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

Leukemic cells of AKR mice contain as constituents of their membranes the murine leukemia virus envelope protein gp70 and the precursor polyprotein of the viral internal (core) structural proteins. Both gp70 and the core polyprotein are represented on the cell surface as glycoproteins, as evidenced by incorporation of [3H]glucosamine into their structure and the binding of these proteins to lectins. The glycosylated core polyprotein exists in at least two serologically distinguishable forms: the 95,000-dalton polyprotein reacts with antisera prepared against the viral proteins p30, p12, and p10, whereas the 85,000-dalton polyprotein reacts with antisera prepared against the viral proteins p30 and p12, but not p10. Additional heterogeneity in these cell surface polyproteins has been observed wtih leukemias induced by exogenous leukemia viruses. Spontaneous leukemia cells of AKR mice invariably express gp70 and the core polyprotein on their cell surface; normal thymocytes of young AKR mice express gp70, but not the core polyprotein on their surface.
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PMID:Viral proteins expressed on the surface of murine leukemia cells. 6 23

The intracellular processing of the murine leukemia virus envelope glycoprotein precursor Pr85 to the mature products gp70 and p15e was analyzed in the mouse T-lymphoma cell line W7MG1. Kinetic (pulse-chase) analysis of synthesis and processing, coupled with endoglycosidase (endo H) and neuraminidase digestions revealed the existence of a novel high molecular weight processing intermediate, gp95, containing endo H-resistant terminally glycosylated oligosaccharide chains. In contrast to previously published conclusions, our data indicate that proteolytic cleavage of the envelope precursor occurs after the acquisition of endo H-resistant chains and terminal glycosylation and thus after the mannosidase II step. In the same W7MG1 cell line, the type and order of murine leukemia virus envelope protein processing events was identical to that for the mouse mammary tumor virus envelope protein. Interestingly, complete mouse mammary tumor virus envelope protein processing requires the addition of glucocorticoid hormone, whereas murine leukemia virus envelope protein processing occurs constitutively in these W7MG1 cells. We propose that all retroviral envelope proteins share a common processing pathway in which proteolytic processing is a late event that follows acquisition of endo H resistance and terminal glycosylation.
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PMID:A novel intermediate in processing of murine leukemia virus envelope glycoproteins. Proteolytic cleavage in the late Golgi region. 131 32

Human Immunodeficiency Virus type 1 (HIV-1) infects CD4+ T lymphocytes and various other cell types, including B cells. Since HIV-1 seropositive individuals have high numbers of B cells carrying Epstein-Barr Virus (EBV), and are at high risk for development of EBV-associated lymphoproliferative diseases, we studied the mode of HIV-1 infection in four EBV-positive lymphoblastoid B-cell lines (LCLs) as well as some molecular and biological features of the B cells infected by both viruses. We found that LCL cells were successfully infected in vitro by HIV-1, despite the lack of CD4 antigen expression on the cell membrane. LCL cells displayed a persistent, productive, and non-cytopathic infection. Moreover, HIV-1 infection induced reactivation of EBV latent genomes in one cell line. Following HIV-1 infection, LCL cells showed a decrease in B-cell activation markers CD23 and CD39, and an increase in CD10 immature B-cell antigen. Not all cells in each LCL expressed HIV-1 antigens, but all CD10+ cells also co-expressed the HIV-1 envelope protein gp 120. Furthermore, HIV-1 infected LCL cells grew as disperse suspensions, and formed more agar colonies than control, non-HIV-1-infected LCLs. These findings raise the possibility that HIV-1 might play a role in EBV reactivation, and in B-cell lymphoma pathogenesis in AIDS patients.
Leukemia 1992
PMID:Morphological and phenotypical changes in EBV positive lymphoblastoid cells infected by HIV-1. 131 75

