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Biomedical subjects

M S Reitz

Publications and source records attributed to M S Reitz.

At least 145 records · Page 8Linked to original sources
PubMed1975

Transcription of 70S RNA by DNA polymerases from mammalian RNA viruses.

DNA polymerases purified by the same procedure from four mammalian RNA viruses, simian sarcoma virus type 1, gibbon ape lymphoma virus, Mason-Pfizer monkey virus, and Rauscher murine leukemia virus are capable of transcribing heteropolymeric regions of viral 70S RNA without any other primer. In this reconstituted system the enzymes from simian sarcoma virus type 1, Mason-Pfizer monkey virus, and Rauscher murine leukemia virus transcribe viral 70S RNA almost as efficiently as the DNA polymerase from the avian myeloblastosis virus, but gibbon ape lymphoma virus DNA polymerase is approximately three-to fivefold less efficient. Although there is a substantial difference among the sizes of these DNA polymerases (160,000 daltons for the avian myeloblastosis virus enzyme, 110,000 daltons for the Mason-Pfizer monkey virus enzyme, and 70,000 daltons for the mammalian type C viral polymerases), the ability to transcribe viral 70S RNA is a characteristic common to these enzymes.

Animals↗
PubMed1974

Systematics of RNA tumor viruses and virus-like particles of human origin.

[(3)H]DNA copies of avian, feline, murine, and primate RNA tumor virus genomes were synthesized in vitro by an RNA-dependent DNA polymerase reaction. These DNAs were hybridized to 60-70S RNA that had been purified from the viruses. The amount of the [(3)H]DNA hybridized yielded a measure of the genetic relatedness among the DNA preparations synthesized by the viruses. When many combinations of DNA and RNA were analyzed, the pattern of hybridization showed in some cases that the DNA copies of the viral RNA were related to each other in the same way that the natural hosts of the viruses are phylogenetically related. This pattern was observed only among the RNA leukemia viruses. The sarcoma component in sarcoma-leukemia viruses from rats and primates appeared to be unusually closely related. The mouse mammary carcinoma virus and two unclassified viruses (MPMV and Visna) appeared to be genetically distinct.A similar analysis of DNA synthesized by an RNA-dependent DNA polymerase associated with a viral-like particle obtained from the cytoplasm of human leukemic white blood cells demonstrated that this DNA occupied a space in the affinity pattern of leukemia viruses which is expected of a nucleic acid from a primate-type-C RNA tumor virus. This observation strengthens earlier evidence that components of RNA tumor viruses are associated with human leukemia.

Animals↗
PubMed1974

Mechanism of stimulation of murine type-C RNA tumor virus production by glucocorticoids: post-transcriptional effects.

We have previously shown that dexamethasone stimulates production of type-C virus from seemingly normal murine fibroblasts (BALB/3T3) and from transformed (Kirsten sarcoma-leukemia virus) nonproducing cells (BALB/K3T3) induced by 5-iododeoxyuridine. In this report, we further examine the mechanism of this effect by using BALB/K3T3 cells. Several observations suggest that this effect is post-transcriptional. The optimal stimulation by dexamethasone is obtained when dexamethasone is given 24 to 48 h after 5-iododeoxyuridine induction. Although this effect is late, time course experiments suggest that dexamethasone does not act to promote release of preformed virions. The stimulation by dexamethasone is blocked when cells are treated with cordycepin (3'-deoxyadenosine) during the first 24 h of induction, but not when cordycepin is added later. Conversely, interferon, which inhibits virus production, interferes with dexamethasone when it is added late or after removal of the steroid. The results of molecular hybridization experiments show that there is no detectable increase in Kirsten sarcoma-leukemia virus-specific RNA in dexamethasone-treated cells (with or without 5-iododeoxyuridine). The results of the time course studies, and the cordycepin, interferon, and hybridization experiments, suggest that the effect of dexamethasone on type-C virus production in this system is post-transcriptional.

Animals↗
PubMed1972

Stimulated normal human lymphocytes contain a ribonuclease-sensitive DNA polymerase distinct from viral RNA-directed DNA polymerase.

