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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The 71,000 dalton glycoprotein (gp71) purified from Rauscher murine leukemia virus (R-MuLV) by affinity chromatography specifically binds to murine but not other mammalian cells in culture. Binding is prevented by specific antiserum raides to gp71 (anti-gp71). The binding assay as described in this report can detect receptors on as few as 300 murine cells, and with 1 X 10(5) cells gives significant binding with 30 sec. The results show that the purified glycoprotein retians biologic activity and can form a stable complex with specific receptors on mouse cell membranes. The assay can therefore be used to characterize the nature of the cellular receptors that are essential for leukemia virus infection. Purified gp71 binding to mouse cells is prevented if the cells are actively producing related ecotropic type C viruses, presumably because the receptors are occupied and are not available to bind exogenously applied gp71. The binding of gp71 to murine cells is enhanced by the presence of calcium ions and low pH. Binding studies performed using an excess of 125I-gp71 indicate the NIH/3T3 cells bind approximately 5.3 X 10(5) molecules of 125I-gp71 per cell.
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PMID:Membrane receptors for murine leukemia viruses: characterization using the purified viral envelope glycoprotein, gp71. 0 13

Revistin, a substance that strongly inhibits the reverse transcriptase activity of murine leukemia virus in our screening system, was obtained from a cultured broth of a soil streptomyces which was closely related to Streptomyces filipinensis. The assay method for the activity was based on the inhibition by a test material of the incorporation of 3H-dTMP into DNA synthesized by the reverse transcriptase of an oncogenic RNA virus. Crude revistin was isolated by serial procedures of salting out with ammonium sulfate and precipitation with cetylpyridinium chloride. The crude material showed neither antibacterial nor antifungal activity. It exhibited against splenomegaly in mice caused by Rauscher leukemia virus infection.
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PMID:Revistin found by screening for inhibitors of reverse transcriptase of an oncogenic virus. 5 48

Three temperature-sensitive mutants of the Rauscher strain of murine leukemia virus are defective in early post-penetration functions required both for leukemia virus infection and for initiation of transformation of cells by their pseudotypes of murine sarcoma virus. In the present study, the reverse transcriptase of one of these mutants (ts 29) is shown to be thermolabile compared with the enzymes of the wild-type virus and several other temperature-sensitive mutants. These findings provide evidence that the reverse transcriptase is required both for leukemia virus infection and for initition of transformation by the replication-defective murine sarcoma virus genome.
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PMID:Thermolabile reverse transcriptase of a mammalian leukemia virus mutant temperature sensitive in its replication and sarcoma virus helper functions. 5 94

We have used a quantitative radiolabelled antibody procedure to measure the amount of certain virus structural antigens on the surface of BALB/c RAG cells producing endogenous B-tropic type C virus. RAG cells expressed group specificities of MuLV p30 on their cell surface but did not express gp70 group specificities. However, type specificities of gp70 were expressed on BALB/c cell lines infected with Moloney leukaemia virus. The majority of p30 antigens detected on the RAG cell surface were removed by trypsin and their reappearance was prevented by cycloheximide, even in the presence of 'conditioned medium' containing MuLV. Passive adsorption of exogenous MuLV p30 to the surface of virus negative BALB/c fibroblasts reached a maximum of 20% of the protein detectable on virus producing RAG cells. These data support the hypothesis that much, but not all, of the surface p30 is expressed de novo on the cell membrane and not derived from passive adsorption of p30 released from shed virus or as a by-product of virus infection of a cell.
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PMID:Expression of virus structural proteins on murine cell surfaces in association with the production of murine leukaemia virus. 6 22

