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Jiři Hejnar - One of the best experts on this subject based on the ideXlab platform.
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identification of new world quails susceptible to infection with Avian Leukosis virus subgroup j
Journal of Virology, 2017Co-Authors: Jiři Plachý, Marketa Reinisova, Dana Kucerova, Filip Senigl, Volodymyr Stepanets, Kateřina Trejbalova, Tomas Hron, Daniel Elleder, Jiři HejnarAbstract:The J subgroup of Avian Leukosis virus (ALV-J) infects domestic chickens, jungle fowl, and turkeys. This virus enters the host cell through a receptor encoded by the tvj locus and identified as Na+/H+ exchanger 1. The resistance to Avian Leukosis virus subgroup J in a great majority of galliform species has been explained by deletions or substitutions of the critical tryptophan 38 in the first extracellular loop of Na+/H+ exchanger 1. Because there are concerns of transspecies virus transmission, we studied natural polymorphisms and susceptibility/resistance in wild galliforms and found the presence of tryptophan 38 in four species of New World quails. The embryo fibroblasts of New World quails are susceptible to infection with Avian Leukosis virus subgroup J, and the cloned Na+/H+ exchanger 1 confers susceptibility on the otherwise resistant host. New World quails are also susceptible to new Avian Leukosis virus subgroup J variants but resistant to subgroups A and B and weakly susceptible to subgroups C and D of Avian sarcoma/Leukosis virus due to obvious defects of the respective receptors. Our results suggest that the Avian Leukosis virus subgroup J could be transmitted to New World quails and establish a natural reservoir of circulating virus with a potential for further evolution. IMPORTANCE: Since its spread in broiler chickens in China and Southeast Asia in 2000, ALV-J remains a major enzootic challenge for the poultry industry. Although the virus diversifies rapidly in the poultry, its spillover and circulation in wild bird species has been prevented by the resistance of most species to ALV-J. It is, nevertheless, important to understand the evolution of the virus and its potential host range in wild birds. Because resistance to Avian retroviruses is due particularly to receptor incompatibility, we studied Na+/H+ exchanger 1, the receptor for ALV-J. In New World quails, we found a receptor compatible with virus entry, and we confirmed the susceptibilities of four New World quail species in vitro We propose that a prospective molecular epidemiology study be conducted to identify species with the potential to become reservoirs for ALV-J.
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Identification of New World Quails Susceptible to Infection with Avian Leukosis Virus Subgroup J
Journal of Virology, 2017Co-Authors: Jiři Plachý, Marketa Reinisova, Dana Kucerova, Filip Senigl, Volodymyr Stepanets, Kateřina Trejbalova, Tomas Hron, Daniel Elleder, Jiři HejnarAbstract:The J subgroup of Avian Leukosis virus (ALV-J) infects domestic chickens, jungle fowl, and turkeys. This virus enters the host cell through a receptor encoded by the tvj locus and identified as Na+/H+ exchanger 1. The resistance to Avian Leukosis virus subgroup J in a great majority of galliform species has been explained by deletions or substitutions of the critical tryptophan 38 in the first extracellular loop of Na+/H+ exchanger 1. Because there are concerns of transspecies virus transmission, we studied natural polymorphisms and susceptibility/resistance in wild galliforms and found the presence of tryptophan 38 in four species of New World quails. The embryo fibroblasts of New World quails are susceptible to infection with Avian Leukosis virus subgroup J, and the cloned Na+/H+ exchanger 1 confers susceptibility on the otherwise resistant host. New World quails are also susceptible to new Avian Leukosis virus subgroup J variants but resistant to subgroups A and B and weakly susceptible to subgroups C and D of Avian sarcoma/Leukosis virus due to obvious defects of the respective receptors. Our results suggest that the Avian Leukosis virus subgroup J could be transmitted to New World quails and establish a natural reservoir of circulating virus with a potential for further evolution. Since its spread in broiler chickens in China and Southeast Asia in 2000, ALV-J remains a major enzootic challenge for the poultry industry. Although the virus diversifies rapidly in the poultry, its spillover and circulation in wild bird species has been prevented by the resistance of most species to ALV-J. It is, nevertheless, important to understand the evolution of the virus and its potential host range in wild birds. Because resistance to Avian retroviruses is due particularly to receptor incompatibility, we studied Na+/H+ exchanger 1, the receptor for ALV-J. In New World quails, we found a receptor compatible with virus entry, and we confirmed the susceptibilities of four New World quail species in vitro We propose that a prospective molecular epidemiology study be conducted to identify species with the potential to become reservoirs for ALV-J. Copyright © 2017 American Society for Microbiology.
Ln Payne - One of the best experts on this subject based on the ideXlab platform.
