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 effect of mouse interferon (ITF) on the expression of Friend leukaemia virus (FLV) an on dimethyl sulphoxide (DMSO)-stimulated haemoglobin synthesis in Friend erythroleukaemic cells (FLC) was studied. Immunofluorescent staining was used to detect intracellular antigens, and incorporation of 3H-uridine into virions to detect extracellular virus release. Interferon markedly inhibited haemoglobin synthesis and FLV production, but enhanced accumulation of virus antigens in the cytoplasm; on the cell surface, however, FLV antigens were present to the same extent whether ITF was present or not. When ITF was removed, virus production rose and intracellular virus antigens fell to the levels of untreated controls.
J Gen Virol 1977 Nov
PMID:Production of Friend leukaemia antigens in chronically-infected cells treated with interferon. 56 23

Leukaemia-resistant C57BL/6 mice inoculated with the Friend complex (FLC) present a transient but definite depression of the ability to develop IgM and IgG antibody-producing cells to sheep red cells (SRC). In this paper it is shown that this immunodepression cannot be attributed solely to the lymphatic leukaemia virus (LLV) component of FLC which is immunodepressive in susceptible mice. This conclusion was reached by investigating the immunological reactivity of C57BL/6 mice following inoculation with two isolates of LLV. Circumstantial evidence obtained by examining the replication of FLC and LLV, the antibody response to E. coli lipopolysaccharide (LPS) and the ability of syngeneic macrophages administered together with the antigen to restore the response to SRC points to the same conclusion. There were also indications that the low sensitivity to depression by viruses of the Friend complex exhibited by the anti-LPS antibody response is due to the mitogenic activity of this antigen.
J Gen Virol 1978 May
PMID:An analysis of the role of lymphatic leukemia virus in the immunodepression exerted by Friend complex in leukaemia-resistant C57BL/6 mice. 56 3

The sizes of non-covalently linked RNA subunits isolated from highly leukaemogenic Friend virus derived from the plasma (PV, plasma virus) of leukaemic mice were compared to the RNA subunits isolated from low leukaemogenic Friend virus grown in tissue culture (TCV, tissue culture virus). Histograms derived from electron microscope measurements showed that about one-half of the plasma virus RNA was 1.4 to 2.5 micron in length, corresponding to a mol. wt. range from 1.8 X 10(6) to 3.2 X 10(6) and the other half less than 1.4 micron. In contrast, approx. 50% of the TCV RNA was only 0.7 to 1.6 micron in length (mol. wt. 0.9 X 10(6) to 2.0 X 10(6)) and the remainder less than 0.7 micron in length regardless of whether the virus RNA was isolated from 3, 9, 36 or 72 h cultures. The histograms suggest size classes for both TCV and PV derived RNA subunits. Data obtained from sucrose gradient sedimentation of heat-denatured FLV RNA agreed with the electron microscope length measurements. The smaller sizes of the TCV RNA subunits are hypothetically related to the limited biological activity of Friend leukaemia virus produced from leukaemic cells in culture. Comparable results were obtained using two different RNA extraction procedures. Contamination of TCV nucleic acid preparations by cellular DNA was observed even when the virions were harvested from short term cultures and purified by isopycnic sucrose gradient centrifugation. Consequently, preparations of intact virus were treated with DNase prior to sucrose gradient purification of the virions.
J Gen Virol 1978 Jun
PMID:The sizes of RNA subunits isolated from high and low leukaemogenic Friend virus. 66 Jan 64

When the partially purified P65-70 proteolytic factor was added at increasing concentrations to 'immature' core sub-particles of Rauscher leukaemia virus (RLV), we observed an increased cleavage of P65-70 (the gag gene product) and P40 (an intermediate cleavage product containing p30) to p30, the major group specific antigen. When examined by electron microscopy the immature cores exhibited a linear decrease in number, with a concomitant increase in the number of mature cores after treatment. Various intermediate structures retaining elements of both immature and mature forms were also observed, suggesting that the in vitro conversion from immature cores to mature cores can occur on a I:I basis.
J Gen Virol 1978 Jul
PMID:Morphological conversion of 'immature' Rauscher leukaemia virus cores to a 'mature' form after addition of the P65-70 (gag gene product) proteolytic factor. 69 Jun 4

Twenty-nine of 100 sera from patients recently infected with varicella-zoster virus (VZV) were found to cross-react with human T cell leukaemia virus type 1 (HTLV-1) antigen in the particle agglutination (PA) assay using HTLV-1 antigen-coated gelatin particles. Anti-VZV IgM antibodies were shown to be responsible for this cross-reactivity. Western blot analysis revealed that PA-positive anti-VZV sera reacted with the HTLV-1 gag p19 protein in HTLV-1-infected cells and recombinant p19 protein produced in Escherichia coli. By using a truncated p19, the cross-reactive region was located to the C-terminal 17 amino acids of p19. One oligopeptide derived from the C terminus, PQIPPPYVEPT (amino acids 115 to 125), was capable of inhibiting PA, suggesting that this peptide carries the cross-reactive epitope. A homologous sequence was found in the VZV gene 22 protein by database analysis, and the oligopeptide TNIPPPLALLR (amino acids 1330 to 1340) had the ability to inhibit PA. These findings suggest that some IgM antibodies against the VZV gene 22 protein produced in the early phase of VZV infection are cross-reactive with the HTLV-1 gag p19 protein because they recognize an antigenic determinant containing an IPPP tetrapeptide.
J Gen Virol 1992 Nov
PMID:Human sera from varicella-zoster virus (VZV) infections cross-react with human T cell leukaemia virus type 1 (HTLV-1): common epitopes in VZV gene 22 protein and HTLV-1 p19 gag protein. 127 4

