Jurkat cell line), which, when alone, had no assayable complex that specifically bound to the GALV enhancer; this complementation gave rise to a specific complex similar to that seen in MLA144 cells. Together, these results suggest that the GALV enhancer can interact with multicomponent protein complexes in a cell-line-specific manner.
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PMID:Multiple components are required for sequence recognition of the AP1 site in the gibbon ape leukemia virus enhancer. 260 94

Gibbon ape leukemia virus (GaLV) is a highly oncogenic C-type retrovirus capable of inducing myeloid leukemia in juvenile gibbons. GaLV is antigenically most closely related to a new world monkey virus, simian sarcoma associated virus (SSAV), and less to the murine and feline C-type leukemia viruses. To begin to understand how this virus induces leukemia at the molecular level, we have sequenced a GaLV genome and shown that it has a "minimal" genetic complement of 5'R-U5-gag-pol-env-U3-R3'. No additional genes could be identified. Such a genetic structure is identical to those of the murine and feline C-type leukemogenic viruses. Despite its suggested murine origin, the GaLV sequence is as closely related to the murine viruses as it is to the feline retroviruses. Finally the GaLV sequence is indistinguishable from that of the fragments of SSAV available indicating that, in fact, SSAV is of gibbon origin.
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PMID:Genetic organization of gibbon ape leukemia virus. 268 60

The gibbon ape leukemia virus, SEATO strain, and human T-cell leukemia virus type I envelope glycoproteins can be functionally assembled with a Moloney murine leukemia virus core into infectious particles. The envelope-host cell receptor interaction is the major determinant of the host cell specificity for these hybrid virions.
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PMID:Formation of infectious hybrid virions with gibbon ape leukemia virus and human T-cell leukemia virus retroviral envelope glycoproteins and the gag and pol proteins of Moloney murine leukemia virus. 278 36

The Fos protein complex and several Fos-related antigens bind directly or indirectly to a common sequence element that is similar to the consensus binding site for HeLa cell activator protein 1 (AP-1). This element is present in a negative regulatory sequence in the differentiation-sensitive adipocyte gene, aP2; in a transcriptional enhancer for the Gibbon ape leukemia virus; and in a region of the human immunodeficiency virus (HIV) long terminal repeat partially characterized as a negative regulatory element. The protein level and binding activity of Fos and Fos-related antigens increase rapidly after calcium ionophore treatment of a CD4+ human lymphoblast cell line, H9. These data suggest that several proteins may associate with the AP-1 binding site. Moreover, temporally regulated control of the level of each protein could represent a mechanism for modulation of these putative mediators of gene expression.
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PMID:The Fos complex and Fos-related antigens recognize sequence elements that contain AP-1 binding sites. 296 84

This study reports the immunohistological detection of serum antibody reacting with the basal aspect of syncytiotrophoblast of human chorionic villi, where SSAV/GaLV (simian sarcoma associated virus/gibbon ape lymphoma virus) type C retrovirus p30 related antigen was observed by an indirect immunofluorescent method using monospecific antibodies against SSAV p28 and GaLV p29. The immunoglobulin class of this antibody activity called 'the anti-basal aspect of syncytiotrophoblast (anti-BAST)', was exclusively IgM and detected in the sera of both female and male patients with SLE and other autoimmune diseases, but rarely in the sera of normal controls. Immunofluorescent absorption and blocking test revealed that anti-BAST specifically reacted with human placenta and cross-reacted with subhuman primate type C RNA retrovirus SSV/SSAV (simian sarcoma virus/simian sarcoma associated virus), but did not cross-react with ATLV (adult T cell leukaemia virus) and BaEV (baboon endogenous retrovirus). These results suggest the presence of a new antigen-antibody system for another human type C retrovirus related antigens(s) and a participation of retrovirus in autoimmune diseases.
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PMID:Serum antibody reacting with placental syncytiotrophoblast in sera of patients with autoimmune diseases--a possible relation to type C RNA retrovirus. 299 Jul 81

Fibroblast cell lines infected in vitro with different strains of gibbon ape leukaemia virus or the related woolly monkey virus (SSAV) synthesized two RNA species of approximately 8.4 kb and 2.9 kb. The former, a complete RNA, represents the gag-pol mRNA, while the latter is a spliced transcript lacking gag and pol, and represents the env mRNA. In contrast, RNA from one T-lymphoid cell line derived from a gibbon ape T-lymphocytic leukaemia (UCD-144) expressed a viral mRNA in addition to gag-pol and env mRNA. This RNA is 6.4 kb and lacks at least 3.0 kb of sequences derived from the internal region of the viral genome, including most or all of the pol gene. These data, as well as data from Southern blots of UCD-144 DNA, suggest that the 6.4 kb mRNA could represent a transcript from a defective recombinant provirus and may contain cell-derived sequences.
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PMID:Gibbon ape leukaemia virus RNA in leukaemic T-lymphoid cell lines: expression of a novel RNA transcript. 301 55


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