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the long view 40 years of Avian Leukosis research
Avian Pathology, 2012Co-Authors: Ln Payne, Venugopal NairAbstract:The present review is aimed at the non-specialist reader and is one of a number being written on important diseases of poultry to celebrate the 40th anniversary of the birth of Avian Pathology, the journal of the World Veterinary Poultry Association. The diseases of the Avian Leukosis complex have a number of features of distinction. They were the first neoplastic diseases in any species to be shown, 100 years ago, to be transmissible and caused by viruses, and have consequently been studied extensively by biomedical scientists as models for the role of viruses in cancer. They also became, from around the 1920s, the major cause of mortality and economic loss to the developed poultry industry, and were studied by agricultural scientists searching to understand and control them. The remit of the review is to cover research carried out over the 40 years since 1971, when the journal was founded. In this review on Avian Leukosis, an introductory summary is given of knowledge acquired over the preceding 60 year...
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Tropism of subgroup J Avian Leukosis virus as detected by in situ hybridization
Avian Pathology, 1999Co-Authors: Siti Suri Arshad, K Howes, L. M. Smith, P.h. Russell, K. Venugopal, Ln PayneAbstract:The HPRS-103 strain of Avian retrovirus is the prototype of subgroup J Avian Leukosis virus (ALV-J) and causes myeloid Leukosis in meat-type chickens. Using immunohistochemical detection of the viral groupspecific antigen (Gag) we have previously demonstrated that the induction of myeloid Leukosis by ALV-J is associated with viral tropism for myelomonocytic cells. In this paper we describe an in situ hybridization (ISH) technique using digoxigenin (DIG)-labelled probes for detecting RNA transcripts in tissues from chickens infected with Avian Leukosis viruses (ALV) of subgroups J (HPRS-103 strain) and A (RAV-1 strain). Virus-specific RNA was detected mainly in the heart, kidney, proventriculus and adrenal in locations similar to those of the Gag protein. Viral gene expression could not be detected in the bone marrow or tumour tissues using this test. Higher levels of viral gene expression in the bursa of Fabricius infected with RAV-1, but not with HPRS-103, might help explain the inability of the latter v...
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Developments in Avian Leukosis research.
Leukemia, 1992Co-Authors: Ln PayneAbstract:Infection by exogenous Avian Leukosis viruses (ALVs) causes economic loss from neoplastic mortality and from impaired performance of subclinically infected chickens. This paper reviews progress in research related to natural infection and its control. Subgroup A ALVs causing lymphoid Leukosis are the most common viruses in the field, but variant viruses can arise and cause losses. In Israel in recent years, epidemic outbreaks of haemangiosarcomas caused by a virus of unusual cytopathogenicity have occurred. In the UK, an ALV belonging to a new subgroup for chickens has been recently isolated; this virus is able to cause myeloid Leukosis and nephromas
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a novel subgroup of exogenous Avian Leukosis virus in chickens
Journal of General Virology, 1991Co-Authors: Ln Payne, K Howes, Judith A Frazier, S R Brown, Nat Bumstead, Margaret E ThoulessAbstract:An Avian Leukosis virus with a wide host range belonging to a new subgroup for chickens was isolated from meat-type chicken lines. The virus, of which HPRS-103 strain is the prototype, was of low oncogenicity in chickens but appeared to behave like an exogenous Leukosis virus. Neutralizing antibodies to the virus were found in three of five meat-type chicken lines, but not in seven layer lines. The virus and its Rous sarcoma virus pseudotype did not replicate in, or transform, mammalian cells.
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Eradication of exogenous Avian Leukosis virus from commercial layer breeder lines.
Veterinary Record, 1991Co-Authors: Ln Payne, K HowesAbstract:On the basis of earlier studies, a programme for eradicating exogenous Avian Leukosis virus from commercial poultry stock was devised and applied to 11 layer breeder lines. After three years of testing, Avian Leukosis virus infection was eradicated completely from all but one, a slow-feathering line.
Jiři Plachý - One of the best experts on this subject based on the ideXlab platform.
