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)

A search for variant endogenous cat viruses led to a novel isolate. Although the major envelope glycoprotein of this virus was similar in size to that of an RD-114-like virus that was coisolated, it was unrelated to RD-114 or feline leukemia virus by immunological and biological criteria. This degree of dissimilarity suggests a different evolutionary progenitor from that for the RD-114 and feline leukemia virus viral envelopes. The novel virus did, however, code for gag gene polypeptides which are closely related to RD-114 virus. Neither the novel isolate nor the RD-114-like coisolate induced foci in S+L- cat cells which restrict focus induction by RD-114 virus. This suggests that the two viruses share a common genomic target of restriction which resides outside of the env region.
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PMID:Isolation from cats of an endogenous type C virus with a novel envelope glycoprotein. 298 93

Polypeptides specific for feline leukemia virus (FeLV) have been identified in the media of cells that produce FeLV as well as in nonproducer cells transformed by feline sarcoma viruses (FeSV). Cat fibroblasts that were persistently infected with FELV release the major virus envelope glycoprotein, whereas cultured cat lymphoma cells shed both glycopeptides related to the virus core gene (gag) and glycopeptides related to the virus envelope gene (env). Mink cells and cat cells transformed by FeSV secrete polypeptides of a wide range of sizes that cross-react with the major virus core protein p27. Differences in the classes of p27-related proteins produced may be related to the strain of virus and the cell type. Cat cells transformed by FeSV release a glycopeptide that appears to be processed differently from those identified in the media of FeSV-transformed mink cells. The possibility that such FeLV-related secretory proteins may interfere with the immune response of the host is discussed.
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PMID:Feline leukemia virus-and feline sarcoma virus-related polypeptides released by virus producer and nonproducer cells. 300 64

Infection of bovines with bovine leukaemia virus (BLV) manifests itself in either of two ways: 30-70% of carriers develop persistent lymphocytosis (PL), with the viral genome integrated at a large number of different sites in the DNA of the affected B-lymphocytes, without causing any chromosomal abnormalities. Only 0,1-10% of carriers develop lymphoid tumours, which also consist of B-lymphocytes. In contrast to PL, however, they are of mono- or oligoclonal origin in terms of the integration site, which is characteristic for each tumour. All cells contain one or more copies of the viral genome, chromosomal aberrations are common and if deletions are present they are invariably found in the 5'-half of the virus DNA sequence. In both types of affected cells transcription is repressed in vivo, but transient virus production can be induced in vitro and detected by means of syncytia induction or haemagglutination. In vivo production of virus in some unknown cell is suggested by the presence of high antibody titres in infected animals, especially against the envelope glycoprotein gp51. This can be detected by various techniques such as immunodiffusion, radioimmune assay or ELISA. Monoclonal antibodies against gp51 have revealed 8 epitopes, 3 of which are recognized by neutralizing antibodies and one by a cytolytic antibody. The BLV genome, about 9 kb in size, have been cloned, and some of the information obtained on its molecular structure and function is discussed. It codes for at least 4 non-glycosylated and 2 glycoproteins. Of special interest is the recently discovered serological relationship between some of the non-glycosylated proteins and those of the human T-cell leukaemia virus. The functional role of BLV in leukaemogenesis is largely unknown. The presence of the viral genome seems to be necessary for the maintenance of the transformed state, but not its continuous expression nor an LTR-mediated promotion of transcription of cellular genes. No oncogene is carried by the virus. Although bovine leukosis is not of major economic importance, its eradication is desirable and feasible in countries with a relatively low incidence, by means of testing and elimination. For endemic situations vaccination would be preferable, and distinct possibilities exist for the development of gp51 based vaccines.
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PMID:Bovine leukaemia virus and enzootic bovine leukosis. 300 47

Murine monoclonal antibodies were developed against the protein products produced by murine C127 cells which had been transfected with a recombinant plasmid clone containing the human T-cell leukemia (lymphotropic) virus type I (HTLV-I) proviral DNA coding regions for part of env, px, and the 3' LTR. Four antibodies with different binding patterns were obtained. One of these antibodies, F1.6, reacted against HTLV-I infected cells but not against noninfected cell lines. This antibody also reacted with sucrose-gradient purified HTLV-I and -II particles with preferential binding against the HTLV-I preparation. The F1.6 antibody bound to two proteins of approximately 21 and 43 kDa in gradient purified HTLV-I preparations, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and Western blots, and to a 43-kDa protein in cell lysates of HTLV-I infected cell lines; the F1.6 antibody did not bind significantly to any HTLV-II proteins in western blots. The three other antibodies F1.1, F1.2, and F1.5, recognized the same size proteins, 21 and 43 kDa in the gradient purified viral preparations of HTLV-I and in the case of the F1.2 antibody, the same size proteins in purified virus preparation of HTLV-II and -III. The F1.2 and F1.5 antibodies bound not only to purified HTLV particles but also to a variety of cellular proteins in HTLV-I infected and noninfected cells suggesting that they recognized epitopes which were shared between HTLV proteins and normal cells. The identity of the 21-kDa viral protein is most likely that of the small envelope glycoprotein. The identity of the larger protein is undetermined.
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PMID:Serological characterization of human T-cell leukemia (lymphotropic) virus, type I (HTLV-I) small envelope protein. 300 30

