Sequence analysis for the complete proviral genome of avian leukosis virus subgroup J associated with haemangiomas, leiomyosarcomas and myelomas in layer flocks

2012 ◽  
Vol 60 (3) ◽  
pp. 343-354 ◽  
Author(s):  
Yue Qu ◽  
Honglei Sun ◽  
Meiyu Sun ◽  
Delong Li ◽  
Liting Qin ◽  
...  

Avian leukosis virus subgroup J (ALV-J) can cause a variety of neoplasms, including mainly myeloid leukosis (myelocytomatosis) and nephromas. Other tumours, such as histiocytic sarcoma (HS), haemangiosarcoma and mesothelioma, may also develop. In a previous article we described a case in which myeloid leukosis, haemangiomas and leiomyosarcomas appeared simultaneously in a commercial layer flock with infection by ALV-J. The present research was completed to understand the molecular characteristics of the ALV-J strain that induced clinical myeloid leukosis, haemangiomas and leiomyosarcomas. Two strains of ALV-J (SDAU1001 and SDAU1002) were isolated and identified, and their full-length sequences were analysed. The complete genome nucleotide sequences of these two isolates were different in length, 7652 nt and 7636 nt, respectively. They shared 98.9% identity with each other, and 93.4% to 97.8% nucleotide identity to the reference ALV-J isolates. A 19-nucleotide repeat sequence was identified in the primer binding site (PBS) leader region of isolate SDAU1001. A base substitution mutation (base 15 C-T) in this insertion was identified. However, the identical insertion at the same site was not found in SDAU1002. Thegagandpolgenes of the two viruses were more conserved than theenvgene. One key deletion in the E element was a common feature of SDAU1001 and SDAU1002. SDAU1001 and SDAU1002, possibly recombinants of ALV-J and another avian retrovirus, may share the same ancestor. Co-infection by SDAU1001 and SDAU1002 isolates is a possible explanation why myeloid leukosis, haemangiomas, and leiomyosarcomas appeared simultaneously in the same commercial layer flock.

2015 ◽  
Vol 89 (9) ◽  
pp. 4712-4719 ◽  
Author(s):  
James Justice ◽  
Sanandan Malhotra ◽  
Miguel Ruano ◽  
Yingying Li ◽  
Guillermo Zavala ◽  
...  

ABSTRACTAvian leukosis virus subgroup J (ALV-J) is a simple retrovirus that can cause hemangiomas and myeloid tumors in chickens and is currently a major economic problem in Asia. Here we characterize ALV-J strain PDRC-59831, a newly studied U.S. isolate of ALV-J. Five-day-old chicken embryos were infected with this virus, and the chickens developed myeloid leukosis and hemangiomas within 2 months after hatching. To investigate the mechanism of pathogenesis, we employed high-throughput sequencing to analyze proviral integration sites in these tumors. We found expanded clones with integrations in theMETgene in two of the five hemangiomas studied. This integration locus was not seen in previous work characterizing ALV-J-induced myeloid leukosis.METis a known proto-oncogene that acts through a diverse set of signaling pathways and is involved in many neoplasms. We show that tumors harboringMETintegrations exhibit strong overexpression ofMETmRNA.IMPORTANCEThese data suggest that ALV-J induces oncogenesis by insertional mutagenesis, and integrations in theMEToncogene can drive the overexpression ofMETand contribute to the development of hemangiomas.


2006 ◽  
Vol 87 (9) ◽  
pp. 2685-2692 ◽  
Author(s):  
Peter M. Chesters ◽  
Lorraine P. Smith ◽  
Venugopal Nair

Among the six subgroups of Avian leukosis virus (ALV) that infect chickens, subgroup J (ALV-J) was isolated from meat-type chickens where it predominantly induces myeloid leukosis (ML) and erythroblastosis (EB). The sequence of HPRS-103, the ALV-J prototype virus, shows several distinct features, one of which is the presence of a distinct hairpin stem–loop structure called the E (also called XSR) element in the 3′ untranslated region. In order to determine the role of the E element in ALV-induced pathogenicity, a comparison was made of the oncogenicity of viruses derived from the provirus clones of parental and E element-deleted HPRS-103 viruses in two genetically distinct lines of birds. In line 15I birds, deletion of the E element had profound effects on virus replication in vivo, as only 55 % of birds showed evidence of infection, compared with 100 % infection by the parental virus. Furthermore, none of the line 15I birds infected with this virus developed tumours, indicating that the E element does contribute to the oncogenicity of the virus. On the other hand, deletion of the E element had only a marginal effect on the incidence of tumours in line 0 birds. These results indicate that, although the E element per se is not absolutely essential for tumour induction by this subgroup of viruses, it does contribute to oncogenicity in certain genetic lines of chicken.


2018 ◽  
Vol 66 (2) ◽  
pp. 622-626 ◽  
Author(s):  
Defang Zhou ◽  
Jingwen Xue ◽  
Ya Zhang ◽  
Guihua Wang ◽  
Yongsheng Feng ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document