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From the complete nucleotide sequence of the genome of the avian sarcoma virus Y73, we have predicted amino acid sequence of p90 gag-yes, the product of the transforming gene. Contrary to previous evidence from molecular hybridization studies p90 gag-yes was found to have much homology with the transforming gene product p60 src of Rous sarcoma virus, suggesting that the cellular counterparts of the two (c-yes and c-src) originated from a common prototype sequence.

A single gene, src of Rous sarcoma virus (RSV) coding for a protein of pp60src, is responsible for the transformation of fibroblasts1–3. DNA sequences homologous to src (the endogenous sarc) are present in uninfected cells of chickens4 and other vertebrates5. Endogenous nucleotide sequences have also been found in the putative transforming genes of MC29 (ref. 6) and avian erythroblastosis virus7. These viruses, however, induce different spectra of tumours in animals. From analysis of a new avian sarcoma virus, Y73, we present here evidence suggesting that multiforms of viral sarcoma genes originated from cellular genetic sequences, and that these viral genes are structurally unrelated, but have similar pathogenicities.

Human T-cell leukaemia virus (HTLV)1–4, previously also reported as ATLV5, is a recently identified retrovirus which is closely associated with adult T-cell leukaemia (ATL) endemic in southwestern Japan6,7 and the Caribbean8. Determination of the total nucleotide sequence of the HTLV genome has revealed no typical onc gene acquired from the cellular sequence9,10. Screening of the HTLV provirus genome in tumour cells4,11,12 has shown that in all cases of ATL examined, the primary tumour cells contained the provirus genome and were monoclonal with respect to the integration site of the provirus13. These findings suggest that ATL leukaemogenesis may be due to insertional mutagenesis in which the provirus genome is integrated into a specific locus on the chromosomal DNA and then activates an adjacent cellular onc gene, a mechanism already demonstrated in avian lymphoma14,15 and erythroblastosis16 induced by avian leukosis viruses. A common site of HTLV provirus integration in leukaemic cells among some ATL patients was reported by Hahn et al.17 but subsequently retracted18. However, this retraction does not imply the random integration of the proviruses. Independently, we have been testing this insertional mutagenesis model in ATL and report here that the provirus did not have a common locus of integration in 35 ATL patients and did not integrate on the same chromosome in 2 ATL patients.

Genes de HTLV-I et de HTLV-II et genes de HIV: nom propose (et derivation), noms anterieurs, masse moleculaire, fonction connue (ou inconnue)