The purpose of this investigation was to search for oncornavirus in primary cell cultures obtained from leukemic cattle organs and lymphocytes and to study their molecular-biological properties and role in the etiology of cattle leukemia. The investigation was carried out on 25 primary trypsinized cell culutres of lymph nodes, spleens, kidneys and lymphocytes from cattle with acute and chronic leukemia. It was demonstrated that all cell cultures from leukemic cattle (in contrast to cell cultures from healthy cattle) released oncornavirus into the culture medium. The virus possesses the main properties of oncornaviruses: it has a virion of C-type structure with a density of 1.16--1.18g/ml in a 20--60 per cent sucrose gradient, which may be induced by 5-bromodeoxyuridine, inhibited by Actino-mycin D, has reverse transcriptase activity, contains 60S RNA, that is annealed in the reaction of molecular hybridization with DNA of lymph nodes of cattle with leukemia. The propagation of the isolated oncornavirus in continuous cell lines of calf kidney culture was demonstrated. Experimental inoculation of purified oncornavirus was carried out on 60 baby calves and 15 lambs from leukosis free herds or flocks. Several of the calves later showed evidence of virus infection.
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PMID:Isolation and characterisation of oncornavirus from primary cultures of tissues from cattle with leukemia. 6 13

Previous studies from this laboratory have mapped resistance and/or susceptibility to radiation-induced leukemia virus (RadLV)-induced neoplasia to the H-2D region. H-2 linked effects on virus replication can be detected subsequent to the initial virus infection, and clear-cut differences in numbers of virus infected thymus cells can be detected as early as 5 wk after RadLV inoculation. Rapid increases in cellular synthesis and cell surface expression of H-2 antigens are detectable immediately after virus inoculation. These changes have been studied by immunofluorescence, absorption, cell surface iodination followed by sodium dodecyl-sulfate-polyacrylamide gel electrophoresis, and two dimensional gel electrophoretic analysis of internally labeled lymphocyte proteins. Expression of H-2K molecules is significantly increased in cells of susceptible and resistant animals. However, significant increases in expression of H-2D antigens occurs only on thymus cells from resistant strains (H-2Dd). Transformed cells of resistant and susceptible H-2 haplotypes adapted to tissue culture lack detectable H-2 antigens as determined by serological absorption studies. It is argued that altered expression of H-2 antigens plays a very significant role in the mechanism of host defense to virus infection.
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PMID:Increased synthesis and expression of H-2 antigens on thymocytes as a result of radiation leukemia virus infection: a possible mechanism for H-2 linked control of virus-induced neoplasia. 7 39

Fv-1b restriction in BALB/3T3 cells is temporarily abrogated following infection with N-tropic murine leukemia virus. The mechanism of this phenomenon was investigated by comparing the inactivation rates for viral infectivity and for the ability of the same virus to abrogate Fv-1 restriction. Inactivation of the abrogating ability of N-tropic murine leukemia virus following graduated doses of gamma radiation proceeded at half the rate of that for viral infectivity. This result indicates that viral RNA must function in abrogating Fv-1b restriction but that only a portion of the viral genome is required. The inactivation kinetics of N-tropic murine leukemia virus were also determined following incubation of virus at 43 degrees C. Abrogating ability of N-tropic murine leukemia virus was found to be about six times as stable under these conditions as was viral infectivity. Interestingly, virion-associated reverse transcriptase activity was inactivated at the same rate as was viral infectivity, indicating that this enzyme may not need to function during abrogation. Virus heated at 43 degrees C was used to study the kinetics of the abrogation phenomenon itself. Abrogation was shown to be transient, requiring 6 to 9 h after virus infection to become maximally effective and beginning to disappear after about 18 h. The data reported here confirm the idea that abrogation of Fv-1 restriction can be separated experimentally from virus replication, and they raise the possibility that a separate biochemical pathway exists for incoming viral RNA in Fv-1 restrictive cells.
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PMID:Abrogation of Fv-1b restriction with murine leukemia viruses inactivated by heat or by gamma irradiation. 7 8

