RNA Tumor Virus

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Jay A. Levy - One of the best experts on this subject based on the ideXlab platform.

  • Xenotropism: The elusive viral receptor finally uncovered
    Proceedings of the National Academy of Sciences of the United States of America, 1999
    Co-Authors: Jay A. Levy
    Abstract:

    Working with knowledge gained from pioneers in the RNA Tumor Virus field (2), the biologic activity of this NZB Virus ultimately was demonstrated in 1970 by cultivating NZB mouse embryo cells with hamster or rat Tumor cells containing a nonreplicating sequence of the murine sarcoma Virus (3). This procedure, using conventional MLV, leads to the rescue of the sarcoma Virus genome in the envelope coat of the replication-competent MLV (2). The newly formed transforming Virus pseudotype now has the host range of the “helper” MLV. SupeRNAtants from the NZB cell coculture demonstrated the presence of a replicating Virus that could induce foci of transformation in rat cells but not mouse embryo cells (3). The NZB MLV host range thus seemed limited to rat cells. Subsequent work demonstrated that the helper MLV visualized in the NZB mouse cells was infectious but was not infectious at all for mouse cells (i.e., complete block). It was infectious only for cells from heterologous species, including those of avian origin (Table 1). Similar Viruses were subsequently found in all laboratory strains of Mus musculus domesticus as …

M G Sarngadharant - One of the best experts on this subject based on the ideXlab platform.

  • natural antibodies to the structural t cell leukemia lymphoma retrovi patients in japan RNA Tumor Virus type c Virus radioimmunoassays japanese adult
    2016
    Co-Authors: V S Kalyanaraman, M G Sarngadharant, Y Nak, Y Ito, T Aoki, R C Gallotil
    Abstract:

    In Japan, adult T-cell leukemias and lymphomas are more common than in the United States and Europe, and in the southwest part of Japan these T-cell malignancy cases appear in clusters. Therefore, we investigated the involvement in these leukemias and lymphomas of the human T-cell leukemia Virus (HTLV) that was previously isolated in one of our laboratories from cultured T cells of some patients in the United States with leukemias and lymphomas involving relatively mature T cells. High titers of antibodies capable of quantitative precipitation of 125I-labeled p24, a well characterized core protein of HTLV, were detected in 12 of 12 patients with untreated adult T-cell leukemia (ATL). (One negative was a patient on chemotherapy.) Ten of the 12 positive samples were from an area where the disease is en- demic. Strong precipitating antibodies were also detected in five of seven cases of T-cell malignant lymphoma (TML) which differs from ATL by having fewer leukemic cells in the peripheral blood. High antibody titers were also observed in one of five cases of acute monoblastic leukemia and one of eight cases of chronic mye- logenous leukemia in the blast phase of the disease. Low to mod- erate titers of antibodies were detected in several categories of leukemia (two cases of blast-phase chronic myelogenous leukemia, two cases of acute lymphoblastic leukemia of the null-cell type, and one case of acute myelogenous leukemia). Among all categories of leukemias, except ATL and TML, more cases were negative than positive for anti-p24 activity. All of 79 sera from normal Japanese, including 39 collected from the endemic ATL area of southwest Japan, were negative for antibodies to HTLV p24. All the positive reactivities observed were highly specific to HTLV. The only com- petition observed in the precipitation of HTLV p24 was with HTLV or with cell lines expressing HTLV and not with various animal retroViruses or a large number of human and subhuman primate cell lines, not known to be producing HTLV. The data strongly indicate an association of HTLV with the increased in- cidence of ATL in parts of Japan, probably with other forms of leukemias in Japan, and, less commonly, with certain T-cell ma- lignancies in the United States.

  • primary structure analysis of the n human type c t cell leukemia Virus human RNA Tumor Virus bovine leukemia Virus retroVirus proteins
    2016
    Co-Authors: Stephen Oroszlan, M G Sarngadharant, V Gilden, Robert C Gallot
    Abstract:

