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)

After a review of the general biological properties of C-type oncorna viruses, results are presented on the structure of an exogenous murine leukemia virus (FLV) and on the serobiological properties of its structural proteins. Our findings suggested a major role of the viral surface glycoprotein gp71 in immunological defense mechanisms. This was confirmed by vaccination experiments with isolated gp71 in mice. The induced immunity was highly specific and not operative against endogenous murine C-viruses belonging to other serotypes. Surprisingly the latter were found to be activated by the vaccination with gp71 of FLV. In heterologous animal species isolated FLV-gp71 induced the formation of broadly reacting antibodies. They were found to be effective in the therapy of infections with FLV in mice as well as with feline leukaemia virus in cats. Most impressive results were obtained with an antiserum prepared against feline leukaemia virus in a goat. This serum completely suppressed sarcomas induced by infection with feline sarcoma virus.
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PMID:[Model studies on virus-induced tumors and their immunological treatment (author's transl)]. 19 2

The feline oncornavirus-associated cell membrane antigen (FOCMA) acts as a target for natural immuno-surveillance against tumor development in the cat. In the present study, mink and rat cells nonproductively transformed by feline sarcoma virus (FeSV) were shown to express FOCMA as well as 5'-terminal feline leukemia virus (FeLV) gag gene proteins, p15 and p12. In contrast, such cells lack detectable levels of other FeLV gag gene-coded proteins or the env gene product, gp70. FOCMA, p15, and p12 antigen expression is initially in the form of an 80,000-100,000 molecular weight precursor which, upon post-translational cleavage, gives rise to a 65,000 molecular weight component that contains FOCMA and a 25,000 molecular weight component containing p15 and p12. Feline lymphoma cells, including those from several tumors that lacked detectable levels of FeLV structural protein expression, were shown to be FOCMA-positive. These findings strongly suggest that FOCMA represents an FeSV-coded transformation specific protein and provide preliminary information regarding the position within the FeSV genome coding for its synthesis.
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PMID:Feline oncornavirus-associated cell membrane antigen: evidence for an immunologically crossreactive feline sarcoma virus-coded protein. 20 59

A radioimmunoassay has been developed that detects a unique antigen encoded by the genome of the feline sarcoma virus (FeSV). Pseudotype viral particles containing an FeSV-specific polyprotein (p85) were used both as a source of antigen and to prepare specific antisera in rabbits. Because p85 contains antigens related to two structural proteins (p15 and p12) of feline leukemia virus (FeLV), antibodies directed to these were adsorbed with purified FeLV proteins. The adsorbed rabbit antiserum bound to antigenic determinants (designated FOCMA-S) which are also present in p85 and reacted specifically in immunofluorescence tests with rat cells transformed by FeSV and with FOCMA-positive cat lymphoid tumor cells. Competition assays detect FOCMA-S in pseudotype type C viruses rescued from FeSV-transformed mink and rat cells but not in heterologous type C helper viruses or in FeLV. A crossreactive antigen was also detected in pseudotypes of Kirsten sarcoma virus. The assay permits the quantitative measurement of an FeSV-coded protein whose expression is associated with viral transformation.
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PMID:Characterization of a feline sarcoma virus-coded antigen (FOCMA-S) by radioimmunoassay. 21 55

The 15,000-molecular-weight polypeptide (p15) of feline leukemia virus (FeLV) was shown to impair normal lymphocyte function in vitro and to abrogate immunity to feline oncornavirus disease in vivo. FeLVp15 suppressed concanavalin A-induced blast transformation of normal feline lymphocytes by 68%, while other virion proteins had no effect. p15 suppression was not due to toxicity, nor was p15 a competitive inhibitor of concanavalin A binding. Capping of receptors for concanavalin A on normal feline lymphocytes also was inhibited by either inactivated FeLV or FeLV p15. Groups of cats were immunized with either killed feline oncornavirus-associated cell membrane antigen bearing tumor cells or tumor cells plus FeLV p15. After challenge with feline sarcoma virus, three of four p15-treated cats developed progressive fatal fibrosarcoma as compared to one of five non-p15-treated cats. The cats receiving p15 also had lower cytotoxic antibody titers against feline oncornavirus-associated cell membrane antigen (mean peak titer, 1:6) than did the non-p15 group (1:74). These data support the hypothesis that the immunosuppression in cats infected with FeLV is mediated by FeLV p15.
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PMID:Immunosuppressive properties of a virion polypeptide, a 15,000-dalton protein, from feline leukemia virus. 21 25

