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

The major non-glycosylated structural proteins of feline leukemia virus have been isolated, and competition immunoassays have been developed for each. These proteins include the 27,000- to 30,000-molecular-weight major internal antigen designated p30, a 15,000-molecular-weight protein (p15), an acidic protein of 12,000 molecular weight (p12), and a highly basic 10,000-molecular-weight protein (p10). Immunologically and biochemically corresponding proteins of feline and murine leukemia viruses have been identified. and, on the basis of analogy to the known sequence of a prototype type C virus of mouse origin, the map order of the gag region of the feline type C viral genome has been tentatively deduced as NH2-p15-p12-p10-COOH. The demonstration of two feline leukemia virus gag gene-coded proteins, p15 and p12, expressed in the form of an uncleaved precursor in a mink cell line nonproductively transformed by feline sarcoma virus provides indirect support for the proposed sequence.
J Virol 1977 Sep
PMID:Feline leukemia virus: biochemical and immunological characterization of gag gene-coded structural proteins. 19 62

A method is described for detecting the synthesis of avian and murine oncornavirus-specific glycoproteins without the use of antibodies raised against viral structural proteins. As applied to cells infected with avian tumor virus, the method served to resolve pr90, the precursor of the major envelope glycoprotein. A virus-specific glycoprotein of about 85,000 daltons, which has several properties expected to a precursor to gp69/71, was detected in cells infected with murine leukemia virus.
J Virol 1977 Sep
PMID:Antibody-independent detection of virus-specific glycoprotein synthesis is oncornavirus-infected cells. 19 73

Exposure of uninfected rat cells in tissue culture to anaerobic culture conditions induces transcription of RNA corresponding to the two principal constituents of rat-derived type-C sarcoma virus genomes: (i) those specific rat cell sequences present in the Kirsten and Harvey murine sarcoma virus genomes, and (ii) an endogenous type-C rat leukemia virus.
Science 1977 Sep 30
PMID:Expression of murine sarcoma virus genes in uninfected rat cells subjected to anaerobic sress. 19 2

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.
Klin Wochenschr 1977 Sep 01
PMID:[Model studies on virus-induced tumors and their immunological treatment (author's transl)]. 19 2

The OK 10 virus complex was isolated from a liver tumour of a chicken which, as an embryo, had been inoculated intravenously with a field isolate of an avian leukosis virus. The OK 10 virus complex contains at least two viruses: the interference assay and serum neutralization test indicate that the helper virus belongs to subgroup A. One of the viruses, OK 10 V, induces distinct foci in chick embryo cells under agar overlay and cells from the foci form colonies in soft agar. These properties allow in vitro assay of the virus. Injection of virus or infected cells into chicks induces acute leukaemia but no local tumours. Another virus, OK 10 AV (associated virus), comprises about 99% of the OK 10 complex. The virus does not induce foci in chick embryo cells. In chickens it causes leukosis 17 months after injection. Electron micrographs of OK 10 virus stocks show typical C type virus particles. These particles have a density of 1.16 g/ml and contain 70S RNA which, after heat denaturation, releases type b RNA subunits. The OK 10 virus complex apparently represents a strain of acute leukaemia viruses.
J Gen Virol 1978 Sep
PMID:OK 10 virus, an avian retrovirus resembling the acute leukaemia viruses. 21 Nov 98

A removal programme, specially designed for catteries or multiple cat households, to reduce the incidence of lymphosarcoma or leukaemia in cats and the spread of feline leukaemia virus (FeLV), is discussed. This removal programme includes annual testing of male stud cats, testing all contacts of FeLV-positive cats they had during the past two years, testing cats imported from abroad and isolation--or, if this is not possible, euthanasia--of cats found to be positive for FeLV-antigen. To detect the FeLV-antigen a simple indirect fluorescent antibody technique (FAT) was used to detect FeLV-antigen. During a period of four years, the following results were obtained when a removal programme was carried out by a large cat breeders' association in the Netherlands. The proportion of catteries, in which FeLV-positive cats were found to be present, decreased from 11.5 per cent in the former half of 1974 to 2.1 per cent in the latter half of 1977. The proportion of FeLV-positive cats and male studs decreased from 4.9 per cent to 1.2 per cent and from 5.9 per cent to 1.0 per cent respectively during this period. It is concluded that the recommended removal programme is a simple and successful procedure.
Tijdschr Diergeneeskd 1978 Sep 15
PMID:[Control of lymphosarcoma or leukaemia in cats and of feline leukaemia virus (author's transl)]. 21 74

