A novel subgroup of exogenous avian leukosis virus in chickens

Payne, L. N.; Brown, Susan; Bumstead, Nat; Howes, K.; Frazier, Judith A.; Thouless, Margaret E.

doi:10.1099/0022-1317-72-4-801

Cited by 333 publications

(205 citation statements)

References 28 publications

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“…Similarly, sequence variation in Tvb accounts for differential interactions with the subgroup B, D, and E Env proteins and susceptibility to the viruses carrying them (32). In contrast, all chicken lines analyzed to date are susceptible to ALV-J (14). Mammalian NHE1 is a housekeeping protein that regulates intracellular pH and cell volume.…”

Section: Discussionmentioning

confidence: 99%

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Na ⁺ /H ⁺ exchanger type 1 is a receptor for pathogenic subgroup J avian leukosis virus

Chai

Bates

2006

Proc. Natl. Acad. Sci. U.S.A.

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Subgroup J avian leukosis virus (ALV-J) is a recently identified avian oncogenic retrovirus responsible for severe economic losses worldwide. In contrast with the other ALV subgroups, ALV-J predominantly induces myeloid leukosis in meat-type chickens. Despite significant homology with the other ALV subgroups across most of the genome, the envelope protein of ALV-J (EnvJ) shares low homology with the others. Pathogenicity and myeloid leukosis induction map to the env gene of ALV-J. A chimeric protein composed of the surface domain of EnvJ fused to the constant region of a rabbit IgG and mass spectrometry were used to identify the chicken Na ؉ ͞H ؉ exchanger type 1 (chNHE1) as a binding protein for ALV-J. Flow cytometry analysis and coprecipitation experiments demonstrated a specific interaction between EnvJ and chNHE1. When introduced into nonpermissive human 293T cells and quail QT6 cells, chNHE1 conferred susceptibility to EnvJ-mediated infection. Furthermore, 293T cells expressing chNHE1 fused with 293T cells expressing EnvJ in a low-pH-dependent manner. Together, these data identify chNHE1 as a cellular receptor for the highly pathogenic ALV-J.retrovirus ͉ viral receptor ͉ viral envelope A vian leukosis viruses (ALV) are a group of avian retroviruses that induce tumors in host birds. The viruses that infect chickens are classified into six subgroups (A-E and J) on the basis of the envelope glycoprotein responsible for specific viral interference patterns, virus neutralization, and host range (1). The most recently identified subgroup, ALV-J, predominantly infects meattype chickens and turkeys (1). ALV-J was identified in 1988 and became widespread in commercial meat-type poultry during the 1990s. The transmission of ALV-J is much higher than other ALV subgroups (2), thus making control and eradication significantly more difficult. The virus also evolves rapidly with sequence variations clustered in hypervariable regions of the envelope protein (Env) (3). In contrast to other subgroups, which primarily cause lymphoma, ALV-J mainly induces myeloid leukosis (4). ALV-J infection causes disease and death in both broiler breeders and egg layers and represents a significant problem for the commercial poultry industry worldwide, with estimated losses of 1.5% per week in excess mortality (5).Retroviruses infect host cells through specific interactions between viral Env and cell surface receptors. The Env surface subunit (SU) directly binds to the receptor, and subsequent conformational changes in the Env transmembrane (TM) subunit drive fusion of the viral and cellular membranes (6). The receptors for all of the other major ALV subgroups (A-E) have been identified (7-10). Receptor distribution is a major determinant of ALV subgroup tropism. Env is also a major determinant for the induction of lymphoid and myeloid tumors by ALV-A and ALV-J, respectively (4), presumably because the specific receptors for ALV-A and ALV-J are differentially expressed on different cell lineages. This hypothesis is supported by the observat...

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Section: Discussionmentioning

confidence: 99%

“…ALV-J appears to be an exception because all lines of chickens screened to date are susceptible to ALV-J infection (14). However, quail and many other avian species are resistant to infection by ALV-J, suggesting that the virus receptor is not broadly conserved in avian species (1).…”

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confidence: 99%

Na ⁺ /H ⁺ exchanger type 1 is a receptor for pathogenic subgroup J avian leukosis virus

Chai

Bates

2006

Proc. Natl. Acad. Sci. U.S.A.

