Subgroup J avian leukosis virus infection in turkeys: Induction of rapid onset tumours by acutely transforming virus strain 966

Venugopal, K.; Howes, K.; Flannery, D. M. J.; Payne, L. N.

doi:10.1080/03079450050118449

Cited by 10 publications

(5 citation statements)

References 14 publications

(18 reference statements)

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“…Another α herpesvirus, herpesvirus of turkeys (HVT) (Meleagrid herpesvirus 1), naturally circulates in turkeys, but is non‐pathogenic (Witter and Solomon 1971). Under experimental conditions, avian leucosis virus, which is closely related to lymphoproliferative disease virus, may potentially infect turkeys (Venugopal and others 2000).…”

Section: Introductionmentioning

confidence: 99%

Diagnostic investigation of Marek's disease in a turkey

Hughes

Archer

Constantino‐Casas

et al. 2016

Vet Record Case Reports

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A six-month-old female turkey from a commercial growing unit was evaluated at postmortem examination for investigation of suspected viral lymphoproliferative disease. Clinically, the turkey was dull and subdued, and relatively unresponsive to external stimuli. The main gross postmortem findings were diffusely enlarged spleen, kidneys and liver, with multifocal cream foci. The lungs were atelectatic, and mild segmental mural thickening of the small intestines was observed. Impression smears taken during postmortem examination confirmed the presence of a population of neoplastic lymphocytes, which, on histological examination, infiltrated multiple organs. Using quantitative real-time PCR analysis, spleen and liver samples were positive for Marek's disease virus and negative for herpesvirus of turkeys. A splenic sample was negative for reticuloendotheliosis virus. This case report details gross, cytological and histological findings in a confirmed case of Marek's disease in a turkey where disease manifests as infiltration of numerous organs with pleomorphic neoplastic lymphocytes.

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Section: Introductionmentioning

confidence: 99%

Diagnostic investigation of Marek's disease in a turkey

Hughes

Archer

Constantino‐Casas

et al. 2016

Vet Record Case Reports

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“…Up to now, there are seven subgroups of ALV in chickens: ALV-A, -B, -C, -D, -E, -J and -K [19,20]. ALV-J was first detected in meat-type chickens in 1987 as a new subgroup [21] and has spread to many countries such as America [22], UK [23], China [24] and so on. Clinical infection is associated with immune tolerance, high mortality, delayed growth, inducing different kinds of tumors [25,26].…”

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: Identification of aberrantly expressed circRNAs in subgroup J avian leucosis virus induced tumor livers by RNA sequencing

Zhang¹,

Yan²,

Lei³

et al. 2018

Oncotarget

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ALV-J (subgroup J avian leucosis virus) is a kind of oncogenic exogenousretrovirus and diseases associated with ALV-J have caused severe reproduction problems in the poultry industry worldwide. However, the pathogenesis of ALV-Jinduced tumor formation is still unclear. In recent years, circRNAs are validated to be related to cancer, which prompts us to explore whether aberrant expression of circRNAs exists in ALV-J-infected tumor samples. In this study, a total of 2822 differentially expressed circRNAs were detected by RNA sequencing in the tumor livers of ALV-J-susceptible chickens (n = 3) and the normal liver samples of ALV-J-resistant chickens (n = 3), among which 2808 circRNAs in the tumor liver samples were detected as unregulated compared to those in the normal liver samples. As circRNAs are considered as miRNA sponge, we predicted top 5 miRNA targets for 24 selected upregulated circRNAs in the ALV-J-induced tumor livers. CircRNA-miRNA-mRNA regulatory axes were also constructed to provide clear interaction relationship among them. Furthermore, Gene Ontology and KEGG pathway analyses were performed for miRNA target genes, the result of which implied that metabolism plays a key role in circRNAs alterations in ALV-J-induced tumor livers. In summary, we identified that circRNAs are involved in ALV-J-induced tumor formation in chickens. However, the pathogenicity mechanism still needs to be further explored.

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“…The acutely transforming ALV-J strain 966 was recovered from a myeloid tumor induced experimentally by HPRS-103 infection (20). This virus transformed peripheral blood monocyte and bone marrow cells and induced rapid-onset tumors in chickens (20) and turkeys (28). Peripheral blood monocytes and bone marrow cells from different lines of chickens showed variation in the relative susceptibility to transformation by ALV-J strain 966 (1).…”

mentioning

confidence: 99%

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

Chesters

Howes

McKay³

et al. 2001

J Virol

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Avian leukosis virus subgroup J (ALV-J) is the newest member of the avian oncogenic retroviruses. After the first isolation of the ALV-J prototype virus, HPRS-103, more than 10 years ago in the United Kingdom (21), viruses belonging to this subgroup have spread rapidly to many countries, becoming one of the major pathogens facing the broiler meat industry worldwide (26). The env gene of ALV-J is closely related to that of a novel group of chicken endogenous retroviral elements designated EAV-HP (24), suggesting that ALV-J has emerged by genetic recombination (17). Compared to the pathogenic ALV subgroups, such as A and B, which primarily induce lymphoid leukosis in genetically susceptible birds (18), ALV-J isolates predominantly induce myeloid leukosis (ML), a property thought to be associated with their tropism for the cells of the myeloid lineage (1). Previous studies have shown that HPRS-103 and other ALV-J isolates do not transform chicken bone marrow cell cultures in vitro and that the tumors induced by these viruses occur after long latent periods (19). These observations and the demonstration that the nucleotide sequence of the viral genome does not carry any viral oncogenes (2, 3) suggested that ALV-J-induced oncogenesis occurs by the activation of oncogenes through the mechanism of insertional mutagenesis (13).Although the tumors induced by HPRS-103 are of late onset, occurring at a median age of 20 weeks (19), we have previously shown that acutely transforming ALVs that induce rapid-onset tumors could be isolated from about 60% of lateonset tumors (20). Many tumors obtained from field cases of ML also contained acutely transforming viruses, suggesting that generation of acutely transforming ALVs is a common feature of ALV-J-induced oncogenesis. Most of these virus isolates were able to transform chicken bone marrow or monocyte cell cultures in vitro and induce rapid-onset tumors when inoculated into susceptible birds, a property attributed to the transduction of oncogenes. The acutely transforming ALV-J strain 966 was recovered from a myeloid tumor induced experimentally by . This virus transformed peripheral blood monocyte and bone marrow cells and induced rapid-onset tumors in chickens (20) and turkeys (28). Peripheral blood monocytes and bone marrow cells from different lines of chickens showed variation in the relative susceptibility to transformation by ALV-J strain 966 (1). This variation was correlated with the relative susceptibility to the induction of ML by HPRS-103, suggesting the involvement of common cell-specific viral and/or host factors in oncogenesis induced by these two viruses. In order to identify the viral genes and oncogenes that are involved in the rapid induction of tumors, we have determined the complete sequence of the proviral genome of ALV-J strain 966. In this paper, we demonstrate the genome structure of the provirus of the 966 strain of ALV-J and compare its sequence with that of HPRS-103 and other acutely transforming avian retroviruses. We also present data demonstratin...

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Subgroup J avian leukosis virus infection in turkeys: Induction of rapid onset tumours by acutely transforming virus strain 966

Cited by 10 publications

References 14 publications

Diagnostic investigation of Marek's disease in a turkey

Diagnostic investigation of Marek's disease in a turkey

WITHDRAWN: Identification of aberrantly expressed circRNAs in subgroup J avian leucosis virus induced tumor livers by RNA sequencing

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

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