    A human type C retroVirus (human T-cell leu- kemia (lymphoma) Virus; HTLV), recently isolated from young adult patients with cutaneous T-cell lymphoma or leukemia, was not detectably related to other known animal retroViruses in mo- lecular hybridization studies, by comparison of reverse transcrip- tase and the major core protein p24. The p24 core protein was purified to homogeneity. The amino acid composition, the COOH- terminal amino acid, and the NH2-terminal amino acid sequence of the first 25 residues of this major inteRNAl structural protein were determined. These results were then compared to the known structure of the inteRNAl core protein of other retroViruses. The compositional data reveal that HTLV p24 is chemically distinct from p30-p24 of other animal retroViruses, in agreement with the earlier immunological analyses. However, HTLV p24 shares the common NH2-terminal proline and COOH-terminal leucine of all mammalian type C viral p30s. In addition, like bovine leukemia Virus (BLV), HTLV lacks the common prolylleucylarginine tri- peptide and the larger conserved region found near the NH2 terminus of the other mammalian type C viral p30s. Align- ment of the amino acid sequence of HTLV p24 with previously determined sequences of other retroVirus proteins, including BLV p24, reveals statistically significant sequence homology only to BLV. The results reported here demonstrate that HTLV p24 is related to but chemically distinct from the major core protein of other retroViruses. Similarly, previous results showed that there was no immunological crossreactivity of the p24 protein and re- verse transcriptase of HTLV with other retroViruses, including BLV, and no nucleic acid sequence homology. However, the pres- ent results, combined with the common size of the p24 and reverse transcriptase, suggest that HTLV may be closer to BLV than any other known retroVirus.

Robert C Gallot - One of the best experts on this subject based on the ideXlab platform.

  • primary structure analysis of the n human type c t cell leukemia Virus human RNA Tumor Virus bovine leukemia Virus retroVirus proteins
    2016
    Co-Authors: Stephen Oroszlan, M G Sarngadharant, V Gilden, Robert C Gallot
    Abstract:

    A human type C retroVirus (human T-cell leu- kemia (lymphoma) Virus; HTLV), recently isolated from young adult patients with cutaneous T-cell lymphoma or leukemia, was not detectably related to other known animal retroViruses in mo- lecular hybridization studies, by comparison of reverse transcrip- tase and the major core protein p24. The p24 core protein was purified to homogeneity. The amino acid composition, the COOH- terminal amino acid, and the NH2-terminal amino acid sequence of the first 25 residues of this major inteRNAl structural protein were determined. These results were then compared to the known structure of the inteRNAl core protein of other retroViruses. The compositional data reveal that HTLV p24 is chemically distinct from p30-p24 of other animal retroViruses, in agreement with the earlier immunological analyses. However, HTLV p24 shares the common NH2-terminal proline and COOH-terminal leucine of all mammalian type C viral p30s. In addition, like bovine leukemia Virus (BLV), HTLV lacks the common prolylleucylarginine tri- peptide and the larger conserved region found near the NH2 terminus of the other mammalian type C viral p30s. Align- ment of the amino acid sequence of HTLV p24 with previously determined sequences of other retroVirus proteins, including BLV p24, reveals statistically significant sequence homology only to BLV. The results reported here demonstrate that HTLV p24 is related to but chemically distinct from the major core protein of other retroViruses. Similarly, previous results showed that there was no immunological crossreactivity of the p24 protein and re- verse transcriptase of HTLV with other retroViruses, including BLV, and no nucleic acid sequence homology. However, the pres- ent results, combined with the common size of the p24 and reverse transcriptase, suggest that HTLV may be closer to BLV than any other known retroVirus.

Geraldine L. Freeman - One of the best experts on this subject based on the ideXlab platform.

  • 19 – REVERSE TRANSCRIPTASE
    The Nobel Prize Winning Discoveries in Infectious Diseases, 2005
    Co-Authors: David Rifkind, Geraldine L. Freeman
    Abstract:

    Publisher Summary Transcription is the process by which a deoxyribonucleic acid (DNA) template codes for an ribonucleic acid (RNA) complement. It is because of the role of reverse transcriptase in RNA Tumor Virus replication, that reverse transcriptases are termed as retroViruses. The retroViruses as the family are comprised of a number of agents that infect both man, and animals. The alpharetroViruses cause leukemias and sarcomas in birds. The deltaretroViruses cause leukemias in man, primates and other animals. The lentiViruses infect a range of animals, including man, and characteristically attack, and depress the immune system. Human Immunodeficiency Virus 1 (HIV-1) is an important example as it causes Acquired Immunodeficiency Syndrome (AIDS) worldwide.

G Steven Martin - One of the best experts on this subject based on the ideXlab platform.

  • The road to Src
    Oncogene, 2004
    Co-Authors: G Steven Martin
    Abstract:

    More than a quarter of a century has elapsed since the identification of the c- src proto-oncogene. During that period, we have learned that cancer arises as the result of mutations in proto-oncogenes and Tumor suppressor genes, and we are now seeing the first fruits of these discoveries, in the form of targeted therapies directed against activated tyrosine kinases such as Bcr-Abl, c-Kit and the EGF receptor. But the discovery of the c- src proto-oncogene was in turn based on decades of study on an avian RNA Tumor Virus, Rous sarcoma Virus (RSV). Here I review the work that led up to the identification of the RSV transforming gene and its protein product, and how this information in turn led to the discovery of cellular Src.