Bovine leukemia virus is horizontally transmitted mainly through infected cells by direct blood transfer. In this report, a cloned bovine leukemia virus (BLV) provirus was examined for its infectivity by direct inoculation into sheep. One hundred micrograms of plasmid DNA containing a complete provirus was mixed with a cationic liposome solution and injected intradermally into five sheep at three different locations. Seroconversion occurred 1 to 2 months after injection as demonstrated by immunodiffusion, indirect ELISA (for the gp51 envelope protein), and blocking ELISA (for gp51 and the major capsid protein, p24). These results demonstrate that BLV infection can be efficiently initiated by direct transfection into sheep. This approach should thus facilitate investigation of the involvement of BLV genetic determinants in the induction of leukemia in ruminants.
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PMID:In vivo transfection of bovine leukemia provirus into sheep. 132 2

We have isolated a cDNA (H52) of 2.8-kb-long encoding an 80-kDa mouse melanoma Ag that is defined by a syngeneic anti-B16 melanoma mAb with an ability to block anti-melanoma cytotoxic T cell responses. H52 transfectants were brightly stained with the antibody, and the 80-kDa molecule was immunoprecipitated from the transfectants. Northern blot analysis showed that this transcript was detected in mouse melanoma cells of C57BL/6 and DBA/2 origin, C1300 A/J neuroblastoma, L cell (C3H) and EL-4 T lymphoma (C57BL/6), faintly in BW5147 (AKR) T lymphoma, but not in other tumors, such as S913 fibrosarcoma (C57BL/10), NIH3T3, 70 Z/3 pre-B lymphoma, and P3U1 plasmacytoma (BALB/c). Since the transcripts were not found in normal C57BL/6 tissues of fetus, newborn, and adult origin, the H52 expression is associated with transforming phenotypes. However, no tissue- or cell type-specific expression was observed. Nucleotide sequence analysis has clearly demonstrated that H52 cDNA encodes the full length of the env gene and long terminal repeat region of endogenous ecotropic murine leukemia provirus of AKV-type, which is defective in C57BL/6. The H52 envelope protein has several amino acid changes compared to those of AKV, one of which is in the env 14 peptide region preferentially associated with MHC molecule, suggesting the possible reason for the difference of antibody reactivity even in H52-positive tumors. We also demonstrate that CTL against H52 transfectant kills B16 melanoma. Thus, the above results are direct evidence that even the endogenous self molecule, when constitutively expressed, does act as a tumor Ag.
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PMID:Molecular cloning and characterization of the gene encoding mouse melanoma antigen by cDNA library transfection. 138 36

Neonatal BALB/c mice were inoculated (ip) with a recombinant Moloney murine leukemia virus-TB. Majority of the inoculated mice developed lymphoma within 5-7 months post infection. The cells from splenic lymphomas were cultured and 3 continuous cell lines (GP1, GP2 and GP3) developed. GP1 was single cell cloned and characterized. Based on Thy 1.2 (98.4%) phenotypic marker, the cell line was categorized as T cell line. The percent positivity for different cell surface markers on analysis with FACS was 98.4, 4.8, 5.5, 2.2, 1.8, 1.2 and 9.5 for Thy 1.2, mu, L3T4, Lyt2, Ia, IL2R and PNA receptor, respectively. A total of 16.5% GP1 cells was also positive for Moloney murine leukemia virus envelope protein (gp 70). Incomplete retrovirus like particles were demonstrated in the cytoplasm of GP1 cells by electron microscopy. The cell line on inoculation(ip) in neonatal BALB/c mice produced lymphomic lesions in almost all the vital organs of the mice.
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PMID:Characterization of a continuous lymphocyte cell line derived from BALB/c mice inoculated with a recombinant Moloney murine leukemia virus-TB. 145 11