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identification of new world quails susceptible to infection with Avian Leukosis virus subgroup j
Journal of Virology, 2017Co-Authors: Jiři Plachý, Marketa Reinisova, Dana Kucerova, Filip Senigl, Volodymyr Stepanets, Kateřina Trejbalova, Tomas Hron, Daniel Elleder, Jiři HejnarAbstract:The J subgroup of Avian Leukosis virus (ALV-J) infects domestic chickens, jungle fowl, and turkeys. This virus enters the host cell through a receptor encoded by the tvj locus and identified as Na+/H+ exchanger 1. The resistance to Avian Leukosis virus subgroup J in a great majority of galliform species has been explained by deletions or substitutions of the critical tryptophan 38 in the first extracellular loop of Na+/H+ exchanger 1. Because there are concerns of transspecies virus transmission, we studied natural polymorphisms and susceptibility/resistance in wild galliforms and found the presence of tryptophan 38 in four species of New World quails. The embryo fibroblasts of New World quails are susceptible to infection with Avian Leukosis virus subgroup J, and the cloned Na+/H+ exchanger 1 confers susceptibility on the otherwise resistant host. New World quails are also susceptible to new Avian Leukosis virus subgroup J variants but resistant to subgroups A and B and weakly susceptible to subgroups C and D of Avian sarcoma/Leukosis virus due to obvious defects of the respective receptors. Our results suggest that the Avian Leukosis virus subgroup J could be transmitted to New World quails and establish a natural reservoir of circulating virus with a potential for further evolution. IMPORTANCE: Since its spread in broiler chickens in China and Southeast Asia in 2000, ALV-J remains a major enzootic challenge for the poultry industry. Although the virus diversifies rapidly in the poultry, its spillover and circulation in wild bird species has been prevented by the resistance of most species to ALV-J. It is, nevertheless, important to understand the evolution of the virus and its potential host range in wild birds. Because resistance to Avian retroviruses is due particularly to receptor incompatibility, we studied Na+/H+ exchanger 1, the receptor for ALV-J. In New World quails, we found a receptor compatible with virus entry, and we confirmed the susceptibilities of four New World quail species in vitro We propose that a prospective molecular epidemiology study be conducted to identify species with the potential to become reservoirs for ALV-J.
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Identification of New World Quails Susceptible to Infection with Avian Leukosis Virus Subgroup J
Journal of Virology, 2017Co-Authors: Jiři Plachý, Marketa Reinisova, Dana Kucerova, Filip Senigl, Volodymyr Stepanets, Kateřina Trejbalova, Tomas Hron, Daniel Elleder, Jiři HejnarAbstract:The J subgroup of Avian Leukosis virus (ALV-J) infects domestic chickens, jungle fowl, and turkeys. This virus enters the host cell through a receptor encoded by the tvj locus and identified as Na+/H+ exchanger 1. The resistance to Avian Leukosis virus subgroup J in a great majority of galliform species has been explained by deletions or substitutions of the critical tryptophan 38 in the first extracellular loop of Na+/H+ exchanger 1. Because there are concerns of transspecies virus transmission, we studied natural polymorphisms and susceptibility/resistance in wild galliforms and found the presence of tryptophan 38 in four species of New World quails. The embryo fibroblasts of New World quails are susceptible to infection with Avian Leukosis virus subgroup J, and the cloned Na+/H+ exchanger 1 confers susceptibility on the otherwise resistant host. New World quails are also susceptible to new Avian Leukosis virus subgroup J variants but resistant to subgroups A and B and weakly susceptible to subgroups C and D of Avian sarcoma/Leukosis virus due to obvious defects of the respective receptors. Our results suggest that the Avian Leukosis virus subgroup J could be transmitted to New World quails and establish a natural reservoir of circulating virus with a potential for further evolution. Since its spread in broiler chickens in China and Southeast Asia in 2000, ALV-J remains a major enzootic challenge for the poultry industry. Although the virus diversifies rapidly in the poultry, its spillover and circulation in wild bird species has been prevented by the resistance of most species to ALV-J. It is, nevertheless, important to understand the evolution of the virus and its potential host range in wild birds. Because resistance to Avian retroviruses is due particularly to receptor incompatibility, we studied Na+/H+ exchanger 1, the receptor for ALV-J. In New World quails, we found a receptor compatible with virus entry, and we confirmed the susceptibilities of four New World quail species in vitro We propose that a prospective molecular epidemiology study be conducted to identify species with the potential to become reservoirs for ALV-J. Copyright © 2017 American Society for Microbiology.
Xiaomei Wang - One of the best experts on this subject based on the ideXlab platform.
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Avian Leukosis virus subgroup a and b infection in wild birds of northeast china
Veterinary Microbiology, 2013Co-Authors: Delong Li, Xiangwei Zeng, Xiaole Qi, Yongqiang Wang, Bo Yang, Xiaomei WangAbstract: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.