A purified 15,000-molecular-weight (Mr) Prague strain Rous sarcoma virus gag gene-coded structural protein, p15, was shown to enzymatically cleave the previously described 130,000 Mr feline sarcoma virus-coded polyprotein, Pr130. Cleavage products included proteins ranging in molecular weight from 12,000 to 110,000. The specificity of this cleavage reactivity was indicated by the fact that, under similar conditions, neither purified type C viral structural proteins nor nonviral proteins such as bovine serum albumin were cleaved to significant extents. Moreover, feline leukemia virus Pr65gag was efficiently cleaved, resulting in the generations of proteins of 30,000 (p30), 15,000 (p15), 12,000 (p12), and 10,000 (p10) Mr. Using enzymatically (p15) treated feline sarcoma virus Pr130 as starting material, we were able to purify a major 72,000 Mr cleavage product and to show it to contain the previously described feline sarcoma virus-coded nonstructural component.
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PMID:Feline sarcoma virus-coded polyprotein: enzymatic cleavage by a type C virus-coded structural protein. 21 52

The genomes of three independent isolates of feline sarcoma virus (FeSV) were compared by molecular hybridization techniques. Using complementary DNAs prepared from two strains, SM- and ST-FeSV, common complementary DNA'S were selected by sequential hybridization to FeSV and feline leukemia virus RNAs. These DNAs were shown to be highly related among the three independent sarcoma virus isolates. FeSV-specific complementary DNAs were prepared by selection for hybridization by the homologous FeSV RNA and against hybridization by fline leukemia virus RNA. Sarcoma virus-specific sequences of SM-FeSV were shown to differ from those of either ST- or GA-FeSV strains, whereas ST-FeSV-specific DNA shared extensive sequence homology with GA-FeSV. By molecular hybridization, each set of FeSV-specific sequences was demonstrated to be present in normal cat cellular DNA in approximately one copy per haploid genome and was conserved throughout Felidae. In contrast, FeSV-common sequences were present in multiple DNA copies and were found only in Mediterranean cats. The present results are consistent with the concept that each FeSV strain has arisen by a mechanism involving recombination between feline leukemia virus and cat cellular DNA sequences, the latter represented within the cat genome in a manner analogous to that of a cellular gene.
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PMID:Nature and distribution of feline sarcoma virus nucleotide sequences. 22 44

The susceptibility of human fibroblasts and human lymphoid cell lines to feline leukemia virus (FeLV) and feline sarcoma virus (FeSV) was investigated. Human cells were highly sensitive to infection by FeLV subgroups B and C and FeSV but resistant to infection by FeLV subgroup A. The cells became infected, produced infectious virus, and displayed no differences in morphology or viability. T-cell lines appeared to be more sensitive to FeLV and FeSV infection and to produce more virus than did autochthonous B-cells. B-cell lines with membrane IgG appeared more resistant to infection than did those with no membrane IgG.
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PMID:Susceptibility of human cell lines to feline leukemia virus and feline sarcoma virus. 22 3

