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)

In vitro infection of human cord blood lymphocytes (CBL) with human T-cell leukemia/lymphoma virus type I (HTLV-I) was found to be reduced by suramin treatment at a concentration ranging from 10-100 micrograms/ml. At higher concentrations (500 micrograms/ml) suramin was toxic to the cells and even resulted in an increased percentage of cells positive for the p19 viral core protein. Suramin treatment at the onset of the CBL coculture with a lethally irradiated HTLV-I donor cell line (MT-2) reduced virus transmission, evaluated as number of p19+ cells, and the consequent amount of integrated provirus in the host genome. The amount of viral RNA transcripts was not reduced in CBL cocultures. On the other hand, suramin affected HTLV-I replication in infected MT-2 cells, when used at a concentration of 50 micrograms/ml, and this might contribute to the reduced infectivity of suramin-treated MT-2 cells. In addition to its antiviral effects, suramin exerted a modest positive regulation on the natural killing activity of CBL and their early proliferative response in mixed lymphocyte/tumor cell culture.
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PMID:Low concentrations of suramin can reduce in vitro infection of human cord blood lymphocytes with HTLV-I during long-term culture. 289 31

A rabbit lymphoid cell line (Ra-1) was established by co-cultivation with a human T-cell line (MT-2) carrying human T-cell leukemia virus (HTLV). The Ra-1 cell line is chromosomally male and is persistently infected with HTLV. Ra-1 cells, with or without mitomycin C treatment, were inoculated intravenously (i.v.) into 3 female rabbits. All 3 animals responded with the production of antibodies to HTLV antigens. Lymphocytes from one of these seroconverters were cultured in the presence of T-cell growth factor (TCGF) and HTLV particles were detected in the TCGF-grown lymphocytes which were chromosomally female. Co-cultivation of lymphocytes from the 2 other seroconverters with lymphocytes from 2 anti-HTLV-negative healthy men gave rise to the establishment of an HTLV-producing T-cell line derived from each individual. Blood transfusion from one of the HTLV-infected rabbits into 2 female rabbits also resulted in the seroconversion of both recipients. An HTLV-carrying lymphoid cell line (Ra-2) was established from one of the transfusion-related seroconverters. The Ra-2 cell line was initially TCGF-dependent but later became TCGF-independent. There results indicate that HTLV can be transmitted to rabbits. These animals may provide a suitable model system for studying the mode of transmission and pathogenicity of HTLV.
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PMID:Infectious transmission of human T-cell leukemia virus to rabbits. 298 84

Rabbits were successfully infected with human T-cell leukemia virus type I (HTLV-I) and produced antibodies to adult T-cell leukemia-associated antigens (ATLA) on intravenous inoculation of the HTLV-producing human cord T-cell line MT-2, or autologous cell lines established by cocultivation with MT-2 cells. Lymphocytes taken from the rabbits between 4 and 14 days after the inoculation of MT-2 cells, but not lymphocytes obtained in earlier or later periods, could be immortalized in vitro and expressed ATLA and type C virus particles. However, lymphocytes harvested during an early culture period (5 to 8 days) were found to be negative for ATLA. The transformed cells had the karyotype of a normal male rabbit. Two rabbits inoculated with the autologous HTLV-producing cell lines did not allow their growth in vivo, but some peripheral blood lymphocytes could be immortalized in vitro. One of these transformed cell lines was examined for the integration of HTLV-I provirus genome. The transformed cells were found to contain the provirus genome and also to be monoclonal with respect to the integration site of the provirus genome, unlike the inoculated cells.
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PMID:Experimental infection of rabbits with human T-cell leukemia virus type I. 298 72

Promoter function for gene expression of the long terminal repeat (LTR) of human T-cell leukemia virus type I (HTLV-I) was studied by constructing plasmids containing the LTR sequence. The gene encoding chloramphenicol acetyltransferase (CATase) was linked to an HTLV-I LTR sequence (pLTR-CAT) by replacing the simian virus 40 promoter in plasmid pSV2-CAT with the LTR sequence. The transient CATase activities of cells transfected with the plasmids were compared. The results are summarized as follows: The HTLV LTR was active even in an epithelial cell line, with efficiency similar to that of the simian virus 40 promoter. pLTR-CAT expressed high CATase activity, 40-200 times that expressed by pSV2-CAT, in HTLV-I-infected T-cell lines, such as the human cell lines MT-2 and HUT-102, or in HTLV-I-infected rat cell lines. This enhanced activity of the LTR seems to be associated with HTLV gene expression, since only low activity of pLTR-CAT was observed in the HTLV-infected cell line MT-1, in which only a small percent of cells express viral antigens. In HTLV-infected rat cell lines, the pX-encoded protein p40x was the only viral protein detected. Thus, we suggest that p40x is the factor associated directly or indirectly with the enhanced activity of the LTR.
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PMID:Functional activation of the long terminal repeat of human T-cell leukemia virus type I by a trans-acting factor. 298 9

