Recombinant avian leukosis viruses of subgroup J isolated from field infected commercial layer chickens with hemangioma and myeloid leukosis possess an insertion in the E element.
BACKGROUND
Five isolates (JS09GY2, JS09GY3, JS09GY4, JS09GY5, and JS09GY6) of avian leukosis virus subgroup J (ALV-J) were isolated from six infected commercial layer flocks displaying both hemangioma and myeloid leukosis (ML), which shared the same parental line, in China in 2009.


RESULTS
All six of the commercial layer chickens examined showed hemangiomas on their body surface or feet. Some developed hemangiomas in their internal organs, causing hepatorrhexis and blood loss. Histopathologically different stages of hemangiomas with ML in the liver, heart, and spleen, were observed. Five viral isolates were obtained from infected DF1 cells incubated with the spleen tissue or serum of the birds from the six flocks. By full genome sequences analysis, a 19-nucleotide repeat sequence was identified in the primer binding site (PBS)-leader region of isolates JS09GY3 and JS09GY6, located between sites 249 and 250 according to the sequence of reference strain HPRS103, and also present in Rous sarcoma virus strain Schmidt-Ruppin B (RSV-SRB), Rous associated virus type 1 (RAV-1), and Rous associated virus type 2 (RAV-2). The predicted Gp85 proteins of isolates JS09GY2, JS09GY3, JS09GY5, and JS09GY6 were highly variable. Interestingly, the E elements of these four examined isolates showed a key deletion at site 30, which produced a new c-Ets-1 binding site. An 11-bp insertion was also found in the E element of isolate JS09GY3 located between bp 66 and 67 according to the sequence of reference strain HPRS103, while almost all previously reported Chinese strains showed an almost identical deletion of 127 bp in the same region.


CONCLUSIONS
Five ALV-J isolates were obtained from six field infected commercial layer chickens. Coexistence of hemangioma and ML were observed in these infected cases both macro- and microscopically. Complete proviral genome sequences of two isolates (JS09GY3 and JS09GY6) and the partial sequences of the other two isolates (JS09GY2 and JS09GY5) were determined. The isolates were found to be recombinants of ALV-J with a PBS-leader sequence originating from other retroviruses. The Gp85 protein with an amino acid deletion, a contiguous 11-bp insertion mutation in the E element, and a novel binding site, were noted in the proviral genomes.
Wu
Xiaoping
X
Key Lab of Jiangsu Preventive Veterinary Medicine, College of Veterinary Medicine, Yangzhou University, No.12 East Wenhui Road, Yangzhou, Jiangsu Province, China, 225009. pingping19781015@yahoo.cn
Qian
Kun
K
Qin
Aijian
A
Shen
Haiyu
H
Wang
Pingping
P
Jin
Wenjie
W
Eltahir
Yassir Mohammed
YM
D000818:Animals; D001353:Avian Leukosis / Q000821:virology*; D001354:Avian Leukosis Virus / Q000145:classification* / Q000235:genetics*; D001483:Base Sequence; D002645:Chickens; D004251:DNA Transposable Elements; D005260:Female; D015967:Gene Expression Regulation, Viral / Q000502:physiology; D005814:Genes, Viral; D014644:Genetic Variation; D016679:Genome, Viral; D006391:Hemangioma / Q000662:veterinary* / Q000821:virology; D008297:Male; D008969:Molecular Sequence Data; D009154:Mutation; D016865:Reassortant Viruses / Q000145:classification / Q000235:genetics
D004251:DNA Transposable Elements