The Experts below are selected from a list of 747 Experts worldwide ranked by ideXlab platform
Peter K. Kaiser - One of the best experts on this subject based on the ideXlab platform.
-
Chicken Anaemia Virus evades host immune responses in transformed lymphocytes
The Journal of general virology, 2018Co-Authors: Efstathios S. Giotis, Daniel Todd, A. N. J. Scott, Lisa Rothwell, Richard Talbot, David W. Burt, Elizabeth Glass, Peter K. KaiserAbstract:Chicken Anaemia Virus (CAV) is a lymphotropic Virus that causes Anaemia and immunosuppression in Chickens. Previously, we proposed that CAV evades host antiviral responses in vivo by disrupting T-cell signalling, but the precise cellular targets and modes of action remain elusive. In this study, we examined gene expression in Marek’s disease Virus-transformed Chicken T-cell line MSB-1 after infection with CAV using both a custom 5K immune-focused microarray and quantitative real-time PCR at 24, 48 and 72 h post-infection. The data demonstrate an intricate equilibrium between CAV and the host gene expression, displaying subtle but significant modulation of transcripts involved in the T-cell, inflammation and NF-κB signalling cascades. CAV efficiently blocked the induction of type-I interferons and interferon-stimulated genes at 72 h. The cell expression pattern implies that CAV subverts host antiviral responses and that the transformed environment of MSB-1 cells offers an opportunistic advantage for Virus growth.
-
Transcriptomic Profiling of Virus-Host Cell Interactions following Chicken Anaemia Virus (CAV) Infection in an In Vivo Model.
PloS one, 2015Co-Authors: Efstathios S. Giotis, A. N. J. Scott, Lisa Rothwell, Richard Talbot, David W. Burt, Elizabeth Glass, Daniel A. Todd, Peter K. KaiserAbstract:Chicken Anaemia Virus (CAV) is an economically important Virus that targets lymphoid and erythroblastoid progenitor cells leading to immunosuppression. This study aimed to investigate the interplay between viral infection and the host's immune response to better understand the pathways that lead to CAV-induced immunosuppression. To mimic vertical transmission of CAV in the absence of maternally-derived antibody, day-old chicks were infected and their responses measured at various time-points post-infection by qRT-PCR and gene expression microarrays. The kinetics of mRNA expression levels of signature cytokines of innate and adaptive immune responses were determined by qRT-PCR. The global gene expression profiles of mock-infected (control) and CAV-infected Chickens at 14 dpi were also compared using a Chicken immune-related 5K microarray. Although in the thymus there was evidence of induction of an innate immune response following CAV infection, this was limited in magnitude. There was little evidence of a Th1 adaptive immune response in any lymphoid tissue, as would normally be expected in response to viral infection. Most cytokines associated with Th1, Th2 or Treg subsets were down-regulated, except IL-2, IL-13, IL-10 and IFNγ, which were all up-regulated in thymus and bone marrow. From the microarray studies, genes that exhibited significant (greater than 1.5-fold, false discovery rate
-
transcriptomic profiling of Virus host cell interactions following Chicken Anaemia Virus cav infection in an in vivo model
PLOS ONE, 2015Co-Authors: Efstathios S. Giotis, A. N. J. Scott, Lisa Rothwell, Richard Talbot, David W. Burt, Elizabeth Glass, Daniel A. Todd, Peter K. KaiserAbstract:Chicken Anaemia Virus (CAV) is an economically important Virus that targets lymphoid and erythroblastoid progenitor cells leading to immunosuppression. This study aimed to investigate the interplay between viral infection and the host's immune response to better understand the pathways that lead to CAV-induced immunosuppression. To mimic vertical transmission of CAV in the absence of maternally-derived antibody, day-old chicks were infected and their responses measured at various time-points post-infection by qRT-PCR and gene expression microarrays. The kinetics of mRNA expression levels of signature cytokines of innate and adaptive immune responses were determined by qRT-PCR. The global gene expression profiles of mock-infected (control) and CAV-infected Chickens at 14 dpi were also compared using a Chicken immune-related 5K microarray. Although in the thymus there was evidence of induction of an innate immune response following CAV infection, this was limited in magnitude. There was little evidence of a Th1 adaptive immune response in any lymphoid tissue, as would normally be expected in response to viral infection. Most cytokines associated with Th1, Th2 or Treg subsets were down-regulated, except IL-2, IL-13, IL-10 and IFNγ, which were all up-regulated in thymus and bone marrow. From the microarray studies, genes that exhibited significant (greater than 1.5-fold, false discovery rate <0.05) changes in expression in thymus and bone marrow on CAV infection were mainly associated with T-cell receptor signalling, immune response, transcriptional regulation, intracellular signalling and regulation of apoptosis. Expression levels of a number of adaptor proteins, such as src-like adaptor protein (SLA), a negative regulator of T-cell receptor signalling and the transcription factor Special AT-rich Binding Protein 1 (SATB1), were significantly down-regulated by CAV infection, suggesting potential roles for these genes as regulators of viral infection or cell defence. These results extend our understanding of CAV-induced immunosuppression and suggest a global immune dysregulation following CAV infection.