Adult T-cell leukemia virus is the member of a human type-C retrovirus family (HTLV) found to be associated with adult T-cell leukemia (ATL) in Japan. In our study, HTLV was isolated from the MT-2 cell line, purified on sucrose gradient and labelled with fluorescein-isothiocyanate (FITC-HTLV). The protein pattern of the virus was determined by SDS-gel electrophoresis and assured by Western blotting using ATL patient serum. Fresh human lymphocytes, separated B and T cells, mouse and rabbit lymphocytes, mouse fibroblasts, and 13 different tumor cell lines were tested in parallel for binding of FITC-HTLV and infectability by the virus. Virus binding to cell receptors was assayed by flow cytometry. Successful infection was monitored by following the expression of HTLV-determined antigen (HTLA). Most of the cells bound FITC-HTLV at levels ranging from 5% to 130% of the MT-2 cell binding. Only fresh human T, mouse and rabbit lymphocytes were infectable by cell-free virus preparations. The results demonstrate that HTLV receptors are present on different types of cells of both human and animal origin, and that infection by the virus is restricted to fewer host cells but not limited to a specific class of human lymphocytes.
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PMID:Host cell range of adult T-cell leukemia virus. I. Viral infectivity and binding to various cells as detected by flow cytometry. 299 Nov 47

A 2.3 kb cDNA was cloned from human T-cell leukaemia virus [HTLV(MT-2)] virion RNA using a vector system, as plasmid pHTLV 707. The restriction endonuclease map of pHTLV 707 revealed that the insert contained the 5' half of the env gene and a portion of the pX region of HTLV, corresponding to the subgenomic RNA derived from 32S defective HTLV. Nucleotide sequence analysis of pHTLV 707 indicated that the clone contained an open reading frame for a 60K mol. wt. protein including the upstream and entire pX IV region. A rabbit antibody raised against a synthetic decapeptide deduced from the nucleotide sequence at the carboxyl terminus of the pX IV region immunoprecipitated gp68, and also 80K and 40K proteins.
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PMID:Molecular cloning of cDNA encoding gp68 of adult T-cell leukaemia-associated antigen: evidence for expression of the pX IV region of human T-cell leukaemia virus. 299 47

The human T-cell lines MT-2 and MT-4 carry the human T-cell leukemia virus type I (HTLV-I). When MT-2 and MT-4 were infected with HTLV-III, the probable etiologic agent of the acquired immune deficiency syndrome (AIDS), rapid cytopathogenic effects and cytotoxicity were observed that made it possible to titrate the biologically active virus in a plaque-forming assay. The cytopathogenic effects were preceded by the rapid induction and increase of HTLV-III antigens as revealed by immunofluorescence and immunoprecipitation. Activities of HTLV-III were neutralized by the human antibodies against the virus when immunofluorescence and plaque assays were used. Essentially the same results were obtained with the lymphadenopathy-associated virus (LAV1).
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PMID:Infection of HTLV-III/LAV in HTLV-I-carrying cells MT-2 and MT-4 and application in a plaque assay. 299 81

