Widespread Presence, in Chickens, of DNA Complementary to the RNA Genome of Avian Leukosis Viruses

Baluda, M A

doi:10.1073/pnas.69.3.576

Cited by 139 publications

(83 citation statements)

References 21 publications

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“…The isolation of cellular RNA and DNA, the isolation of 35S[3H]RNA from purified virions labeled with [3H]uridine and [3H]cytidine, and the hybridization of viral RNA with cellular DNA either on filters when RNA was in excess or in liquid when DNA was in excess, and the separation of single-and double-stranded nucleic acids by hydroxylapatite chromatography followed published procedures (19)(20)(21)(22) The hybridization conditions are described in legend of Fig. 1.…”

mentioning

confidence: 99%

Host induced alteration of avian sarcoma virus B-77 genome.

Shoyab¹,

Markham²,

Baluda³

1975

Proc. Natl. Acad. Sci. U.S.A.

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The genome of an avian oncornavirus was altered after infection of a heterologous host. This was studied with avian sarcoma virus B-77 in duck embryonic fibroblasts (DEF) and chicken embryonic fibroblasts (CEF). To detect alteration of the viral genome, we hybridized 35S B-77 RNA with normal duck DNA by either one of two techniques: when viral RNA was in excess and when DNA was in excess. The RNA of B-77 passaged only in gs-chf-CEF does not have homology with duck DNA. However, after several passages of B-77 through DEF the viral genome acquired duck specific RNA sequences. After 4 and 10 passages, B-77 RNA acquired 2.2 and 6.6%, respectively, complementarity to normal duck DNA. The duck specific RNA sequences were found to be covalently linked to the B-77 RNA genome. Also, the host specific sequences acquired by the virus appear to be from a region of the duck DNA which is repeated four to six times per cell. After 5 back passages in CEF some of the duck specific RNA sequences in the viral genome were lost.Avian oncornaviruses have the ability to be modified by the host through which they are passaged. Even Rous sarcoma virus (RSV) may have had to be adapted to induce tumors and replicate in chickens (1). After the isolation of chicken tumor no. 1 by Rous in 1911, the tumor cells could cause sarcomas only in chickens of the same strain as that in which the tumor originated and only by inoculation of large numbers of tumor cells. Subsequently, tumors could be induced in other strains of chickens but only after several more passages could sarcomas be induced by a cell-free filtrate. After more than 60 years of laboratory manipulations, RSV can now rapidly induce tumors in a wide host range including primates (2, 3). DuranReynals reported that after several passages in ducks, a duck adapted variant of RSV appeared (4). In addition to the ability to cause tumors in ducks, the duck-adapted virus had acquired new tissue affinities causing tumors in bone, skin, and digestive tract, whereas the original RSV did not. Furthermore, the duck-adapted virus had altered surface antigenic properties. A similar phenomenon has also been noted with RSV that has been rescued from transformed rat cells (5-12). These findings led Altaner and Temin (6) to suggest that the alteration of physical and biological properties in the virus may reflect recombination between viral and host genetic material. Host-induced alterations of murine sarcoma viruses have also been reported after passage in rat cells (13). Kirsten and Harvey sarcoma viruses appear to contain murine and rat oncornavirus specific RNA sequences but these sequences have Abbreviations: DEF, duck embryo fibroblasts; CEF, chicken embryo fibroblasts; RSV, Rous sarcoma virus; AMV, avian myeloblastosis virus; Cot, nucleotide concentration (mol/l) X time (sec); TCA, trichloroacetic acid.1031 not been shown to be covalently linked. Also, in those studies the DNA probe synthesized in vitro with reverse transcriptase may have contained cellular as well as viral sequences sin...

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confidence: 99%

Host induced alteration of avian sarcoma virus B-77 genome.

Shoyab¹,

Markham²,

Baluda³

1975

Proc. Natl. Acad. Sci. U.S.A.

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“…Preparations from noninfected cells gave a 14-fold lower value which was still significantly above background. Since virus-specific DNA sequences are present in uninfected chicken cells (23)(24)(25) and virus-specific RNA occurs in noninfected fibroblasts from certain chicken embryos (26), these in vitro results may be meaningful.…”

Section: Resultsmentioning

confidence: 99%

In Vitro Synthesis of Rous Sarcoma Virus-Specific RNA is Catalyzed by a DNA-Dependent RNA Polymerase

Rymo

Parsons

Coffin

et al. 1974

Proc. Natl. Acad. Sci. U.S.A.