Recent studies have indicated that both the replication-defective spleen focus-forming virus (SFFV) in the Friend virus complex and the helper-independent mink cell focus-inducing (MCF) viruses derived from AKR-murine leukemia virus (MuLV) are env gene recombinants between ecotropic virus and xenotropic virus. In an attempt to isolate additional env gene recombinants between Friend murine leukemia virus (F-MuLV) and xenotropic virus, we have inoculated cloned ecotropic F-MuLV into newborn NIH Swiss mice and analyzed MuLV released from preleukemic and leukemic spleens of infected mice. Two helper-independent MCF strains of F-MuLV have been isolated. Like the previously described AKR-MCF viruses, the Friend MCF viruses are env gene recombinants between an ecotropic virus (F-MuLV) and a mouse xenotropic virus, as shown by host range, interference pattern, and tryptic peptide analysis of the gp70s of these MuLV. Furthermore, RNA from the Friend MCF viruses hybridizes completely to cDNAsffv, a nucleic acid probe which detects that portion of SFFV which was not derived from P-MuLV. The ability to isolate replicating MCF viruses derived from F-MuLV FURTHER strengthens the parallels between the Friend erythroleukemia system and the AKR thymic leukemia system. Finally, the potential relationship of helper-independent env gene recombinants between F-MuLV and xenotropic virus to be highly leukemogenic SFFV is discussed.
J Exp Med 1978 Sep 01
PMID:Helper-independent mink cell focus-inducing strains of Friend murine type-C virus: potential relationship to the origin of replication-defective spleen focus-forming virus. 21 4

Ecotropic murine leukemia viruses, both N-tropic FN-2 (purified helper component of Friend leukemia virus) and B-tropic WNB-2 (purified WN1802B BALB/c-derived endogenous virus), were partially restricted in rat NRK cells. In NRK cells, they produced obscure small plaques at reduced efficiencies relative to their plaque-producing efficiencies in mouse SC-1 cells (10-fold for FN-2 and 100-fold for WNB-2). After three or four passages in NRK cells, the plaquing efficiencies of the viruses in NRK cells increased to levels close to their efficiencies in mouse cells, and the plaques in NRK cells became larger and clearer. The adaptation was more complete with FN-2 than with WNB-2. The adaptation was not due to simple selection of a virus in the FN-2 stock, but was host induced, as the viruses had been submitted to successive limiting dilutions in SC-1 cells before propagation in NRK cells. Possible commitment of xenotropic virus in the adaptation was excluded. The change was stable, even if the adapted viruses were propagated back into SC-1 cells. The NRK-adapted viruses were restricted in other rat cell lines of different origins, and the virus adapted in another rat cell line, RFL, was still restricted in NRK cells. The adaptation was mainly brought about by increased viral growth within the rat cells and not by an increased efficiency of viral penetration into the rat cells. This inversely suggests that the restriction of the ecotropic murine leukemia viruses in NRK cells was a mainly intracellular event. The mobilities of gp69/71 and p30 in sodium dodecyl sulfatepolyacrylamide gel electrophoresis remained unchanged after adaptation of FN-2 in NRK cells.
J Virol 1978 Sep
PMID:Intracellular restriction of ecotropic murine leukemia virus in rat NRK cells and its abolishment by adaptation. 21 84

Inhibitors of elongation steps in protein synthesis such as cycloheximide and anisomycin mimic interferon treatment in that they specifically inhibit the synthesis of certain viral proteins. These specific effects are seen only at very low concentrations of the antibiotics, under conditions where host cellular protein synthesis, as well as cell viability, are not severely reduced. A qualitatively as well as quantitatively close correlation between the effects of the two types of agents has been established for encephalomyocarditis virus, vesicular stomatitis virus and murine leukemia virus protein synthesis. It is concluded that one of the primary mechanisms of interferon action may be a nonspecific retardation of one or more elongation steps, and that this may be sufficient to account for its effects on the replication of certain viruses such as encephalomyocarditis and vesicular stomatitis viruses.
J Virol 1978 Sep
PMID:Specificity of interferon action in protein synthesis. 21 87

NIH 3T3 cells infected with Moloney murine sarcoma virus (murine leukemia virus) produce virions which contain about 99% murine sarcoma virus RNA and 1% murine leukemia virus RNA. This report describes experiments which measured intracellular concentrations of proviral DNA and RNA transcripts for each of the viruses. We found that three to four copies of proviral DNA from each virus were integrated into the cellular DNA. Measurements of RNA specific for each of the genomes by hybridization to specific cDNA reagents revealed a 10- to 15-fold difference in concentration in both nuclear and polysomal RNA fractions, with murine sarcoma virus RNA predominating in both cases. Unless there are major differences in stability between the two viral RNAs, our results suggest that transcriptional control is responsible for much of the difference in final levels of virus synthesis.
J Virol 1978 Sep
PMID:Viral gene expression in murine sarcoma virus(murine leukemia virus)-infected cells. 21 92


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