Purified feline leukemia virus, UV light-inactivated feline leukemia virus, and a synthetic peptide (CKS-17) homologous to a well-conserved region of the transmembrane components of several human and animal retroviruses were each studied for their effects on IgG production by feline peripheral blood lymphocytes. Using a reverse hemolytic plaque assay, both the viable virus and the UV-inactivated feline leukemia virus, but not the CKS-17, activated B lymphocytes to secrete IgG. When staphylococcal protein A, a polyclonal B-cell activator, was used to stimulate IgG synthesis by feline lymphocytes, the viable virus, the UV-inactivated virus, and the CKS-17 peptide each strongly suppressed IgG secretion without compromising viability of the lymphocytes. These findings suggest that the immunosuppressive influences of feline leukemia virus on immunoglobulin synthesis may reside in a conserved portion of the envelope glycoprotein that includes the region homologous to CKS-17.
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PMID:Suppressive effect on polyclonal B-cell activation of a synthetic peptide homologous to a transmembrane component of oncogenic retroviruses. 302 58

Cats persistently infected with a type C retrovirus (feline leukemia virus; FeLV) were treated either by the extracorporeal perfusion of their plasma through filter columns containing staphylococcal protein A (SPA) or by the intraperitoneal injection of SPA for up to 32 treatments. The clearance of evidence of viral infection occurred during treatment with SPA in 67% of the treated cats with chronic viral infection that had FeLV-related abnormalities other than overt malignancy. This rate of viral clearance is more than 30 times greater than the incidence of spontaneous clearance of persistent FeLV viremia in the untreated cat. Actual clearance of viremia occurred in 28% of all cats treated. Regression of malignancy, which occurred in four of 12 (33%) treated cats, was demonstrated by reductions in tumor size and bone marrow neoplastic cell populations. Immediately preceding or concurrent with these remissions from viral infection and malignant disease, a marked though transient elevation in the plasma level of circulating gamma-like interferon occurred in some responding cats and was followed by the appearance and rising titer of a complement-dependent cytotoxic antibody that reacted with FeLV-infected cells. This IgG antibody was shown by several analyses to be specific for the major viral envelope glycoprotein gp70. Further investigations demonstrated that high levels of FeLV at the cellular level might be responsible for the reduced ability of normal feline lymphocytes to secrete gamma-interferon in response to mitogenic stimuli in vitro. These findings may provide some clue to the variation in the responsiveness of individual cats to immunotherapy with staphylococcal protein A.
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PMID:Clearance of retroviremia and regression of malignancy in cats with leukemia-lymphoma during treatment with staphylococcal protein A. 303 40

The binding of normal cat IgG, heat-aggregated cat IgG and specific immune complexes (IC) containing cat IgG to a silica matrix containing covalently bound Staphylococcus aureus protein A was evaluated. The amounts of serum relative to protein A-silica, the flow rates and the perfusion times were representative of those existing when protein A-silica columns are used for therapeutic extracorporeal immunoadsorption of IgG and IC from humans and animals. When cat IgG was present in a large excess, approximately one molecule was bound to the matrix per molecule of solid-phase protein A with a KA of 1.5 X 10(6) 1/mol. Aggregated and immune complexed IgG bound to the matrix with relatively higher affinity. IC prepared in vitro between the purified envelope glycoprotein of the feline leukemia virus (FeLV gp70) and affinity-purified cat antibodies bound to the matrix even though normal IgG was present in greater than 10,000-fold excess. Once bound, IC were not eluted from columns upon further perfusion with normal serum. However, bound IgG was eluted from columns by further perfusion of normal serum or IC. IC were at least five-fold more efficient than normal IgG in exerting this effect. The results suggest that protein A-silica columns can be used for preferential removal of IC from plasma in a clinical or experimental setting.
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PMID:Selective removal of antigen-complexed IgG from cat plasma by adsorption onto a protein A-silica matrix. 303 6

