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Avian Leukosis

The Experts below are selected from a list of 204 Experts worldwide ranked by ideXlab platform

Jiři Hejnar – 1st expert on this subject based on the ideXlab platform

  • identification of new world quails susceptible to infection with Avian Leukosis virus subgroup j
    Journal of Virology, 2017
    Co-Authors: Jiři Plachý, Marketa Reinisova, Dana Kucerova, Filip Senigl, Volodymyr Stepanets, Tomas Hron, Kateřina Trejbalova, Daniel Elleder, Jiři Hejnar

    Abstract:

    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.

  • Identification of New World Quails Susceptible to Infection with Avian Leukosis Virus Subgroup J
    Journal of Virology, 2017
    Co-Authors: Jiři Plachý, Marketa Reinisova, Dana Kucerova, Filip Senigl, Volodymyr Stepanets, Tomas Hron, Kateřina Trejbalova, Daniel Elleder, Jiři Hejnar

    Abstract:

    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 – 2nd expert on this subject based on the ideXlab platform

  • the long view 40 years of Avian Leukosis research
    Avian Pathology, 2012
    Co-Authors: Ln Payne, Venugopal Nair

    Abstract:

    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…

  • Tropism of subgroup J Avian Leukosis virus as detected by in situ hybridization
    Avian Pathology, 1999
    Co-Authors: Siti Suri Arshad, K Howes, L. M. Smith, P.h. Russell, K. Venugopal, Ln Payne

    Abstract:

    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…

  • Developments in Avian Leukosis research.
    Leukemia, 1992
    Co-Authors: Ln Payne

    Abstract:

    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

Jiři Plachý – 3rd expert on this subject based on the ideXlab platform

  • identification of new world quails susceptible to infection with Avian Leukosis virus subgroup j
    Journal of Virology, 2017
    Co-Authors: Jiři Plachý, Marketa Reinisova, Dana Kucerova, Filip Senigl, Volodymyr Stepanets, Tomas Hron, Kateřina Trejbalova, Daniel Elleder, Jiři Hejnar

    Abstract:

    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.

  • Identification of New World Quails Susceptible to Infection with Avian Leukosis Virus Subgroup J
    Journal of Virology, 2017
    Co-Authors: Jiři Plachý, Marketa Reinisova, Dana Kucerova, Filip Senigl, Volodymyr Stepanets, Tomas Hron, Kateřina Trejbalova, Daniel Elleder, Jiři Hejnar

    Abstract:

    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.