T- and B-cell counts, estimation of Ig receptor fluidity, and expression of virus-coded antigens were correlated with histological findings during the development of virus-induced mouse lymphoma. Tested were BALB/c mice after infection with the strongly oncogenic Moloney leukemia virus (MLV), the moderately oncogenic (in BALB/c mice) Gross passage A virus (GLV-A), and the essentially non-oncogenic Gross 3T3 tissue culture virus (GLV-T). Methods included immunofluorescence microscopy with antisera against T-cells, B-cells and MLV intact virus, routine histology, and electron microscopy. Following time sequence of changes was observed in mice with oncogenic MLV- and GLV-A infection but not in GLV-T infection: Significant decrease of Ig receptor fluidity and expression of virus antigen were observed already at the initial investigation, i.e. 2 weeks post virus infection. This was followed by significant decreases in percent T-cells 5--8 weeks later, accompanied by histologic atrophy of the thymus and of thymus-dependent regions of lymphatic tissues. Another 2--8 weeks after the decrease in percent T-cells occurred, the first lymphomatous foci became obvious in the thymus. Clinically overt and generalized lymphoma was diagnosed at 20--30 weeks post virus infection. Ultrastructurally, some changes in the arrangement and quantity of cytoplasmic microfilaments were noted in proliferating lymphoblasts and in lymphoma cells. It is concluded, that the described changes were related to the oncogenic potential of mouse C-type RNA viruses and not just to virus infection per se.
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PMID:Sequential changes of T- and B-cells, virus antigen expression and primary histologic tumor diagnosis in virus-induced lymphomagenesis of mice. 15 4

The effects of a single non-carcinogenic dose of 15 mg/kg methylnitrosourea (MNU) on the immune and hematopoietic systems of adult specific-pathogen-free (SPF) cats were determined. The cell-mediated-immune (CMI) system was markedly suppressed, as evidenced by: (i) Prolonged cutaneous allograft retention time (41-84 days); (ii) Decreased lymphocyte blast transformation response to mitogens (2% of pretreatment response to pokeweed mitogen or concanavalin A) and antigen (12% of untreated control cat response to keyhole limpet hemocyanin); (iii) Reduced number of absolute erythrocyte-rosetting T-cells in the peripheral blood. This immunosuppression lasted at least 3 months, the duration of the experiment. Suppression of the hematopoietic system was also noted as evidenced by: (i) Peripheral lymphopenia lasting 3 months and neutropenia lasting 3 weeks; (ii) Bone marrow hypocellularity lasting 3 weeks; (iii) Hypoplasia of neutrophilic precursors lasting 3 weeks and erythroid precursors lasting 4 days. It was concluded that a single non-carcinogenic dose of MNU induces a prolonged suppression of the CMI system and a brief suppression of hematopoiesis in adult SPF cats. The immunosuppression may in part be responsible for the previously observed increased susceptibility to feline leukemia virus infection and disease of adult SPF cats treated with MNU.
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PMID:The effects of methylnitrosourea on the immune system and hematopoietic system of adult specific pathogen free cats. 16 45

Feline leukemia virus (FeLV) infection is common among cats where contact is high. The virus can be transmitted readily between cats. It causes a variety of haemopoietic and lymphoid neoplasms; the most common types are alimentary, multicentric and thymic lymphosarcoma and lymphatic leukaemia. The virus is involved in the aetiology of certain other diseases including anaemia, glomerulonephritis and an immunosuppressive syndrome which predisposes cats to intercurrent infections. Many infected cats mount an immune response and do not suffer from any of these. The immune status is shown by serum antibody levels to feline leukaemia virus associated cell membrane antigens. Cats with a titre of 32 or more are most unlikely to suffer any ill effects and may eliminate the virus infection. The outcome of infection in an individual cat depends on the immunological competence of the cat, the dose of virus received and its ability to induce immunosuppression. FeLV infection can be detected by examination of tissues by electron microscopy, and by culture of virus from plasma and other tissues. In the United States, a method is now in use for the detection of leukaemia virus antigen in peripheral blood leukocytes; this is carried out on ordinary blood films. Successful prototype vaccines have been developed against FeLV. This paper describes the natural history of the virus, the diseases in which it is implicated and discusses recently developed diagnostic methods.
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PMID:Feline leukaemia virus and its clinical effects in cats. 16 15


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