We have prepared two new mouse monoclonal antibodies (MAbs) named TARM-34 (IgM) and TAG-34 (IgG1), that react with surface antigens of lines of human lymphocytes bearing a human T-cell leukemia virus type-I (HTLV-I). The characters of these antibodies are compared with those of anti-HTLV-1 gp21 MAb (TA-21, IgG1), anti-HTLV-I p19 MAb (GIN-14, IgG1) and human antibodies from patients with adult T-cell leukemia (ATL). An indirect membrane immunofluorescence assay showed that TARM-34, TAG-34 and TA-21 all reacted specifically with cell-surface antigens of HTLV-I-positive T- and B-cell lines and cultured peripheral blood lymphocytes from HTLV-I-infected adults. Radioimmunoassay showed that serum antibodies from the ATL patients interfered with the binding of TA-21 antibody to cells of the HTLV-I-positive T-cell line MT-2, but not with the bindings of TARM-34 and TAG-34 antibodies. TARM-34 and TAG-34 both precipitated a 34-kd glycoprotein (gP34), while TA-21 precipitated gp21 from a lysate of 3H-glucosamine-labelled MT-2 cells. TARM-34 and TAG-34 also precipitated the 34-kd protein from lysates of MT-2 and HUT 102 cells labelled with 125I- or 35S-cysteine. Interestingly, TARM-34 and TAG-34 also precipitated 35-kd protein from a lysate of other HTLV-I-positive cells (F-Taj cell line) derived from an ATL patient. TA-21 precipitated the 21-kd protein from the lysates of 35S-cysteine-labelled HTLV-IMT-2 virions, but TARM-34 and TAG-34 did not precipitate any protein from this lysate. TARM-34 lysed HTLV-I-bearing cells in the presence of rabbit complement. These results indicate that TARM-34 and TAG-34 both recognize a glycoprotein antigen that is expressed on the surface of HTLV-I-infected cells.
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PMID:A glycoprotein antigen detected with new monoclonal antibodies on the surface of human lymphocytes infected with human T-cell leukemia virus type-I (HTLV-I). 299 42

Human T-cell leukaemia virus (HTLV1/ATLV), which causes adult T cell leukaemia (ATL), is an infectious, lymphotrophic retrovirus unique for humans. The present study was undertaken to determine whether HTLV1 had any pathogenetic role for systemic lupus erythematosus (SLE). The incidence of antibodies to ATL cell-associated antigens (ATLA) in sera from patients with SLE and other collagen diseases was investigated by an indirect immunofluorescent cytoplasmic staining of an HTLV1-infected cell line (MT-1). A radioimmunoassay was also performed to detect antibodies to HTLV1 protein and crude membrane fraction derived from an HTLV1-producing cell line MT-2. Furthermore, an Epstein-Barr virus (EBV)-transformed B cell line (ES-1) was constructed from an SLE patient, which produced a monoclonal antibody (IgG, lambda) reactive to an HTLV1-related cell-membrane antigen expressed on MT-1 and MT-2 cells. The specific reactivity of the monoclonal antibody was analysed by an indirect immunofluorescent cell-membrane staining and a microcytotoxicity test. The incidence of anti-ATLA antibodies was not different among SLE and other collagen diseases. The monoclonal antibody produced by ES-1 stained and killed HTLV1-infected cell lines specifically, but did not react with other human lymphoid cell lines. This monoclonal antibody failed to react with peripheral blood mononuclear cells (PBMC), mitogen-induced T cell blasts, and iododeoxyuridine-treated T cells from SLE patients. Thus, a possible role of HTLV1 in the aetiology of SLE was not established.
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PMID:Production of a monoclonal antibody to a membrane antigen of human T-cell leukaemia virus (HTLV1/ATLV)-infected cell lines from a systemic lupus erythematosus (SLE) patient: serological analyses for HTLV1 infections in SLE patients. 299 59

The cross-reactivity of antibodies to adult T-cell leukemia (ATL)-associated antigens (ATLA) in human and monkey sera was investigated by indirect immunoperoxidase and immunoferritin methods using a human cell line (MT-2) carrying a type C virus (HTLV), two monkey cell lines (Si-1 and Si-3) carrying HTLV, and a monkey cell line (Si-2) carrying a type C virus isolated from an anti-ATLA-positive monkey. Anti-ATLA-positive but not-negative human and monkey sera gave positive immunoperoxidase reaction with all four virus-positive cell lines when studied by light microscopy. Electron microscopic findings revealed ferritin or peroxidase labeling of virus particles and plasma membranes of these four cell lines with antibody-positive but not-negative human and monkey sera. These results clearly indicate the cross-reactivity of anti-ATLA antibodies in human and monkey sera at light and electron microscopic levels, and the presence of antigenic determinants common to the surface of type C virus particles of human and monkey origin.
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PMID:Immunoelectron microscopic study on the cross-reactivity of antibodies to adult T-cell leukemia-associated antigens in human and monkey sera. 300 Jan 31


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