Ribonuclease-sensitive DNA synthesis is demonstrated in a cytoplasmic particulate fraction of normal human blood lymphocytes stimulated with phytohemagglutinin, but not in unstimulated lymphocytes. DNA polymerase purified from this fraction does not transcribe the heteropolymeric regions of 70S RNA from RNA tumor viruses, thus distinguishing this enzyme from the RNA-directed DNA polymerase (reverse transcriptase) found in oncogenic RNA viruses and human leukemic cells.

Centrifugation, Density Gradient↗
PubMed1969

Alpha-hydroxyglutarate oxidoreductase of Pseudomonas putida.

Oxidation of d-alpha-hydroxyglutarate to alpha-ketoglutarate is catalyzed by d-alpha-hydroxyglutarate oxidoreductase, an inducible membrane-bound enzyme of the electron transport particle [ETP; a comminuted cytoplasmic membrane preparation with enzymic properties and chemical composition resembling beef heart mitochondrial ETP (1)] of Pseudomonas putida P2 (P2-ETP). Treatment of P2-ETP with a nonionic detergent yields a preparation with the sedimentation characteristics of a soluble enzyme, but which retains an intact electron transport chain. Oxygen acts solely as a terminal electron acceptor and may be replaced by ferricyanide, 2,6-dichlorophenol indophenol, or mammalian cytochrome c. The oxidoreductase is specific for the d-isomer (K(m) = 4.0 x 10(-4)m for dl-alpha-hydroxyglutarate) and is distinct both from l- and d-malate dehydrogenases. Spectral studies suggest that the carrier sequence is substrate --> flavine or nonheme iron --> cyt b --> [cyt c] --> oxygen.

Alcohol Oxidoreductases↗
PubMedDate not supplied

Cell lines producing human T-cell lymphoma virus show altered HLA expression.

Human T-cell leukaemia/lymphoma virus (HTLV) can be identified in fresh and cultured T-lymphocytes from patients with adult T-cell malignancies. HLA typing of the peripheral blood lymphocytes and cultured cell lines from the patient from which the virus was originally isolated suggested the expression of additional HLA-A and -B locus antigens on the HTLV positive cultured T-cells that were not present on the EBV transformed B-cell line or on the peripheral blood lymphocytes. Peripheral blood lymphocytes (PBLs) and T-cell lines established from patients and cord blood lymphocytes, infected with virus by co-culture with T-cell lines, were typed for HLA antigens with alloantisera and in addition tested for reactivity with a monoclonal antibody (4D12) which recognizes a polymorphic HLA class-I antigen. In all HTLV positive cells, with demonstrable provirus replication, altered HLA alloantigen expression was observed. This may be explained by the observations reported in the accompanying paper which shows homology between the envelope gene region of HTLV and the region of an HLA-B locus gene which codes for the extracellular portion of a class I histocompatibility antigen.

Antigens, Surface↗
PubMedDate not supplied

Homology of human T-cell leukaemia virus envelope gene with class I HLA gene.

Human T-cell leukaemia virus (HTLV), first isolated in the United States from a patient with cutaneous T-cell lymphoma, is a unique horizontally transmitted retrovirus which is highly associated with certain adult T-cell malignancies. Also, HTLV can be transmitted in vitro to cord blood T-lymphocytes. In the accompanying paper it was shown that all T cells producing HTLV, whether cultured from infected persons or infected in vitro, bind a monoclonal antibody (4D12) which recognizes an epitope shared by certain cross-reactive class I major histocompatibility antigens. This antigen may account for the extra HLA-A and -B specificities detected in HTLV-infected cells using alloantisera. Because of the unusual findings of apparently inappropriate HLA antigens in HTLV infected cells, we had previously looked for rearrangement of class I-related genes in HTLV infected cells but failed to find any. Here, using molecular clones of HTLV and human major histocompatibility antigen DNA, we have shown homology between the envelope gene region of HTLV and the region of an HLA-B locus gene which codes for the extracellular portion of a class I histocompatibility antigen.

Antigens, Viral↗