T cells primed specifically for the envelope glycoprotein of Friend murine leukemia helper virus (F-MuLV) were prepared by immunizing mice with a recombinant vaccinia virus that expressed the entire env gene of F-MuLV. Significant proliferative responses of F-MuLV envelope-specific, H-2a/b T cells were observed when the T cells were stimulated with antigen-pulsed peritoneal exudate cells (PEC) having the b allele at the K, A beta, A alpha, and E beta loci of the H-2. On the other hand, PEC having only the kappa allele at these loci did not induce the envelope-specific T cell proliferation, even when the PEC had the b allele at the E alpha, S, or D loci. F-MuLV envelope-specific proliferation of H-2a/b T cells under the stimulation of antigen-pulsed, H-2a/b PEC was specifically blocked with anti-I-Ab and anti-I-Ek mAbs but not with anti-Kb, anti-Kk, or anti-I-Ak mAbs. Moreover, (B10.MBR x A/WySn)F1 mice that have the b allele only at the K locus but not in I-A subregion were nonresponders to the envelope glycoprotein, and the bm12 mutation at the A beta locus completely abolished the T cell responsiveness to this antigen. These results indicate that proliferative T cells recognize a limited number of epitopes on F-MuLV envelope protein in the context of I-Ab, hybrid I-Ak/b, and/or hybrid I-Ek/b class II MHC molecules but fail to recognize the same envelope protein in the context of I-Ak or I-Ek molecules. This influence of the H-2I region on T cell recognition of the envelope glycoprotein appeared to control in vivo induction of protective immunity against Friend virus complex after immunization with the vaccinia-F-MuLV env vaccine. Thus, these results provide, for the first time, direct evidence for Ir gene-controlled responder/nonresponder phenotypes influencing the immune response to a pathogenic virus of mice.
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PMID:Genetic control of T cell responsiveness to the Friend murine leukemia virus envelope antigen. Identification of class II loci of the H-2 as immune response genes. 314 52

Since a retroviral envelope glycoprotein, gp70, present in sera is prominently involved in the pathogenesis of murine systemic lupus erythematosus (SLE), the detection of gp70-anti-gp70 immune complexes (gp70 IC) is particularly useful for the study of murine SLE. To facilitate the detection of gp70 and gp70 IC, we have developed a simple and sensitive enzyme-linked immunosorbent assay (ELISA). Using an affinity column coupled with whole mouse serum proteins containing serum gp70 or with Rauscher murine leukaemia virus (MuLV), antibodies specific to serum gp70 or to Rauscher MuLV gp70 were purified from hyperimmune goat anti-Rauscher MuLV gp70 antisera. Only affinity-purified anti-serum gp70 fraction, but not anti-Rauscher MuLV gp70 fraction, was able to detect serum gp70 efficiently in the ELISA, because only a minor fraction of goat anti-Rauscher MuLV gp70 antibodies is cross-reacting with serum gp70. This procedure could be applied to other antigen-antibody systems, in which only antibodies to heterologous cross-reacting antigens are available, to detect free and antibody-complexed antigens in pathological sera.
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PMID:Enzyme-linked immunosorbent assay for detection of retroviral gp70 and gp70-anti-gp70 immune complexes in sera from SLE mice. 334 48

Biological activities of antisera against synthetic oligopeptides were examined. The peptide antisera were directed against amino acids 6 to 12 (pep1), 124 to 131 (pep2), 256 to 262 (pep3), 283 to 290 (pep4) and 434 to 441 (pep5) of the viral envelope glycoprotein (gp70). Peptide-specific antisera did not neutralize viral infectivity. However, antibodies to pep4 and pep5, which bound to the hydrophobic part of gp70, mediated the complement-dependent lysis of Friend murine leukaemia virus (FLV)-infected cells. STU mice were immunized against FLV-induced erythroleukaemia with synthetic oligopeptides. Vaccines containing only one of these peptides (single-peptide vaccines) as well as multi-peptide vaccines containing pep1, -4, -5 or pep1, -2, -3, -4, -5 were used. Whereas the immunizations with single-peptide vaccines did not protect the immunized mice from FLV-induced erythroleukaemia, multi-peptide vaccines enhanced the survival rate and incubation period after FLV challenge. These results revealed that immunological reactions distinct from neutralizing antibodies can be evoked by immunization with synthetic peptides and can confer limited protection against FLV-induced erythroleukaemia.
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PMID:Synthetic vaccines against Friend murine leukaemia virus-induced erythroleukaemia: in vivo and in vitro studies with synthetic oligopeptides and sequence-specific antisera. 346 23


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