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)

Interference to superinfection by murine leukemia viruses (MuLV) was analyzed in cells chronically infected with other MuLVs. A new sensitive focal immunofluorescence assay employing monoclonal antibodies was used to detect foci of virus infection in live cell monolayers. Monoclonal antibodies were chosen which reacted with the challenge virus but not with the interfering virus. The results obtained confirmed some of the findings of previous workers using Moloney sarcoma virus pseudotypes as challenge viruses on mouse and nonmouse cells. In addition, SC-1 mouse cells nonproductively infected with defective spleen focus-forming virus were found to be resistant to superinfection by recombinant dual-tropic viruses. Furthermore, results indicated that interference patterns between some pairs of viruses differed in different cell types. Thus, xenotropic MuLV blocked superinfection by recombinant dual-tropic viruses in SC-1 feral mouse cells, but not in two lines of NZB mouse cells. Also, in a Mus dunii tail fibroblast cell line some unique patterns of interference were observed. One ecotropic MuLV blocked infection by two xenotropic viruses and three recombinant dual-tropic viruses. Two other ecotropic viruses blocked infection by only one of the two xenotropic viruses tested. These two ecotropic viruses also differed from each other in their ability to block the three recombinant viruses. In addition, two strains of amphotropic MuLV also differed in their interference capacity. As expected, strain 1504A did not block any viruses tested, whereas strain 4070A surprisingly blocked one xenotropic and one ecotropic MuLV. The lack of homogeneity in interference patterns seen in the Mus dunii cells suggested either that a large number of heterogeneous virus receptors were present on this cell line or that interference in these cells might operate through a mechanism other than blocking of virus receptors by the envelope protein of the interfering virus.
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PMID:Different murine cell lines manifest unique patterns of interference to superinfection by murine leukemia viruses. 298 94

An immunological focus assay using monoclonal antibodies on live adherent in vitro cell lines was employed to detect and isolate different types of murine leukemia viruses (MuLVs) from spleen and thymus cells of young (less than 1 month of age) AKR/J mice. In agreement with earlier studies, ecotropic viruses were detected from cells of both tissues in all mice tested, although only trace levels of ecotropic MuLV infectious centers were found with thymus cells from mice of this age. Polytropic MuLVs were not detected in mice less than 3 weeks of age; however, between the ages of 3 and 4 weeks, polytropic viruses were detectable in assays of spleen cells from 50% of the mice. No polytropic MuLVs were detected in assays of thymocytes from any mice of this age. Several polytropic MuLVs obtained from spleens of young mice were further characterized. All of the isolates were infectious for both mink and SC-1 (feral mouse) cells, and exhibited interference properties typical of polytropic MuLVs. However, none of the viruses induced obvious cytopathic effects (CPE) on mink cells. All of the viruses appeared antigenically similar with regard to their reactivities to a panel of 12 monoclonal antibodies directed at envelope antigens of polytropic MuLVs. RNase T1-resistant oligonucleotide analysis of a polytropic MuLV from a 26-day-old mouse indicated that its entire env gene was derived from nonecotropic sequences while the remainder of its genome was indistinguishable from the ecotropic parent. The isolate thus exhibited a genome structure typical of Class II polytropic MuLVs and is the first example of this type of MuLV isolated from AKR/J mice. Examination of polytropic MuLVs derived from the spleens and thymuses of 5- to 6-month-old mice indicated that only 2 of 10 isolates examined induced CPE on mink cells. Furthermore, most of the CPE-negative viruses isolated from spleen and thymus cells of these mice exhibited in vitro host ranges and antigenic reactivities similar to isolates from young mice, suggesting that this type of polytropic MuLV may originate in the spleen, subsequently spread to other tissues, and persist throughout the preleukemic period. The detection of polytropic viruses in a large proportion of very young mice is in contrast to previous studies which have not detected polytropic virus production in AKR mice less than 5 to 6 months of age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of polytropic MuLVs from three-week-old AKR/J mice. 301 82

Various 3'-azido, 3'-amino, 2',3'-unsaturated, 2',3'-dideoxy, and 5-substituted analogues of pyrimidine deoxyribonucleosides have been prepared and tested against Moloney-murine leukemia virus (M-MULV), a mammalian T-lymphotropic retrovirus in vitro. Among these compounds, the 3'-azido analogues of thymidine, 2'-deoxy-5-bromouridine, and 2'-deoxy-5-iodouridine, the 2',3'-unsaturated analogue of thymidine and and 2'-deoxycytidine, and 2',3'-dideoxycytidine were found to be most active, with ED50 values of 0.02, 1.5, 3.0, 2.5, 3.7, and 4.0 microM, respectively. These active compounds were nontoxic to the host SC-1 cells up to 100 microM concentration. The 3'-azido analogues of thymidine and 2'-deoxy-5-bromouridine were also tested in vitro against HTLV-III/LAV/AAV ("AIDS" virus) and found to be significantly active, with ED50 values of 0.23 and 2.3 microM, respectively. The structure-activity relationships are discussed.
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PMID:Synthesis and antiviral activity of various 3'-azido, 3'-amino, 2',3'-unsaturated, and 2',3'-dideoxy analogues of pyrimidine deoxyribonucleosides against retroviruses. 364 84