The human T-cell leukemia virus type I (HTLV-I) envelope protein is synthesized as a gp61 precursor product cleaved into two mature proteins, a gp45 exterior protein and a gp20 anchoring the envelope at the cell membrane. Using N-glycosylation inhibitors and site-directed mutagenesis of the potential glycosylation sites, we have studied the HTLV-I envelope intracellular maturation requirements for syncytium formation. We show here that experimental conditions resulting in the absence of precursor cleavage (tunicamycin, monensin treatments, and use of inhibitors of the reticulum steps of the N glycosylations) also result in no cell surface expression of envelope protein. The lack of syncytium formation observed in these cases is thus explained by incorrect intracellular transport. When the precursor is cleaved in the Golgi stack (no treatment or treatment with inhibitors of the Golgi steps of the N glycosylations), it is transported to the cell surface in all the cases examined. Syncytium formation is markedly reduced, however, when Golgi glycosylations are incorrect, which shows that the sugar moieties are involved in the envelope functions. Site-directed mutagenesis demonstrates that each of the five potential glycosylation sites is actually glycosylated. Glycosylation of sites 1 and 5 is required for normal maturation, whereas that of sites 2, 3, and 4 is dispensable. Glycosylation of each site, however, is required for normal syncytium formation. Altogether, the restraints exerted by the cell for the HTLV-I envelope to be transported and functional are very high, which might play a role in the observed conservation of the envelope amino acid sequence between various strains.
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PMID:Human T-cell leukemia virus type I envelope protein maturation process: requirements for syncytium formation. 153 Sep 80

High sequence variability in the envelope gene of human immunodeficiency virus has provoked interest in nonenvelope antigens as potential immunogens against retrovirus infection. However, the role of core protein antigens encoded by the gag gene in protective immunity against retroviruses is unclear. By using recombinant vaccinia viruses expressing the Friend murine leukemia helper virus (F-MuLV) gag gene, we could prime CD4+ T-helper cells and protectively immunize susceptible strains of mice against Friend retrovirus infection. Recovery from leukemic splenomegaly developed more slowly after immunization with vaccinia virus-F-MuLV gag than with vaccinia virus-F-MuLV env; however, genetic nonresponders to the envelope protein could be partially protected with Gag vaccines. Class switching of F-MuLV-neutralizing antibodies from immunoglobulin M to immunoglobulin G after challenge with Friend virus complex was facilitated in mice immunized with the Gag antigen. Sequential deletion of the gag gene revealed that the major protective epitope was located on the N-terminal hydrophobic protein p15.
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PMID:Protection against Friend retrovirus-induced leukemia by recombinant vaccinia viruses expressing the gag gene. 153 53

Low toxic and synthetic adjuvants were investigated in the induction of protective immunity against Friend murine retrovirus-induced erythroleukaemia by immunization with inactivated Friend murine leukaemia helper virus (F-MuLV). 6-O-(2-tetradecyl-hexadecanoyl)-N-acetylmuramyl-L-alanyl-D-isoglutamine (B30-MDP) showed a significant enhancement of the protective immunity against Friend virus-induced erythroleukaemia not only in H-2a/b mice known to make good immune responses to F-MuLV envelope, but also in H-2a/a mice which are usually unable to respond to F-MuLV envelope protein. Another analogue of N-acetylmuramyl-D-isoglutamine (MDP), N alpha-acetylmuramyl-L-alanyl-D-isoglutaminyl-N epsilon-stearoyl-L-lysine [MDP-Lys(L18)], which has been shown to enhance non-specific protective activity against bacterial and viral infections, however, showed no adjuvant activity in the present system. A combined adjuvant of the synthesized mycobacterial cord factor, trehalose dimycolate (TDM) and detoxified bacterial endotoxin, monophosphoryl lipid A from Salmonella minnesota, gave good protection which was comparable to complete Freund's adjuvant in both H-2a/b and H-2a/a mice.
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PMID:Use of low toxicity adjuvants and killed virus to induce protective immunity against the Friend murine leukaemia retrovirus-induced disease. 157 22

Several aspects of turnover and degradation of cell membrane proteins were studied in an NIH 3T3 cell clone expressing the env gene of Moloney murine leukemia virus ts1. Both internalization and shedding of the extracellular domain of the envelope protein gp70 occurred at the cell surface, albeit, in the case of shedding, only a very small fraction of gp70 was shed. The turnover rate of gp70 at the cell surface was similar to that of the same protein in the postendoplasmic reticulum intracellular compartment. In the presence of L-methionine methyl ester, the transmembrane domain of the envelope protein Prp15E was degraded faster than gp70.
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PMID:Studies on compartmentation and turnover of murine retrovirus envelope proteins. 158 31


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