Induction of neoplasms by subgroup E recombinants of exogenous and endogenous avian retroviruses (Rous-associated virus type 60)

Crittenden, L. B.; Hayward, William S.; Hanafusa, Hidesaburô; Fadly, A. M.

doi:10.1128/jvi.33.2.915-919.1980

Cited by 50 publications

(15 citation statements)

References 26 publications

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“…Even though the RAV-O is a competent replicating virus, it does not, despite a clear homology with the ALV viruses, induce any neoplasia in domestic chickens. Previous studies suggested, but did not prove, that the crucial difference in oncogenic potential resides within the LTR (6,24,29). Both hybridization and T1 oligonucleotide fingerprinting experiments show that the major differences between the ALVs and RAV-O are in the region at the 3' end of viral RNA, and my sequence analysis has demonstrated that the differences lie mostly within the U3 region.…”

Section: Discussionmentioning

confidence: 83%

“…There are several possibilities, some more likely than others. It is possible the RAV-O cannot infect the appropriate target cell, although this is unlikely since subgroup E ALVs are oncogenic (6,24). It is also possible, though unlikely, that RAV-O activates c-myc but kills the target cell.…”

Section: Discussionmentioning

confidence: 99%

“…Since the long terminal repeat (LTR) region of viral DNA appears to contain the sequences necessary for the initiation of transcription, termination of RNA and addition of the polyadenylate tail, and is intimately involved in integra-192 HUGHES tion, whichever model proves correct, the crucial difference(s) may reside within the LTR of the virus. By T1 oligonucleotide fingerprinting (3), hybridization (22), and analysis with restriction enzymes (25), the major differences detected between the ALVs and RAV-0 lie in the 3' end of the RNA genome, and studies with in vivo recombinants suggest, but do not prove, that this is the region responsible for the difference in oncogenic potential between the ALVs and RAV-0 (6,24,29). I have cloned unintegrated circular RAV-0 DNA and shown that the DNA gives rise to replicating RAV-0 virus upon transfection.…”

mentioning

confidence: 99%

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Sequence of the Long Terminal Repeat and Adjacent Segments of the Endogenous Avian Virus Rous-Associated Virus 0

Hughes

1982

J Virol

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Rous-associated virus 0 (RAV-0), an endogenous chicken virus, does not cause disease when inoculated into susceptible domestic chickens. An infectious unintegrated circular RAV-0 DNA was molecularly cloned, and the sequence of the long terminal repeat (LTR) and adjacent segments was determined. The sequence of the LTR was found to be very similar to that of replication-defective endogenous virus EV-1. Like the EV-1 LTR, the RAV-0 LTR is smaller (278 base pairs instead of 330) than the LTRs of the oncogenic members of the avian sarcoma virus-avian leukosis virus group. There is, however, significant homology. The most striking differences are in the U3 region of the LTR, and in this region there are a series of small segments present in the oncogenic viruses which are absent in RAV-0. These differences in the U3 region of the LTR could account for the differences in the oncogenic potential of RAV-0 and the avian leukosis viruses. I also compared the regions adjacent to the RAV-0 LTR with the available avian sarcoma virus sequences. A segment of approximately 200 bases to the right of the LTR (toward gag) is almost identical in RAV-0 and the Prague C strain of Rous sarcoma virus. The segment of RAV-0 which lies between the end of the env gene and U3 is approximately 190 bases in length. Essentially this entire segment is present between env and src in the Schmidt-Ruppin A strain of Rous sarcoma virus. Most of this segment is also present between env and src in Prague C; however, in Prague C there is an apparent deletion of 40 bases in the region adjacent to env. In Schmidt-Ruppin A, but not in Prague C, about half of this segment is also present between src and the LTR. This arrangement has implications for the mechanism by which src was acquired. The region which encoded the gp37 portion of env appears to be very similar in RAV-0 and the Rous sarcoma viruses. However, differences at the very end of env imply that the carboxy termini of RAV-0, Schmidt-Ruppin A, and Prague C gp37s are significantly different. The implications of these observations are considered.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Sequence of the Long Terminal Repeat and Adjacent Segments of the Endogenous Avian Virus Rous-Associated Virus 0

Hughes

1982

J Virol

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“…On the one hand, recarbination analysis indicated that the sequence may be inportant for viral replication (15,16). On the other hand, some investigators have sought to inplicate "c" in leukemogenesis by avian leukosis viruses, which otherwise have no apparent genetic locus devoted to tunmrigenesis (1,17,18). In order to explore the structural boundaries and possible functions of "c", we have determined the sequence of over 900 rucleotides at the 3' end of the genome of the Schmidt-RLppin sugroup A strain of ASV (SR-A ASV).…”

