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Journal of Virology, May 2001, p. 4219-4225, Vol. 75, No. 9
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.9.4219-4225.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Acutely Transforming Avian Leukosis Virus Subgroup J Strain 966: Defective Genome Encodes a 72-Kilodalton Gag-Myc Fusion Protein

P. M. Chesters,1 K. Howes,1 J. C. McKay,2 L. N. Payne,1 and K. Venugopal1,*

Institute for Animal Health, Compton, Berkshire RG20 7NN,1 and Ross Breeders Ltd., Newbridge, Midlothian EH28 8SZ,2 United Kingdom

Received 23 August 2000/Accepted 31 January 2001

Avian leukosis virus subgroup J (ALV-J), the most recent member of the avian retroviruses, is predominantly associated with myeloid leukosis in meat-type chickens. We have previously demonstrated that the acutely transforming virus strain 966, isolated from an ALV-J-induced tumor, transformed peripheral blood monocyte and bone marrow cells in vitro and induced rapid-onset tumors, suggesting transduction of oncogenes (L. N. Payne, A. M. Gillespie, and K. Howes, Avian Dis. 37:438-450, 1993). In order to understand the molecular basis for the rapid transformation and tumor induction, we have determined the complete genomic structure of the provirus of the 966 strain. The sequence of the 966 provirus clone revealed that its genome is closely related to that of HPRS-103 but is defective, with the entire pol and parts of the gag and env genes replaced by a 1,491-bp sequence representing exons 2 and 3 of the c-myc gene. LSTC-IAH30, a stable cell line derived from turkey monocyte cultures transformed by the 966 strain of ALV-J, expressed a 72-kDa Gag-Myc fusion protein. The identification of the myc gene in 966 virus as well as in several other ALV-J-induced tumors suggested that the induction of myeloid tumors by this new subgroup of ALV occurs through mechanisms involving the activation of the c-myc oncogene.

* Corresponding author. Mailing address: Institute for Animal Health, Compton, Berkshire RG20 7NN, United Kingdom. Phone: 44 (0) 1635 578411. Fax: 44 (0) 1635 577237. E-mail: venu.gopal{at}bbsrc.ac.uk.

Journal of Virology, May 2001, p. 4219-4225, Vol. 75, No. 9
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.9.4219-4225.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Chesters, P. M., Smith, L. P., Nair, V. (2006). E (XSR) element contributes to the oncogenicity of Avian leukosis virus (subgroup J). J. Gen. Virol. 87: 2685-2692 [Abstract] [Full Text]  
  • Carrasco, M. L., Duch, M., Pedersen, F. S. (2004). Strand transfer to the 5' part of a tRNA as a mechanism for retrovirus patch-repair recombination in vivo. J. Gen. Virol. 85: 1965-1969 [Abstract] [Full Text]  
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  • Chesters, P. M., Howes, K., Petherbridge, L., Evans, S., Payne, L. N., Venugopal, K. (2002). The viral envelope is a major determinant for the induction of lymphoid and myeloid tumours by avian leukosis virus subgroups A and J, respectively. J. Gen. Virol. 83: 2553-2561 [Abstract] [Full Text]  


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