Novel endogenous retroviral sequences in the chicken genome closely related to HPRS-103 (subgroup J) avian leukosis virus.

Smith, Lorraine P.; Toye, Ayo A.; Howes, K.; Bumstead, Nat; Payne, L. N.; Venugopal, K.

doi:10.1099/0022-1317-80-1-261

Cited by 73 publications

(41 citation statements)

References 22 publications

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“…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).…”

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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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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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“…The EAV-HP (also designated ev/J), the most recently identified members of the endogenous avian retrovirus (EAV) family, are present in Gallus species as 10 to 15 copies per genome (12). Four different structures of EAV-HP proviruses have been identified in the chicken genome.…”

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Intact EAV-HP Endogenous Retrovirus in Sonnerat's Jungle Fowl

Sacco

Howes

Venugopal

2001

J Virol

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The EAV-HP group of chicken endogenous retrovirus elements was previously shown to be defective, with large deletions of the pol gene. In this report, we demonstrate that genomes of other Gallus species also maintain EAV-HP elements with similar deletions. The chicken EAV-HP1 locus was detected in both red (Gallus gallus gallus) and Sonnerat's (Gallus sonneratii) jungle fowl with identical integration sites, indicating that these elements had integrated before separation of the Gallus species. Furthermore, we demonstrate for the first time that the G. sonneratii genome carries EAV-HP elements with intact pol regions.The EAV-HP (also designated ev/J), the most recently identified members of the endogenous avian retrovirus (EAV) family, are present in Gallus species as 10 to 15 copies per genome (12). Four different structures of EAV-HP proviruses have been identified in the chicken genome. Three of these 4-kbplong provirus structures, designated types I, II, and III, show large deletions spanning the entire pol gene and parts of the gag and env regions. Each structure has a different gag-env deletion junction, with the type II and III provirus deletions extending an additional 57 and 86 bp, respectively, than the smallest (type I) provirus deletion size (9, 10). These proviruses are found at multiple loci, with the type I provirus appearing to be the most abundant, based on its frequency in clones randomly screened from separate chicken genomic DNA libraries (9, 10). A single clone, designated ev/J clone 4-1, forms the fourth type of proviral structure, comprising a cDNA of the env subgenomic transcript bounded by long terminal repeats (LTRs) (9). The EAV-HP proviruses are more than 97% identical to the newly emerged subgroup J avian leukosis virus (ALV-J) env gene and demonstrate Ͼ96% sequence identity to other EAV family members in the R and U5 regions, the 5Ј untranslated region, and portions of the gag gene (6, 9, 10).Because of their distribution in several Gallus species, the EAV family is considered an ancient group of retroviruses that integrated into a common ancestor. The genus Gallus is composed of four species: the Sonnerat's or grey jungle fowl (SJF; G. sonneratii), the green jungle fowl (GJF; G. varius), the Ceylonese jungle fowl (CJF; G. lafayettei), and the red jungle fowl (RJF; G. gallus), of which domesticated chickens are a subspecies (G. gallus domesticus) (4). EAV-HP proviruses have also been detected in both RJF and SJF by hybridization of env and LTR sequences and PCR amplification of the env region (10, 12). In this study, we have used a PCR approach to examine whether (i) the EAV-HP proviruses in RJF and SJF have the same pol region deletions as in chickens, (ii) the EAV-HP1 and EAV-HP2 loci, present in chickens, could be detected in the jungle fowls, and (iii) the genomic deletion and integration events occurred before or after the separation of Gallus species.The EMBL accession numbers for the sequences described here are AJ292966 for clone EAV-JF1 and AJ292967 for EAV-JF2, which includ...

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“…Because retroviral integration can be considered random, each ERV is present at a unique chromosomal location (Stoye, 2012). The overwhelming majority of ERVs have been identified using hybridization (Hayward and Hanafusa, 1975;Martin et al, 1981;Chambers et al, 1986;Smith et al, 1999) and polymerase chain reaction (PCR) strategies by amplifying conserved viral sequences (Smith et al, 1999;Xiao et al, 2008) in various animal species. Herniou et al (1998) identified ERVs in reptilian, amphibian, and piscine vertebrates using PCR to amply viral sequence-coding protease and reverse transcriptase.…”

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confidence: 99%

Avian sarcoma and leukosis virus gag gene in the Anser anser domesticus genome

Zhu¹,

Huang²,

Lian³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Endogenous retroviruses are regarded as ideal genetic markers for evolutionary analyses. Birds were some of the initial vertebrates found to contain endogenous retroviruses. However, few studies have investigated the presence and distribution of endogenous retroviruses in goose. In this study, we detected the avian sarcoma and leukosis virus gag gene in the genomic DNA of 8 Chinese native breeds using polymerase chain reaction method. The results indicated that a 1.2-kb avian sarcoma and leukosis virus gag sequence was integrated into all 8 goose breeds. The mean genetic pairwise distance was 0.918% among the investigated geese. To the best of our knowledge, this is the 14380 F. Zhu et al. ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 14379-14386 (2015) first report demonstrating the presence of the endogenous retroviruses in the domestic goose genome. The genetic structure should be further examined in the domestic goose.

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Novel endogenous retroviral sequences in the chicken genome closely related to HPRS-103 (subgroup J) avian leukosis virus.

Cited by 73 publications

References 22 publications

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

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

Intact EAV-HP Endogenous Retrovirus in Sonnerat's Jungle Fowl

Avian sarcoma and leukosis virus gag gene in the Anser anser domesticus genome

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