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confidence: 99%

The nucleotide sequence of an untranslated but conserved domain at the 3′ end of the avian sarcoma virus genome

et al. 1980

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The genomes of numerous avian retroviruses contain at their 3' termini a conserved domain denoted "c". The precise boundaries and function of "c" have been enigmas. In an effort to resolve these issues, we determined the sequence of over 900 nucleotides at the 3' end of the genome of the Schmidt-Ruppin subgroup A strain of avian sarcoma virus (ASV). We obtained the sequence from a suitable fragment of ASV DNA that had cloned into the single-stranded DNA phage M13mp2. Computer-assisted analysis of the sequence revealed the following structural features: i) the length of "c" - 473 nucleotides; ii) the 3' terminal domain of src, ending in an amber codon at the 5'boundary of "c"; iii) terminator codons that preclude continuous translation from "c"; iv) suitably located sequences that may serve as signals for the initiation of viral RNA synthesis and for the processing and/or polyadenylation of viral mRNA; v) a repeated sequence that flanks src and that could facilitate deletion of this gene; vi) repeated sequences within "c"; and vii) unexplained homologies between sequences in "c" and sequences in several other nucleic acids, including the 5' terminal domain of the ASV genome, tRNATrp and its inversion, the complement of tRNATrp and its inversion, and the 18S RNA of eukaryotic ribosomes. We conclude that "c" probably does not encode a protein, but its sequence may nevertheless serve several essential functions in viral replication.

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“…Because of the long latencies, the apparant monoclonality of T-cell lymphomas, and the lack of in vitro transforming activity of murine leukemia viruses (MuLV), it appears that leukemogenesis involves an indirect mechanism. Several possibilities have been presented, including formation of oncogenic recombinant viruses (6,10,15), induction of transformation by an effect due to viral integration (6), and promotion of somatic events giving rise to transformation due to chronic immune stimulation brought about by viral replication (20,34). One way to distinguish among these possibilities is to study the characteristics of individual lymphoma cell lines with regard to their virological and immunological properties.…”

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confidence: 99%

Characterization of a unique defective type C virus associated with a Moloney leukemia virus-induced splenic T-cell lymphoma cell line

Horak¹,

Lee²,

Enjuanes³

1980

J Virol

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Moloney leukemia virus (MoLV) induces lymphomas in BALB/c mice which either involve an immature thymic T-cell subpopulation or a splenic mature T-cell subpopulation. To investigate further the possible virological and immunological differences in these lymphomas, several lymphoma cell lines were derived. Although the majority of these cell lines expressed only the parental MoLV, one lymphoma cell line (5F4) was found which expressed only a defective virus. 5F4 virions lacked detectable reverse transcriptase activity and by immunoprecipitation lacked a serologically detectable reverse transcriptase. The lack of reverse transcriptase did not appear to be due to a deletion in the viral genome. Intracellularly 5F4 cells synthesized normal gag gene precursors but had little, if any, detectable Pr180gag-pol or an altered precursor. These results suggest that the defect of the 5F4 virus is associated with the inability to translate the appropriate precursor for reverse transcriptase. The possible origin of the detective 5F4 virus was also examined by competition radioimmunoassays. These results demonstrate that the type-specific proteins, gp71 and p12, are serologically identical to those of the endogenous ecotropic virus and distinct from the MoLV proteins. Competition assays of 5F4 cell extracts further demonstrated the lack of any detectable MoLV type-specific proteins, although the tumor was presumably induced by MoLV. The significance of these observations to leukemogenesis is discussed.

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Induction of neoplasms by subgroup E recombinants of exogenous and endogenous avian retroviruses (Rous-associated virus type 60)

Cited by 50 publications

References 26 publications

Sequence of the Long Terminal Repeat and Adjacent Segments of the Endogenous Avian Virus Rous-Associated Virus 0

Sequence of the Long Terminal Repeat and Adjacent Segments of the Endogenous Avian Virus Rous-Associated Virus 0

The nucleotide sequence of an untranslated but conserved domain at the 3′ end of the avian sarcoma virus genome

Characterization of a unique defective type C virus associated with a Moloney leukemia virus-induced splenic T-cell lymphoma cell line

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