A Mus dunni cell line has been developed that is permissive for all four classes of murine leukemia viruses (MuLV): ecotropic, amphotropic, xenotropic, and mink cell focus-forming viruses. The M. dunni cells contain fewer MuLV-related sequences than do feral or domestic mouse, rat, or mink cells. Infection of the line by ecotropic MuLV induces a distinct cytopathic effect, and the cells can be readily transfected by MuLV DNA. The M. dunni line has been used to isolate an endogenous MuLV from the SC-1 feral mouse cell line.
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PMID:A Mus dunni cell line that lacks sequences closely related to endogenous murine leukemia viruses and can be infected by ectropic, amphotropic, xenotropic, and mink cell focus-forming viruses. 609 93

LCV, a murine retrovirus released by L929 mouse cell fibroblasts, is non-infectious when inoculated into SC-1, mink, D-17 or Vero cells. Ultrastructural examination by thin sectioning, freeze-etching or negative staining revealed the absence, on the viral envelope, of the radially disposed spikes. Polyacrylamide gel electrophoresis of radiolabelled viral components showed the absence of the glycosylated protein gp70 as well as of the p15E cleavage product of the polyprotein precursor gPr90env. The premature loss of the gp70 molecule from LCV to the culture medium was ruled out since no peak of D-[14C]glucosamine-labelled glycoprotein was detected by affinity chromatography or immunoprecipitation of concentrated medium. The ultrastructural and biochemical results all supported the hypothesis that the absence of infectivity was due to the lack of gp70 glycoprotein in the envelope of LCV. A possible block at a translational or post-translational level was also investigated by immunofluorescence studies with antisera directed against ecotropic or xenotropic gp70; Moloney murine leukaemia virus-infected or NZB cells were used as positive controls for eco- or xenotropic viruses respectively. The absence of fluorescent stain in L929 cells further supported these results and suggested that LCV and the L929 parental cell line lack the uncleaved precursor and the final product of the env gene translation process.
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PMID:Ultrastructural and biochemical evidence that the L929 cell retrovirus lacks the env gene translation product. 619 51

We investigated the nature of a common tumor rejection antigen(s) in chemically induced murine fibrosarcomas. Two methylcholanthrene-induced fibrosarcomas, previously demonstrated to contain a common tumor rejection antigen(s), released infectious ecotropic murine leukemia virus and expressed the murine leukemia virus proteins, a glycoprotein with a molecular weight of 70,000 (gp70) and an envelope protein with a molecular weight of 15,000. To determine whether an antigen(s) specified by a murine leukemia virus might serve as a common tumor rejection antigen(s), primary cultures of syngeneic embryo cells or cultures of an allogeneic embryo cell line were infected with an endogenous ecotropic murine leukemia virus obtained from one of the cross-reacting fibrosarcomas; expression of infectious virus and/or viral proteins by infected and uninfected embryo cells was monitored and correlated with the results of transplantation protection tests. Uninfected allogeneic embryo cells (SC-1) did not release infectious virus or the viral protein gp70; mice immunized with SC-1 cells did not inhibit tumor growth. Uninfected syngeneic embryo cells did not release infectious virus but did release micrograms quantities of gp70 into supernatant fluids; mice immunized with uninfected syngeneic cells inhibited tumor growth in two of seven experiments. Virus-infected syngeneic and allogeneic embryo cells released both infectious ecotropic murine leukemia virus and gp70; mice immunized with virus-infected cells inhibited tumor growth in 11 of 11 experiments. Growth of the two cross-reacting fibrosarcomas was inhibited in mice immunized with virus-infected embryo cells. The results indicate that antigens coded for by endogenous murine leukemia virus may function as common tumor rejection antigen on chemically induced murine fibrosarcomas.
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PMID:Immunoprophylaxis of transplantable methylcholanthrene-induced murine fibrosarcomas by immunization with embryo cells expressing endogenous murine leukemia virus antigens. 627 79