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development of an antigen capture elisa for the detection of Avian Leukosis virus p27 antigen
Journal of Virological Methods, 2013Co-Authors: Delong Li, Xiaole Qi, Guan Wu, Yongqiang Wang, Xiaomei WangAbstract:Abstract An antigen-capture enzyme-linked immunosorbent assay (AC-ELISA) employing monoclonal and polyclonal antibodies against p27 was developed for the detection of the Avian Leukosis virus (ALV). The specificity of the optimized AC-ELISA was evaluated using Avian Leukosis virus subgroup J (ALV-J), Avian Leukosis virus subgroup A (ALV-A), Avian Leukosis virus subgroup B (ALV-B), Avian infectious bronchitis virus (IBV), Marek's disease virus (MDV), Avian infectious laryngotracheitis virus (ILTV), Fowlpox virus (FPV), infectious bursal disease virus (IBDV), Newcastle disease virus (NDV), Avian reovirus (ARV), reticuloendotheliosis virus (REV), Avian influenza virus (AIV) and Escherichia coli . The only specimens that yielded a strong signal were ALV-J, ALV-A and ALV-B, indicating that this assay is suitable for the detection of ALV. The limit of detection of this assay was 1.25 ng/ml of rp27 protein and 10 1.79 TCID 50 units of HLJ09MDJ-1 (ALV-J). Moreover, this AC-ELISA can detect ALV in cloacal swabs of chickens experimentally infected as early as 12 days post-infection. The AC-ELISA detected the virus in the albumin and cloacal swabs of naturally infected chickens, and the results were confirmed by PCR, indicating that the AC-ELISA was a suitable method for the detection of ALV. This test is rapid and sensitive and could be convenient for epidemiological studies and eradication programs.
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Novel sequences of subgroup J Avian Leukosis viruses associated with hemangioma in Chinese layer hens
Virology Journal, 2011Co-Authors: Yongqiang Wang, Xiaole Qi, Xiaomei WangAbstract:Background 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.
Hongmei Li - One of the best experts on this subject based on the ideXlab platform.
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gga-miR-375 plays a key role in tumorigenesis post subgroup J Avian Leukosis virus infection.
PLOS ONE, 2014Co-Authors: Hongxin Li, Huiqing Shang, Huanmin Zhang, Jun Ji, Hongmei LiAbstract:Avian Leukosis is a neoplastic disease caused in part by subgroup J Avian Leukosis virus J (ALV-J). Micro ribonucleic acids (miRNAs) play pivotal oncogenic and tumour-suppressor roles in tumour development and progression. However, little is known about the potential role of miRNAs in Avian Leukosis tumours. We have found a novel tumour-suppressor miRNA, gga-miR-375, associated with Avian Leukosis tumorigenesis by miRNA microarray in a previous report. We have also previously studied the biological function of gga-miR-375; Overexpression of gga-miR-375 significantly inhibited DF-1 cell proliferation, and significantly reduced the expression of yes-associated protein 1 (YAP1) by repressing the activity of a luciferase reporter carrying the 3′-untranslated region of YAP1. This indicates that gga-miR-375 is frequently downregulated in Avian Leukosis by inhibiting cell proliferation through YAP1 oncogene targeting. Overexpression of gga-miR-375 markedly promoted serum starvation induced apoptosis, and there may be the reason why the tumour cycle is so long in the infected chickens. In vivo assays, gga-miR-375 was significantly downregulated in chicken livers 20 days after infection with ALV-J, and YAP1 was significantly upregulated 20 days after ALV-J infection (P
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gga mir 375 plays a key role in tumorigenesis post subgroup j Avian Leukosis virus infection
PLOS ONE, 2014Co-Authors: Hongxin Li, Huiqing Shang, Huanmin Zhang, Jun Ji, Hongmei LiAbstract:Avian Leukosis is a neoplastic disease caused in part by subgroup J Avian Leukosis virus J (ALV-J). Micro ribonucleic acids (miRNAs) play pivotal oncogenic and tumour-suppressor roles in tumour development and progression. However, little is known about the potential role of miRNAs in Avian Leukosis tumours. We have found a novel tumour-suppressor miRNA, gga-miR-375, associated with Avian Leukosis tumorigenesis by miRNA microarray in a previous report. We have also previously studied the biological function of gga-miR-375; Overexpression of gga-miR-375 significantly inhibited DF-1 cell proliferation, and significantly reduced the expression of yes-associated protein 1 (YAP1) by repressing the activity of a luciferase reporter carrying the 3′-untranslated region of YAP1. This indicates that gga-miR-375 is frequently downregulated in Avian Leukosis by inhibiting cell proliferation through YAP1 oncogene targeting. Overexpression of gga-miR-375 markedly promoted serum starvation induced apoptosis, and there may be the reason why the tumour cycle is so long in the infected chickens. In vivo assays, gga-miR-375 was significantly downregulated in chicken livers 20 days after infection with ALV-J, and YAP1 was significantly upregulated 20 days after ALV-J infection (P<0.05). We also found that expression of cyclin E, an important regulator of cell cycle progression, was significantly upregulated (P<0.05). Drosophila inhibitor of apoptosis protein 1 (DIAP1), which is related to caspase-dependent apoptosis, was also significantly upregulated after infection. Our data suggests that gga-miR-375 may function as a tumour suppressor thereby regulating cancer cell proliferation and it plays a key role in Avian Leukosis tumorigenesis.
