The LTR, v-src, LTR provirus generated in the mammalian genome by src mRNA reverse transcription and integration

Bodor, Josef; Svoboda, Jan

doi:10.1128/jvi.63.2.1015-1018.1989

Cited by 20 publications

(4 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The hypothesis that the defective cauliflower mosaic virus is generated by reverse transcription and encapsidation of a spliced viral RNA is supported by our results. This phenomenon is also reminiscent of the finding that the spliced mRNAs of some retroviruses (e.g., Rous sarcoma virus and mouse mammary tumor virus [4,17,27]) can be encapsidated and subsequently integrated into the genome after reverse transcription. This is not the case, however, for retroviruses whose major cis-acting encapsidation sequences are located downstream of the splice donor site (e.g., Moloney murine leukemia virus and human immunodeficiency virus [1,7,16,18,19]).…”

mentioning

confidence: 79%

Defective hepatitis B virus particles are generated by packaging and reverse transcription of spliced viral RNAs in vivo

Terre

Petit

Bréchot

1991

J Virol

101

View full text Add to dashboard Cite

Generation of replicative defective viruses is frequently observed during viral infections. We now report that encapsidation and reverse transcription of spliced viral RNA is an additional mechanism for synthesis of defective viral particles. We have investigated the in vivo synthesis of a spliced hepatitis B virus (HBV) RNA. By using the polymerase chain reaction with different sets of primers on DNA purified from infected livers and the HepG2 HBV cell line, we detected a subgenomic HBV DNA complementary to the spliced viral RNA. Its nucleotide sequence was found to be identical to that previously described for the spliced RNA. This HBV RNA is packaged and reverse transcribed in vivo, the cDNA being incorporated into circulating particles. This finding establishes the synthesis of spliced HBV RNA in vivo and indicates that its reverse transcription can give rise to defective viruses.

show abstract

mentioning

confidence: 79%

Defective hepatitis B virus particles are generated by packaging and reverse transcription of spliced viral RNAs in vivo

Terre

Petit

Bréchot

1991

J Virol

101

View full text Add to dashboard Cite

show abstract

“…The clonal line F6K4 of transformed quail cells was used for DNA cloning. The proviral DNA in this cell line has lost its replication competence due to a deletion of all viral genes except v-src (Bodor and Svoboda, 1989). The viral DNA was released with BamHI and HindIII from lambda F6K4c1.2 (Svoboda et al, 1992) and cloned into the same restriction sites of pUC18.…”

Section: Preparation and Inoculation Of V-src Proviral Dnamentioning

confidence: 99%

Protective Effects of Type I and Type II Interferons toward Rous Sarcoma Virus-Induced Tumors in Chickens

Plachý

Weining

Kremmer³

et al. 1999

Virology

View full text Add to dashboard Cite

Growth of tumors induced by Rous sarcoma virus (RSV) is controlled by alleles at the major histocompatibility complex locus in chickens, indicating that immunological host defense mechanisms play a major role. We show here that the resistance phenotype of CB regressor chickens can be partially reverted by treating the animals with a monoclonal antibody that neutralizes the major serotype of chicken type I interferon, ChIFN-alpha. Injection of recombinant ChIFN-alpha into susceptible CC progressor chickens resulted in a dose-dependent inhibition of RSV-induced tumor development. This treatment was not effective, however, in CC chickens challenged with a DNA construct expressing the v-src oncogene, suggesting that the beneficial effect of type I interferon in this system resulted from its intrinsic antiviral activity and probably not from indirect immunmodulatory effects. By contrast, recombinant chicken interferon-gamma strongly inhibited tumor growth when given to CC chickens that were challenged with the v-src oncogene, indicating that the two cytokines target different steps of tumor development.

show abstract

“…We have previously described a functional proviral structure that consists of LTR, v-src, LTR sequences integrated in the hamster tumor H-19 and that, according to restriction mapping and sequencing, corresponds to the reverse-transcribed src mRNA (4,10,30). This provirus can be rescued if the nonpermissive H-19 cells are complemented by fusion with Rous-associated virus RAV-1-infected chicken fibroblasts and the v-src proviral transcript is encapsidated in RAV-1 virions (10, 27).…”

mentioning

confidence: 99%

“…For hybridization, 32P-labeled plasmid probes, gag 2, src 11, and LTR 2 (10,15,19), detecting specifically the viral genome regions spanning nucleotides 532 to 1916, 8098 to 8671, and 8992 to 9335, respectively, were used. arrangement of cellular DNA direct repeats in the ancestral H-19 provirus (4).…”

mentioning

confidence: 99%

A transformation-competent recombinant between v-src and Rous-associated virus RAV-1

Svoboda¹,

Kandala²,

Geryk³

et al. 1990

J Virol

Self Cite

View full text Add to dashboard Cite

The LTR, v-src, LTR provirus, which arose by the reverse transcription and integration of src mRNA in the H-19 hamster tumor, has been successfully rescued by fusion with chicken fibroblasts infected with Rous-associated virus RAV-1. One rescued virus, E6, acquired 1 kilobase of the 5' end of the gag gene structure. Recombination took place in the region of 15-nucleotide homology exactly between v-src exon (position 7054) and gag (position 1417). This recombination resulted in the alteration of src splice acceptor site sequences, but this site is maintained as a functional splice acceptor site. The nucleotide structure of the long terminal repeat of recombinant E6 virus suggests that it arose by the intermolecular jump of reverse transcription from RAV-1 to src mRNA and then the switch of templates between already depicted regions of homology. The second jump of reverse transcription was apparently an intramolecular event. The acquisition of 1 kilobase of the 5' gag by E6 resulted in maintaining the balance of unspliced and spliced E6 RNAs and assured the replication advantage of rescued E6 virus over rescued F6 virus, the genome of which corresponds to that present in ancestral H-19 cells.

show abstract

The LTR, v-src, LTR provirus generated in the mammalian genome by src mRNA reverse transcription and integration

Cited by 20 publications

References 38 publications

Defective hepatitis B virus particles are generated by packaging and reverse transcription of spliced viral RNAs in vivo

Defective hepatitis B virus particles are generated by packaging and reverse transcription of spliced viral RNAs in vivo

Protective Effects of Type I and Type II Interferons toward Rous Sarcoma Virus-Induced Tumors in Chickens

A transformation-competent recombinant between v-src and Rous-associated virus RAV-1

Contact Info

Product

Resources

About