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Synthesis of Rous sarcoma virus RNA was examined in vitro with a new assay for radioactive virus-specific RNA. Nuclei from infected and uninfected cells were incubated with ribonucleoside [a-$'2Ptriphos-phates, Mn++, Mg++ and (NH4)2SO4. Incorporation into total and viral RNA proceeded with similar kinetics for up to 25 min at 37°. About 0.5% of the RNA synthesized by the infected system was scored as virus-specific, compared to 0.03% of the RNA from the tuninfected system and 0.005% of the RNA synthesized by monkey kidney cell nuclei. Preincubation with DNase or actinomycin D completely suppressed total and virus-specific RNA synthesis. a-Amanitin, a specific inhibitor of eukaryotic RNA polymerase Il. completely inhibited virus-specific RNA synthesis, while reducing total RNA synthesis by only 50%. We conclude that tumor virus-specific RNA is synthesized on a DNA template, most probably by the host's RNA polymerase II.Temin's model for tumor virus RNA replication postulates that the infecting viral RNA is transcribed into DNA, which is then integrated into the host genome. Progeny RNA would subsequently be produced by transcription of the DNA (1-3). While-the first part of the hypothesis is supported by a number of findings (1-3), the only evidence for DNA-dependent viral RNA synthesis is provided by the observations that actinomycin D inhibits virus formation (4, 5) and that virus mutants are generated by exposure of infected cells to brornodeoxyuridine (6). Although the inhibition experiment demonstrates the requirement for a DNA-dependent step, it does not show that the inhibitor is acting directly on viral RNA synthesis, rather than, for instance, by preventing synthesis of protein(s) required for viral RNA replication. Failure to find tumor virus-specific minus strands in infected cells (J. Duffy, H. Diggelthann, and C. Weissmann, unpublished results; see however ref. (7) for an opposite result) argues against the alternative pathway of RNA-directed RNA replication.In order to clarify the nature of template and enzyme involved in Rous sarcoma virus RNA replication we developed a cell-free system of RNA synthesis in which about 0.5% of the RNA synthesized is virus-specific. Virus-specific RNA synthesis is as sensitive to actinomycin D and DNase as cellular RNA synthesis, supporting the view that the template involved is DNA. The high sensitivity of virus RNA synthesis to a-amanitin suggests that DNA-dependent RNA polymerase II is responsible for tufmor virus RNA synthesis. MATERIALS AND METHODSDNase I (electrophoretically purified, from Worthington Biochemical Corp., Freehold, N.J.) was treated with iodoacetate to eliminate RNase activity (8). RNase T1 was from Calbiochem; crude RNase T2 was prepared as described (9). a-Amanitin was a gift from Prof. T. Wieland. Ribonucleoside [a-32PItriphosphates were synthesized by a method based on published procedures (10, 11). All information regarding cells, cell lines, viruses, labeled viral nucleic acids, and other materials has been published (12,16). Chicke...

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“…RAV-0 was discovered as a complete infectious endogenous virus and we soon showed that several strains of chicken had latent, yet activatable, endogenous ALV genomes which could recombine with infectious RSV (Weiss et al, 1973). ALV 'ev' genomes were also detected by DNA hybridization (Baluda, 1972;Varmus et al, 1972). Ev expression provided resistance to exogenous infection by pseudotype RSV with the same envelope .…”

Section: Endogenous Retrovirusesmentioning

confidence: 98%

The oncologist's debt to the chicken

Weiss

1998

Avian Pathology

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Our understanding of avian tumour virology has laid the groundwork for much basic cancer research. Most outstanding has been the delineation of oncogenes. These were first discovered in avian leukosis and sarcoma viruses, but are of fundamental importance in most types of non-viral cancer too, both in animals and humans. Avian tumour viruses gave us the tools to probe the complex signalling pathways in the cell that go awry in cancer. Avian retroviruses have also aided medical research in other ways: HIV infection is treated by anti-retroviral drugs directed against enzymes, such as reverse transcriptase, first discovered in chicken retroviruses. Endogenous viral genomes are becoming linked to normal development, to disease and to concern over xenotransplantation; again, the chicken provided the initial knowledge. Retroviral vectors used to deliver human gene therapy have borrowed extensively from natural oncogenic and genetically-engineered avian retroviruses. Marek's disease virus (MDV) has served as a model transforming lymphotropic herpesvirus for human lymphomas and lymphoproliferative disease caused by EpsteinBarr virus. Unravelling a novel human herpesvirus causing Kaposi's sarcoma also owes a debt to the chicken, not only to MDV, but also to the chorioallantoic membrane assay as a model for tumour angiogenesis.

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Widespread Presence, in Chickens, of DNA Complementary to the RNA Genome of Avian Leukosis Viruses

Cited by 139 publications

References 21 publications

Host induced alteration of avian sarcoma virus B-77 genome.

Host induced alteration of avian sarcoma virus B-77 genome.

In Vitro Synthesis of Rous Sarcoma Virus-Specific RNA is Catalyzed by a DNA-Dependent RNA Polymerase

The oncologist's debt to the chicken

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