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“…Subgroup A ALVs are more commonly isolated from affected flocks than any other subgroup (Payne & Fadly, 1997). However, subgroup J ALV (ALV-J), first described in the United Kingdom in 1989 and later in other countries, has been found to be associated primarily with myeloid leukosis (ML) in meat-type chickens (Payne et al, 1991a;Payne et al, 1991b;Payne et al, 1992;Fadly & Smith, 1999). In general, fewer studies of the prevalence of ALV in meat lines have been made compared with those in egg lines.…”

Section: Introductionmentioning

confidence: 99%

“…Lesions of ML are usually found in liver, spleen, kidney and sternum. Microscopically, affected tissues are infiltrated with immature myelocytes with characteristic eosinophilic cytoplasmic granules (Payne et al, 1991a(Payne et al, , 1991b(Payne et al, , 1992.…”

Section: Clinical Diseasementioning

confidence: 99%

Isolation and identification of avian leukosis viruses: A review

Fadly

2000

Avian Pathology

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Avian leukosis virus (ALV) is the most common naturally occurring avian retrovirus that can cause a variety of neoplastic disease conditions in chickens. In addition to causing neoplasia, ALV is known to be associated with reduced productivity and other production problems in affected flocks. Biological and molecular assays for the detection of ALV are very useful in identification and classification of new isolates, safety testing of vaccines and in testing pathogen-free and other breeder flocks for freedom of virus infection. However, such assays are not particularly helpful in the diagnosis of virus-induced neoplastic disease of poultry, as avian oncogenic viruses are widespread and infection in the absence of tumor formation is common. Current technology based on molecular and antigenic characteristics of the virus is being used to develop more sensitive and specific procedures for isolation and identification of ALV. This review is primarily focused on the discussion of current technology most commonly used in isolation and identification of ALV associated with clinical disease in chickens.

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“…Since it was first isolated in the UK in 1991 (Payne et al, 1991), ALV-J has spread rapidly worldwide. Moreover, the pathogenicity of ALV-J has increased in China in recent years and has induced a greater diversity of tumours compared with the ALV-J prototype virus, HPRS-103, such as myeloid leukosis, haemangioma, histiocytic sarcoma, fibrosarcoma and erythroblastoma in both broilers and layers (Cheng et al, 2010;Gao et al, 2010Gao et al, , 2012Ji et al, 2012;Lai et al, 2011;Pan et al, 2011;Qu et al, 2012;Shi et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Identification of avian leukosis virus subgroup J-associated acutely transforming viruses carrying the v-src oncogene in layer chickens

Wang

et al. 2016

Journal of General Virology

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To elucidate the molecular basis for the rapid oncogenicity of an acutely transforming avian leukosis virus (ALV), isolated from fibrosarcomas in Hy-Line Brown commercial layer chickens infected with ALV subgroup J (ALV-J), the complete genomic structure of the provirus was determined. In addition to ALV-J replication-complete virus SDAU1102, five proviral DNA genomes, named SJ-1, SJ-2, SJ-3, SJ-4 and SJ-5, carrying different lengths of the v-src oncogene were amplified from original tumours and chicken embryo fibroblasts (CEFs) infected with viral stocks. The genomic sequences of the SJ-1-SJ-5 provirus were closely related to that of SDAU1102 but were defective. The results of Western blot analysis and immunohistochemical staining also showed overexpression of the p60 v-src protein in infected CEFs and tumour tissue. To the best of our knowledge, this is the first report of the isolation and identification of acutely transforming viruses carrying the v-src oncogene with ALV-J as the helper virus. It also offers insight into the generation of acutely transforming ALVs carrying the v-src oncogene.

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A novel subgroup of exogenous avian leukosis virus in chickens

Cited by 333 publications

References 28 publications

Na ⁺ /H ⁺ exchanger type 1 is a receptor for pathogenic subgroup J avian leukosis virus

Na ⁺ /H ⁺ exchanger type 1 is a receptor for pathogenic subgroup J avian leukosis virus

Isolation and identification of avian leukosis viruses: A review

Identification of avian leukosis virus subgroup J-associated acutely transforming viruses carrying the v-src oncogene in layer chickens

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A novel subgroup of exogenous avian leukosis virus in chickens

Cited by 333 publications

References 28 publications

Na + /H + exchanger type 1 is a receptor for pathogenic subgroup J avian leukosis virus

Na + /H + exchanger type 1 is a receptor for pathogenic subgroup J avian leukosis virus

Isolation and identification of avian leukosis viruses: A review

Identification of avian leukosis virus subgroup J-associated acutely transforming viruses carrying the v-src oncogene in layer chickens

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Na ⁺ /H ⁺ exchanger type 1 is a receptor for pathogenic subgroup J avian leukosis virus

Na ⁺ /H ⁺ exchanger type 1 is a receptor for pathogenic subgroup J avian leukosis virus