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 new antiviral substance phosphonoformate (PFA) has been tested in a cell-free system for its effect on reverse transcriptases from an avian retrovirus (avian myeloblastosis virus, AMV) and from mammalian retroviruses (Rauscher leukaemia virus, RMuLV; bovine leukaemia virus; baboon endogenous virus; simian sarcoma virus; visna virus). The observed inhibitory effect of PFA has been compared with that of a structurally related substance, phosphonoacetate (PAA). Phosphonoformate, at a concentration of 100 microM, reduced the activities of all the above mentioned polymerases by 90% when (rA)n.(dT)10 was used as a template/primer. The dose-response curves for AMV and RMuLV polymerases primed with (rA)n.(dT)10 showed PFA to be a 1000-fold more active than PAA; the RMuLV polymerase activity was reduced to 50% after incubation with 0.7 microM-PFA and 0.7 mM-PAA, respectively. There was no difference in PFA inhibition of virus-associated and purified reverse transcriptase activity. Results with various synthetic templates showed that both the RNA- and the DNA-dependent polymerase activities of reverse transcriptase were inhibited by PFA. The endogenous polymerase activity of AMV was inhibited to 50% at 100 microM-PFA, while PAA had no effect. The PFA inhibition was dependent on whether Mg2+ or Mn2+ was used as divalent cation in the assay. Phosphonoformate arrested DNA synthesis immediately after being added to the assay system. The mechanism of inhibition of the AMV polymerase was non-competitive with respect to substrate and template and the apparent inhibition constants were 16 microM and 9 microM, respectively.
J Gen Virol 1979 Nov
PMID:Phosphonoformate inhibits reverse transcriptase. 9 44

Bone marrow of leukaemic patients, non-leukaemic patients and normal individuals were co-cultivated with the canine cell line A7573. These co-cultures were screened for retrovirus antigens by means of the indirect cytoplasmic immunofluorescence assay (IFA). Rabbit antisera directed against the major structural protein (p30) of woolly monkey (simian) sarcoma leukaemia virus (grown in human lymphoid cells) and Rauscher murine leukaemia virus were used for testing. After 2 months in culture, 6 of 17 co-cultures containing cells from leukaemic patients showed positive staining in the IFA with the anti-simian virus serum. In control dog cells fluorescence was never observed. Five of the six positive cultures were derived from leukaemic children. One of 12 co-cultures of the non-leukaemic group and one of nine normal bone marrow co-cultures were positive with the simian virus antiserum. None of the 38 co-cultures stained positive in the IFA with Rauscher virus antiserum. Absorption of the simian virus antiserum with calf serum or mouse mammary tumour virus had no dramatic effect in the IFA on positive control cells or on cells of a positive co-culture. However, absorption with purified simian virus (grown in rat cells) completely abolished these fluorescence reactions. The results provide evidence that simian sarcoma-leukaemia virus related information was present in the original bone marrow samples and that co-cultivation with permissive mammalian cells enabled the detection of virus footprints.
J Gen Virol 1979 Dec
PMID:Type-C virus antigen detection in co-cultures of human leukaemic bone marrow and dog cells. 9 49

Relatives of probands with histologically confirmed Alzheimer's disease had excessive morbidity from Alzheimer's disease, Down's syndrome, and hematologic malignancies. These associations coupled with two previously reported ones, the indistinguishable histopathological changes in brain in Alzheimer's disease and Down's syndrome, and the 20-fold increased incidence of leukemia among persons with Down's syndrome, are evidence that some instances of those disorders are associated with a unitary genetic etiology. The genetic defect may be expressed through disorganization of microtubules. Other evidence suggests that the same process may be involved in aging and in other chromosomal aberrations.
Arch Gen Psychiatry 1977 Aug
PMID:The genetics of Alzheimer's disease: associations with hematologic malignancy and Down's syndrome. 14 59

The protein and glycoprotein composition of Kirsten murine leukaemia-sarcoma virus (KiMSV(KiMuLV) was studied using SDS-polyacrylamide gel electrophoresis. Twenty-three polypeptides and three glycoproteins were detected following electrophoresis by staining with Coomassie blue and PAS or by autoradiography of isotopically labelled virus. Protein components were assigned positions in the virus particle, envelope, nucleoid or intermediate area based on iodination with lactoperoxidase and sedimentation in potassium citrate equilibrium gradients. The KiMSV (KiMuLV) envelope contained 11 polypeptides and three glycoproteins. The virus nucleoid and intermediate area were each composed of six proteins. The protein composition of KiMSV(KiMuLV) was highly reproducible when virus was harvested from cells of the same subcluture generation. However, the protein profiles were altered with repeated in vitro passages of the virus-producing cell line.
J Gen Virol 1975 Jan
PMID:Proteins of Kirsten murine leukaemia-sarcoma virus: localization within the virus particle by iodination and fractionation techniques. 16 14

N-tropic Friend leukaemia virus (FLV) was serially passaged in a B-type C57BL/6 mouse cell line, YH-7. After a single passage, the infectious efficiency of FLV in the restrictive YH-7 cells was significantly increased. This adapted character of FLV could be reversed by a single passage in permissive N-type MLg cells. The true host range conversion from N to NB was accomplished after eleven to twelve passages in YH-7 cells. In contrast, the host range conversion of N-tropic murine sarcoma pseudotype, MuSV(FLV), took place after two passages.
J Gen Virol 1975 Oct
PMID:Adaptation of N-tropic Friend leukaemia virus and its murine sarcoma virus pseudotype of non-permissive B-type C57BL/6 mouse cell line. 17 32

