Article

Molecular Epidemiology of Avian Leukosis Virus Subgroup J in Layer Flocks in China

Division of Avian Infectious Diseases, State [corrected] Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, China.
Journal of clinical microbiology (Impact Factor: 4.23). 12/2011; 50(3):953-60. DOI: 10.1128/JCM.06179-11
Source: PubMed

ABSTRACT Avian leukosis virus subgroup J (ALV-J) was first isolated from meat-type chickens in 1988. No field cases of ALV-J infection or tumors in layer chickens were observed worldwide until 2004. However, layer flocks in China have experienced outbreaks of this virus in recent years. The molecular epidemiology of ALV-J strains isolated from layer flocks was investigated. The env genes of 77.8% (21/27) of the ALV-J layer isolates with a high degree of genetic variation were significantly different from the env genes of the prototype strain of ALV-J (HPRS-103) and American and Chinese strains from meat-type chickens (designated ALV-J broiler isolates). A total of 205 nucleotides were deleted from the 3' untranslated region of 89.5% (17/19) of the ALV-J layer isolates. Approximately 94.7% (16/17) of the layer isolates contained a complete E element of 146 to 149 residues. The U3 sequences of 84.2% (16/19) of the ALV-J layer isolates displayed less than 92.5% sequence homology to those of the ALV-J broiler isolates, although the transcriptional regulatory elements that are typical of avian retroviruses were highly conserved. Several unique nucleotide substitutions in the env gene, the U3 region, and the E element of most of the ALV-J layer isolates were detected. These results suggested that the env gene, E element, and U3 region in the ALV-J layer isolates have evolved rapidly and were significantly different from those of the ALV-J broiler isolates. These findings will contribute to a better understanding of the pathogenic mechanism of layer tumor diseases induced by ALV-J.

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Available from: Xiaole Qi, Jul 29, 2015
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    • "One of these subgroups shared high identity with the UK prototype HPRS-103, while the other clustered in a new branch that was distinct from all meat-type chicken isolates and earlier layer isolates. Meanwhile, some isolates showed differences in the leader sequences or in the 3 0 -untranslated region of the E (XSR) element (Gao et al., 2012). "
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    ABSTRACT: Cases of myeloid leukosis and hemangioma associated with avian leukosis virus subgroup J (ALV-J) are becoming more frequent in China in commercial layer chickens and breeders of egg-type chickens. In this study, two strains of ALV-J (SCAU11-H and SCAU11-XG) associated with hemangioma and myelocytoma were isolated from commercial broiler breeder animals in 2011. Their full-length proviral sequences were analyzed, revealing several unique genetic differences between the two isolates, and suggesting that the two viruses were derived from two distinct lineages. Strain SCAU11-H showed high sequence homology to early Chinese isolates associated with hemangioma, while strain SCAU11-XG was genetically closer to the prototype strain, HPRS-103. The complete genomic nucleotide sequences of SCAU11-H and SCAU11-XG were 7471bp and 7727bp in length, respectively. They shared 94.8% identity with each other, and had 94.0-96.8% nucleotide identity to ALV-J reference isolates. Homology analysis of the env, pol, and gag genes of the two isolates and other references strains showed that the gag and pol genes of the two viruses were more conserved than the env gene. In addition, the two isolates had significant deletions and substitutions in their 3'-UTR regions, compared to HPRS-103. These results suggest that the env gene and the 3'-UTR regions in these ALV-J isolates have evolved rapidly, and might be involved in the oncogenic spectrum of ALV-J. The results of this study contribute to our further study of the relationship between ALV integration patterns and multi-pathotypes associated with ALV-J.
    Veterinary Microbiology 06/2013; 166(3-4). DOI:10.1016/j.vetmic.2013.06.007 · 2.73 Impact Factor
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    • "Avian leukosis viruses (ALVs), which belong to the genus alpharetrovirus of the Retroviridae family, cause neoplastic diseases and other reproduction problems in the poultry industry worldwide (Gao and Wang, 2012). Avian leukosis viruses are divided into 10 well-characterized subgroups, A to J, based on receptor usage group and host range in chickens. "
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    ABSTRACT: To analyze the status of wild birds infected with avian leukosis virus (ALV) in China, we collected 300 wild birds from various areas. Virus isolation and PCR showed that wild birds were infected by ALV-A and ALV-B. Two ALV-A and 4 ALV-B env sequences were obtained by PCR using primers designed to detect ALV-A and -B respectively. Our results showed that the gp85 genes of the 2 ALV-A strains have the highest homology with RAV-1, 99.8%, and more than 92% homology with other American strains. However, the gp85 genes of the two ALV-A strains showed slightly lower homology with Chinese strains (87.2-92.6%). Additionally, the 4 ALV-B strains have high homology with the prototype strain (RAV-2), from 99.1 to 99.4%, but they have slightly lower identity with Schmidt-Ruppin B and Prague subgroup B, from 93.3 to 98.4%. The 4 ALV-B strains showed the lowest identity with SDAU09C2 and SDAU09E3 (90%). In total, these results suggested that avian leukosis virus has infected wild birds in China.
    Veterinary Microbiology 05/2013; 163(3-4):257-63. DOI:10.1016/j.vetmic.2013.01.020 · 2.73 Impact Factor
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    ABSTRACT: Avian leukosis virus subgroup J (ALV-J) preferentially induces myeloid leukosis (ML) in meat-type birds. Since 2008, many clinical cases of hemangioma rather than ML have frequently been reported in association with ALV-J infection in Chinese layer flocks. Three ALV-J strains associated with hemangioma were isolated and their proviral genomic sequences were determined. The three isolates, JL093-1, SD09DP03 and HLJ09MDJ-1, were 7,670, 7,670, and 7,633 nt in length. Their gag and pol genes were well conserved, with identities of 94.5-98.6% and 97.1-99.5%, respectively, with other ALV-J strains at the amino acid level (aa), while the env genes of the three isolates shared a higher aa identity with the env genes of other hemangioma strains than with those of ML strains. Interestingly, two novel 19-bp insertions in the U3 region in the LTR and 5' UTR, most likely derived from other retroviruses, were found in all the three isolates, thereby separately introducing one E2BP binding site in the U3 region in the LTR and RNA polymerase II transcription factor IIB and core promoter motif ten elements in the 5' UTR. Meanwhile, two binding sites in the U3 LTRs of the three isolates for NFAP-1 and AIB REP1 were lost, and a 1-base deletion in the E element of the 3' UTR of JL093-1 and SD09DP03 introduced a binding site for c-Ets-1. In addition to the changes listed above, the rTM of the 3' UTR was deleted in each of the three isolates. Our study is the first to discovery the coexistence of two novel insertions in the U3 region in the LTR and the 5' UTR of ALV-J associated with hemangioma symptoms, and the transcriptional regulatory elements introduced should be taken into consideration in the occurrence of hemangioma.
    Virology Journal 12/2011; 8(1):552. DOI:10.1186/1743-422X-8-552 · 2.09 Impact Factor
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