The env and gag genes from feline leukaemia virus were expressed in a thymidine kinase-negative feline herpes-virus and a baculovirus. Cats were vaccinated with various combinations of these recombinant viruses and 100% protection against feline leukaemia virus challenge was achieved using an immunization schedule which utilized both env and gag products delivered at both a mucosal and systemic site.
J Gen Virol 1992 Jul
PMID:The use of feline herpesvirus and baculovirus as vaccine vectors for the gag and env genes of feline leukaemia virus. 132 Dec 14

In order to test components of feline leukaemia virus (FeLV) as subunit vaccines, we have constructed recombinant baculoviruses that express the FeLV envelope glycoprotein gp85 [Autographa californica nuclear polyhedrosis virus (AcNPV)-gp85] and the structural protein, gag (AcNPVgag). The gag protein is expressed and shed into the medium of infected cells as particles which have a buoyant density on sucrose gradients and appearance by electron microscopy similar to those of authentic FeLV virions. The gag precursor protein within the particles is not fully processed and appears to be a result of partial cleavage of the gag polypeptide. Insect cells that are coinfected with AcNPVgag and AcNPVgp85 shed particles that contain both the gag protein and the gp85 glycoprotein.
J Gen Virol 1992 Jul
PMID:Expression of feline leukaemia virus gp85 and gag proteins and assembly into virus-like particles using the baculovirus expression vector system. 132 Dec 15

The Fv-4 resistance (Fv-4r) gene is a truncated endogenous murine leukaemia virus (MuLV) containing a 3' portion of pol, the entire env gene and the 3' long terminal repeat. Env expression renders mice resistant to infection by ecotropic MuLVs, probably via receptor interference. Previous studies have suggested that the flanking cellular sequences are also important for Fv-4 env gene expression. To establish how the truncated retrovirus was generated and the nature of the cellular sequences involved, the Fv-4 susceptible (Fv-4s) allele DNA was cloned, and its restriction map and nucleotide sequence were compared with those of the Fv-4r allele. A likely mechanism for generation of the truncated endogenous MuLV is suggested by the results; integration of a prototype MuLV provirus at a site within the Fv-4s allele about 6 to 8 kb downstream of a non-retroviral promoter region, followed by deletion of the 5' half of the provirus, with an accompanying loss of only 7 or 10 bp of cellular flanking sequences. The deletion may have led to the expression of the Fv-4r env gene under control of the non-retroviral promoter.
J Gen Virol 1992 Aug
PMID:Scheme for the generation of a truncated endogenous murine leukaemia virus, the Fv-4 resistance gene. 132 54

Feline leukaemia viruses (FeLVs) are classified into subgroups A, B and C by their use of different host cell receptors on feline cells, a phenotype which is determined by the viral envelope. FeLV-A is the ubiquitous, highly infectious form of FeLV, and FeLV-C isolates are rare variants which are invariably isolated along with FeLV-A. The FeLV-C isolates share the capacity to induce acute non-regenerative anaemia and the prototype, FeLV-C/Sarma, has strongly age-restricted infectivity for cats. The FeLV-C/Sarma env sequence is closely related to that of common, weakly pathogenic FeLV-A isolates. We now show by construction of chimeric viruses that the receptor specificity of FeLV-A/Glasgow-1 virus can be converted to that of FeLV-C by exchange of a single env variable domain, Vr1, which differs by a three codon deletion and nine adjacent substitutions. Attempts to dissect this region further by directed mutagenesis resulted in disabled proviruses. Sequence analysis of independent natural FeLV-C isolates showed that they have unique Vr1 sequences which are distinct from the conserved FeLV-A pattern. The chimeric viruses which acquired the host range and subgroup properties of FeLV-C retained certain FeLV-A-like properties in that they were non-cytopathogenic in 3201B feline T cells and readily induced viraemia in weanling animals. They also induced a profound anaemia in neonates which had a more prolonged course than that induced by FeLV-C/Sarma and which was macrocytic rather than non-regenerative in nature. Although receptor specificity and a major determinant of pathogenicity segregate with Vr1, it appears that sequences elsewhere in the genome influence infectivity and pathogenicity independently of the subgroup phenotype.
J Gen Virol 1992 Nov
PMID:Partial dissociation of subgroup C phenotype and in vivo behaviour in feline leukaemia viruses with chimeric envelope genes. 133 Dec 90

The presence of human T-cell leukemia virus (HTLV-1) in patients with adult T-cell leukemia (ATL) was investigated by Southern blotting and in situ hybridization. In all seven patients, HTLV-1 provirus was detected. A large and variable number of labeled restriction fragments were observed, indicating multiple integrations. Two of the patients analyzed by in situ hybridization had two, while the third patient had three, sites of viral integration on six different chromosomes, suggesting random integration. A single site of integration was shared by two patients, which was on chromosome 10 at bands p11-->p15. One of these sites was on an apparently normal chromosome 10 and the other was on a derivative chromosome 10,t(10;14)(p12;q32). The interleukin 2 receptor (IL2R) has previously been localized to this region (10p14-->p15). The alpha-chain of the IL2R is continuously expressed on affected T-cells in this disease. Southern blotting with pIL2R showed the presence of a novel 3.5 kb fragment in five out of the seven patients. This novel fragment has not been previously reported. No direct correlation was found between the novel 3.5 kb fragment, present in patients both cytogenetically normal and abnormal, and viral integration in the 10p11-->p15 region in two patients. Therefore, it is suggested that the presence of the 3.5 kb fragment and the numerous chromosomal breaks associated with this disease may not be direct results of viral integration.
Mol Gen Genet 1992 Sep
PMID:Chromosomal localization of HTLV-1 viral integration sites using in situ hybridization: detection of a novel IL2R fragment. 135 40


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