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Journal of Virology, October 2004, p. 10525-10535, Vol. 78, No. 19
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.19.10525-10535.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Assessing the Roles of Endogenous Retrovirus EAV-HP in Avian Leukosis Virus Subgroup J Emergence and Tolerance

Melanie A. Sacco,^* Ken Howes, Lorraine P. Smith, and Venugopal K. Nair

Institute for Animal Health, Compton, Newbury, Berkshire, United Kingdom

Received 22 February 2004/ Accepted 12 May 2004

Avian leukosis virus (ALV) subgroup J is thought to have emerged through a recombination event between an unknown exogenous ALV and the endogenous retrovirus elements designated EAV-HP. All EAV-HP elements identified to date in the chicken genome show large deletions, including that of the entire pol gene. Here we report the identification of four segregating chicken EAV-HP proviruses with complete pol genes, one of which shows exceptionally high sequence identity and a close phylogenetic relationship with ALV-J with respect to the env gene. Embryonic expression of EAV-HP env has been suggested as a factor associated with immunological tolerance induction in a proportion of ALV-J-infected meat-type chickens. In support of this, env gene transcripts expressed from two of the four newly identified EAV-HP proviruses were demonstrated in chicken embryos. However, when ALV-J-infected outbred meat-type chickens were assessed, the presence of intact EAV-HP proviruses failed to directly correlate with ALV-J tolerance. This association was further examined using F₂ progeny of two inbred lines of layer chicken that differed in EAV-HP status and immunological responses to ALV-J. Immunological tolerance developed in a small proportion of F₂ progeny birds, reflecting the expected phenotypic ratio for inheritance of a double-recessive genotype; however, the status of tolerance did not show any direct correlation with the presence of the intact EAV-HP sequence. Nevertheless, identification of an intact chicken EAV-HP locus showing a uniquely close relationship to the ALV-J prototype clone HPRS-103 in the env region provides the strongest evidence of its contribution to the emergence of ALV-J by recombination.

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* Corresponding author. Present address: Boyce Thompson Institute for Plant Research, Cornell University, Tower Rd., Ithaca, NY 14853. Phone: (607) 254-1348. Fax: (607) 254-7423. E-mail: mas289{at}cornell.edu.

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Journal of Virology, October 2004, p. 10525-10535, Vol. 78, No. 19
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.19.10525-10535.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

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