By a biological assay system using phenotypically mixed ecotropic and xenotropic murine leukemia viruses, we investigated whether in the virions of a xenotropic virus there is N- or B-tropic Fv-1 determinant in active form. The existence of N-tropic Fv-1 determinant was demonstrated in SL-XT-1 xenotropic virus isolated from the spleen of a 3-month-old SL mouse, and the N-tropic Fv-1 tropism was confirmed by analysis of the phenotypically mixed viruses harvested from clonal SC-1 cells doubly infected with the SL-XT-1 and B-tropic ecotropic viruses. However, neither N- nor B-tropic Fv-1 determinant was demonstrated in any xenotropic viruses isolated from embryo cells of BALB/c, NZB, or DBA/2 mice, or Cas E #1-IU, and xenotropic-like virus isolated from a wild mouse.
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PMID:Fv-1 determinants in xenotropic murine leukemia viruses studied with biological assay systems: Isolation of xenotropic virus with N-tropic Fv-1 activity in the cryptic form. 628 53

During the course of serial passage of 50 human xenografts in the athymic mouse over a period of 5 years we have observed two cases of induction of sarcomas in the murine stromal tissue associated with the human xenografts. Both times the growth of the murine sarcomas overtook that of the human xenograft. This change was monitored by analysis of the lactate dehydrogenase isozyme profile and histology of each passage of the human xenografts in the athymic mice. The two murine sarcomas were subsequently established in tissue culture. The sarcoma cell lines were found to be malignant by morphological and growth characteristics and were tumorigenic. They contained large amounts of murine leukemia virus when assayed for reverse transcriptase activity by infection of mouse SC-1 cells and BALB/c and NIH Swiss fibroblasts with filtered supernates, and some type C virus particles were observed by electron microscopy in tumor tissues. However, we were unable to demonstrate the presence of murine sarcoma virus by in vitro transformation of fibroblasts or sarcoma formation in vivo will cell free filtrates. Preliminary biochemical data indicate that the sarcomas are extremely high in plasma membrane ATP phosphohydrolase.
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PMID:Induction of sarcomas in athymic mice. 628 53

Chromosome-mediated transfer of murine leukaemia (MuLV) and murine sarcoma (MuSV) virus genetic information to uninfected recipient cells was investigated. Metaphase chromosomes from AKR MuLV-infected SC-1 mouse cells were incubated with NIH/3T3 cells. After several passages (1 to 3 weeks), infectious virions exhibiting reverse transcriptase activity and the characteristic host range of ecotropic, N-tropic AKR virus appeared in the supernatant fluids of the treated cells. Restriction endonuclease analysis of genomic DNA from transfected cells indicated that AKR proviral DNA was associated with the high molecular weight DNA of the host. These results demonstrate that the AKR MuLV genome can be stably transferred to uninfected recipient cells via isolated metaphase chromosomes. Although AKR virions are not able to infect heterologous cells, chromosome-mediated transfection resulted in the establishment of productive AKR MuLV infection in mink cells. Thus, the use of chromosomes to transfer virus genes can circumvent the natural host restriction barrier. In other experiments, it was shown that normal NIH/3T3 cells were transformed after exposure to metaphase chromosomes isolated from an MuSV-infected, non-producer line. Foci were detected 14 to 21 days after chromosome treatment and were shown to contain true viral transformants since transforming virus was produced after superinfection with MuLV.
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PMID:Transfer of murine leukaemia and murine sarcoma virus genetic information by transfection with isolated metaphase chromosomes. 629 50

We studied the infectivity of endogenous ecotropic murine leukemia virus genomes contained in high-molecular-weight DNA prepared from virus-free cells of the AKR-2B line, and from RF, BALB/c, B6, and (BALB/c x B6)F(1) mouse embryo cells. When DNA prepared from virus-free AKR-2B cells was transfected into NIH-3T3 cells, no virus-positive cultures were observed, a result consistent with previous reports. However, when DNAs from virus-free AKR-2B cells or virus-free cells containing the RF/J or BALB/c ecotropic proviruses were transfected into chicken embryo cells that were then cocultivated with SC-1 (mouse) cells, virus-positive cultures were recovered. The specific infectivities of the AKR provirus(es) contained in virus-free cells and the molecularly cloned Akv-1 provirus were similar when chicken embryo cells were used as primary recipients. Virus-positive cultures were also observed when secondary mouse embryo cells were used as recipients for DNA from virus-free AKR-2B and RF/J cells. The transfected chicken embryo-SC-1 cultures produced XC-positive murine leukemia virus that is N-tropic. Virus-positive recipient cultures were observed 10- to 100-fold more frequently when AKR-2B DNA was used than when BALB/c DNA was used as the donor DNA. Our studies indicate that some nonexpressed ecotropic murine leukemia virus proviruses are activated upon transfection into chicken embryo cells. Such studies suggest that there are different factors governing the expression of murine leukemia virus after transfection into established cell lines (NIH-3T3) and into nonestablished secondary cultures (chicken and mouse).
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PMID:Activation of nonexpressed endogenous ecotropic murine leukemia virus by transfection of genomic DNA into embryo cells. 630 Apr 65


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