Extrachromosomal DNA purified from mink cells acutely infected with the Snyder-Theilen strain of feline sarcoma virus (FeSV) was digested with restriction endonucleases, and the DNA fragments were electrophoretically separated, transferred to a solid substrate, and hybridized with radiolabeled DNA transcripts complementary to different portions of the FeSV RNA genome. Major DNA species 8.4 and 5.0 kilobase pairs (kbp) long represent the linear, unintegrated proviruses of Snyder-Theilen feline leukemia virus and FeSV, respectively. Transfection experiments performed with electroeluted DNAs showed that the 8.4-kbp form led to the production of replicating nontransforming virus in mink and cat cells; in contrast, the 5.0-kbp DNA produced helper virus-independent foci of transformation in mouse NIH/3T3 cells and helper virus-dependent foci in mink cells at an efficiency comparable to that obtained with unfractionated extrachromosomal DNA. Sites of restriction endonuclease cleavage for six enzymes were oriented with respect to one another within the FeSV provirus. EcoRI recognized cleavage sites at 0.3 to 0.4 kbp from each terminus of FeSV DNA, reducing the 5.0-kbp DNA to molecules 4.3 kbp long; this enzyme excised a large internal proviral DNA fragment of corresponding size from the DNA of FeSV-transformed mink nonproducer cells. By using DNA transcripts complementary to different portions of the FeSV genome, sarcoma-specific sequences (the FeSV src gene) were positioned within 2.1 and 3.4 kbp from the 5' end of the proviral DNA with respect to the viral RNA genome. The src gene is flanked at both ends by sequences shared in common with feline leukemia virus. The localization of src sequences to this region suggests that a portion of an FeSV polyprotein which contains feline oncornavirus-associated cell membrane antigen (FOCMA-S) is the major product of this gene.
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PMID:Restriction endonuclease mapping of unintegrated proviral DNA of Snyder-Theilen feline sarcoma virus: localization of sarcoma-specific sequences. 22 70

In cats, horizontally transmitted viruses cause leukemia and lymphoma under natural conditions. As with other retroviruses, feline leukemia virus (FeLV) contains products of 3 major genes; the virus core gag gene products, the polymerase, and the virus envelope glycoprotein. When cells are transformed in vitro by the related feline sarcoma virus (FeSV), an additional protein, FOCMA is expressed at the cell membrane. FOCMA, which is FeSV-coded, is transformation and/or tumor specific and expressed regardless of whether or not the cells make virus or contain virus structural antigens. Lymphoid leukemia cells also express FOCMA, both when FeLV is used to induce the disease in laboratory cats and when the tumors occur under natural conditions. FOCMA is expressed on both T and B lymphoid leukemia cells, but not expressed on non-malignant lymphoid cells, even when they are infected with FeLV. About one-third of the naturally occurring lymphoid tumors of cats lack detectable FeLV proteins and varying portions of the FeLV provirus. Despite this, they regularly express FOCMA, which is the target of an immuno-surveillance response that functions effectively under most conditions. FOCMA thus provides a useful model for antigens that might be expressed in "virus-negative" leukemias of man.
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PMID:Leukemia specific antigens: FOCMA and immune surveillance. 23 69

An experimental approach to the immunoprophylatic control of feline oncornavirus-mediated diseases has included induction of antivirus immunity and antibodies to the feline oncornavirus-associated membrane (tumor) antigens. A suitable model for exploring the effectiveness of killed oncornavirus vaccines in the cat has been provided by the use of feline sarcoma virus. Immunization of seven pregnant queens over a 6-week period with ultraviolet light-inactivated Gardner-Arnstein feline sarcoma virus resulted in significant protection among 12 kittens challenged with a tumor-forming Dose 90 at 7 days of age. This immunity was not present in kittens challenged at 35 days of age. Among 12 kittens born of queens immunized during pregnancy with ultraviolet light-inactivated Kawakami-Theilen feline leukemia virus and challenged with the same live virus at 4 days of age, significant protection was noted, ranging from prolongation of survival time to complete protection in 3 kittens. In general, the higher the antibody titer in the mother, the more effective the protection afforded the kittens. Immunization of 43 kittens during their first 5 weeks of life with the same vaccines used in adult cats did not immunize sufficiently to protect against feline sarcoma virus challenge at 5 weeks of age. Neutralizing antibody responses in these kittens were significantly lower than in pregnant queens. That kittens of this age are immunologically responsive was established, since complete protection of 9 kittens to feline sarcoma virus was obtained by immunization with a crude tumor extract inactivated with 5 to 7 megarads of gamma-irradiation. All these kittens developed feline oncornavirus-associated membrane antibodies while 3 developed demonstrable levels of virus-neutralizing antibodies. The results of these studies are believed indicative that killed virus vaccines and tumor vaccines can be effective immunoprophylatic measures in the control of RNA tumor virus oncogenesis in the cat. Developments in this model system should be relevant to any consideration given similar vaccines in humans.
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PMID:Experimental oncornavirus vaccines in the cat. 94 34


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