Mouse and cat cells were each examined for the mode of restriction of endogenous xenotropic oncornavirus. Murine xenotropic helper virus (MuX) and its pseudo-type of Moloney murine sarcoma virus (MSV(MuX)) were grown in cat cells to high titre. MuX alone did not replicate in any mouse cell tested including normal or transformed outbred Swis 3T3 cells or SC-I cells, but did grow in a variety of other mammalian cells. MSV(MuX) was not able to achieve that intracellular state from which it could be rescued by mouse leukaemia virus (MuLV) in any mouse cell tested with the exception of SC-I cells. Detection of MSV(MuX) foci with appropriate helper virus was as sensitive in SC-I cells as in the cells of several other species. Sequential passage of MSV(MuX) virus complex in SC=I cells resulted in a loss of infectious sarcoma and helper viruses, but transformed, MSV rescuable cells were retained. If cat embryo cells were infected with either the feline endogenous xenotropic virus (FeX) or its MSV pseudotype (MSV(FeX), two analogous states of restriction were observed. FeX alone did not replicate in cat cells as measured by release of progeny virus or by FeX group-specific antigen induction. Cat cells could be susceptible or insusceptible to the entry of MSV(FeX) as measured by MSV rescue with appropriate ecotropic feline leukaemia virus. The sensitivity of detection of MSV(FeX) foci in some cat cells in the presence of feline ecotropic virus was comparable to that exhibited by cells of other mammalian species. A single strain of cat cells underwent a change in its restrictive capacity for MSV(FeX) on prolonged passage. Late passage cat cells became very insusceptible to MSV(FeX) but not to other pseudotypes of MSV. Infectious FeX or its group-specific antigens were not detected in the insusceptible cells. The major glycoprotein of FeX did appear as a surface antigen of the insusceptibel cells. It is apparent that two levels of cellular restriction can be distinguished in each of two mammalian cell systems by the susceptibility to penetration of MSV coated with endogenous xenotropic oncornavirus.
J Gen Virol 1975 Oct
PMID:Two levels of restriction by mouse or cat cells of murine sarcoma virus coated by endogenous xenotropic oncornavirus. 17 36

An assay is described for feline leukaemia virus pseudotypes of murine sarcoma virus which increased the virus titre by about 100-fold over conventional assays. The titre is independent of dilution and no secondary focus formation occurs. The assay may be used to study virus neutralization and to detect and type feline leukaemia virus in feline embryo cells by interference.
J Gen Virol 1976 Apr
PMID:An improved assay for feline leukaemia virus pseudotypes of murine sarcoma virus. 17 26

Scanning electron microscopy of AKR cells chronically infected with AKR mouse leukaemia virus revealed that the number of budding virions was greatly increased in interferon-treated cells. These results, together with previous biochemical findings, suggest that in this system, interferon inhibits a late stage of virus assembly or release.
J Gen Virol 1977 Feb
PMID:Interferon inhibits mouse leukaemia virus release: an electron microscope study. 19 Mar 48

Five temperature-sensitive mutants (ts I to 5) were isolated from a stock of the Moloney strain of murine sarcoma leukaemia virus complex which had been mutagenized by ultraviolet irradiation or N-methyl-N'-nitro-N-nitrosoguanidine. In mouse cells at the non-permissive temperature the mutants formed fewer foci of transformed cells than at the permissive temperature. The ts mutants were characterized by testing: (I) murine leukaemia virus (MuLV) clones from the ts complex, (2) the effect of additional wild type MuLV on focus formation, (3) focus formation in rat cells and (4) focus formation with pseudotypes rescued from non-producer cells. Two mutants (ts 1 and ts 3) were found to be ts MuLVs which did not possess heat labile virion proteins and were not ts in post-penetration helper functions necessary for the fixation of sarcoma virus transformation. The remaining three mutants (ts 2, ts 4 and ts 5) were ts murine sarcoma viruses which, however, showed no temperature-sensitive effect on the maintenance of transformed cell morphology nor on colony forming efficiency in soft agar.
J Gen Virol 1977 Aug
PMID:Isolation and preliminary characterization of temperature-sensitive mutants of the murine sarcoma leukaemia virus complex. 19 2

Some morphological, biological, immunological and biochemical characterizations of a virus, rat helper virus pseudotype Kirsten sarcoma virus, KiMSV(RHHV), have been presented here. KiMSV(RHHV) has a type C virus ultrastructure. It is strictly rat tropic and is able to transform rat cells in vitro. The possibility of its being a xenotropic mouse virus has been carefully ruled out by exhaustive analyses of host range and immunological studies. Antigenically KiMSV(RHHV) demonstrates cross reactivity with an antiserum specific against rat leukaemia virus, no cross reactivity with antiserum against Moloney leukaemia virus, and only minor cross reactivity with antiserum against cat leukaemia virus. Analysis of virus proteins and glycoproteins by equilibrium acrylamide gradient gel electrophoresis showed that the virus complex possesses both a gp70 fraction and a p30 fraction. KiMSV(RHHV) sediments isopycnically in a linear sucrose gradient at 1.145 to 1.155 g/ml and possesses RNA and reverse transcriptase activity.
J Gen Virol 1978 Feb
PMID:Properties of a transforming virus, KiMSV(RHHV), isolated from a co-culture of rat HTC-H1 cells with K-NRK cells. 20 53


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