A. N. J. Scott - One of the best experts on this subject based on the ideXlab platform.
-
Chicken Anaemia Virus evades host immune responses in transformed lymphocytes
The Journal of general virology, 2018Co-Authors: Efstathios S. Giotis, Daniel Todd, A. N. J. Scott, Lisa Rothwell, Richard Talbot, David W. Burt, Elizabeth Glass, Peter K. KaiserAbstract:Chicken Anaemia Virus (CAV) is a lymphotropic Virus that causes Anaemia and immunosuppression in Chickens. Previously, we proposed that CAV evades host antiviral responses in vivo by disrupting T-cell signalling, but the precise cellular targets and modes of action remain elusive. In this study, we examined gene expression in Marek’s disease Virus-transformed Chicken T-cell line MSB-1 after infection with CAV using both a custom 5K immune-focused microarray and quantitative real-time PCR at 24, 48 and 72 h post-infection. The data demonstrate an intricate equilibrium between CAV and the host gene expression, displaying subtle but significant modulation of transcripts involved in the T-cell, inflammation and NF-κB signalling cascades. CAV efficiently blocked the induction of type-I interferons and interferon-stimulated genes at 72 h. The cell expression pattern implies that CAV subverts host antiviral responses and that the transformed environment of MSB-1 cells offers an opportunistic advantage for Virus growth.
-
Transcriptomic Profiling of Virus-Host Cell Interactions following Chicken Anaemia Virus (CAV) Infection in an In Vivo Model.
PloS one, 2015Co-Authors: Efstathios S. Giotis, A. N. J. Scott, Lisa Rothwell, Richard Talbot, David W. Burt, Elizabeth Glass, Daniel A. Todd, Peter K. KaiserAbstract:Chicken Anaemia Virus (CAV) is an economically important Virus that targets lymphoid and erythroblastoid progenitor cells leading to immunosuppression. This study aimed to investigate the interplay between viral infection and the host's immune response to better understand the pathways that lead to CAV-induced immunosuppression. To mimic vertical transmission of CAV in the absence of maternally-derived antibody, day-old chicks were infected and their responses measured at various time-points post-infection by qRT-PCR and gene expression microarrays. The kinetics of mRNA expression levels of signature cytokines of innate and adaptive immune responses were determined by qRT-PCR. The global gene expression profiles of mock-infected (control) and CAV-infected Chickens at 14 dpi were also compared using a Chicken immune-related 5K microarray. Although in the thymus there was evidence of induction of an innate immune response following CAV infection, this was limited in magnitude. There was little evidence of a Th1 adaptive immune response in any lymphoid tissue, as would normally be expected in response to viral infection. Most cytokines associated with Th1, Th2 or Treg subsets were down-regulated, except IL-2, IL-13, IL-10 and IFNγ, which were all up-regulated in thymus and bone marrow. From the microarray studies, genes that exhibited significant (greater than 1.5-fold, false discovery rate
-
transcriptomic profiling of Virus host cell interactions following Chicken Anaemia Virus cav infection in an in vivo model
PLOS ONE, 2015Co-Authors: Efstathios S. Giotis, A. N. J. Scott, Lisa Rothwell, Richard Talbot, David W. Burt, Elizabeth Glass, Daniel A. Todd, Peter K. KaiserAbstract:Chicken Anaemia Virus (CAV) is an economically important Virus that targets lymphoid and erythroblastoid progenitor cells leading to immunosuppression. This study aimed to investigate the interplay between viral infection and the host's immune response to better understand the pathways that lead to CAV-induced immunosuppression. To mimic vertical transmission of CAV in the absence of maternally-derived antibody, day-old chicks were infected and their responses measured at various time-points post-infection by qRT-PCR and gene expression microarrays. The kinetics of mRNA expression levels of signature cytokines of innate and adaptive immune responses were determined by qRT-PCR. The global gene expression profiles of mock-infected (control) and CAV-infected Chickens at 14 dpi were also compared using a Chicken immune-related 5K microarray. Although in the thymus there was evidence of induction of an innate immune response following CAV infection, this was limited in magnitude. There was little evidence of a Th1 adaptive immune response in any lymphoid tissue, as would normally be expected in response to viral infection. Most cytokines associated with Th1, Th2 or Treg subsets were down-regulated, except IL-2, IL-13, IL-10 and IFNγ, which were all up-regulated in thymus and bone marrow. From the microarray studies, genes that exhibited significant (greater than 1.5-fold, false discovery rate <0.05) changes in expression in thymus and bone marrow on CAV infection were mainly associated with T-cell receptor signalling, immune response, transcriptional regulation, intracellular signalling and regulation of apoptosis. Expression levels of a number of adaptor proteins, such as src-like adaptor protein (SLA), a negative regulator of T-cell receptor signalling and the transcription factor Special AT-rich Binding Protein 1 (SATB1), were significantly down-regulated by CAV infection, suggesting potential roles for these genes as regulators of viral infection or cell defence. These results extend our understanding of CAV-induced immunosuppression and suggest a global immune dysregulation following CAV infection.
-
Investigation of the unstable attenuation exhibited by a Chicken Anaemia Virus isolate.
Avian pathology : journal of the W.V.P.A, 2003Co-Authors: Daniel Todd, Brian M. Meehan, A. N. J. Scott, Julie L. Creelan, Thomas J. Connor, N. W. Ball, Gerard F. Mckenna, M. S. McnultyAbstract:An attenuated Chicken Anaemia Virus (CAV) isolate, cloned isolate 10, which was molecularly cloned from the Cuxhaven-1 CAV after 173 cell-culture passages, was shown previously to recover pathogenicity following 10 passages in young chicks. The consensus nucleotide sequence of the 'revertant' (Rev) Virus, present as a tissue homogenate, differed from cloned isolate 10 at a single nucleotide residue (nucleotide 1739) that changed amino acid 287 of the capsid protein from alanine to aspartic acid. Subjecting Rev Virus to 10 cell-culture passages reselected Viruses with an alanine at this amino acid position. Experimental infections using a molecularly cloned Rev Virus isolate demonstrated that the mutation at nucleotide 1739 was not in itself responsible for the recovery of pathogenicity exhibited by the Rev Virus. Additional sequence analyses of cloned amplicons provided evidence that the Rev Virus population comprised minor, genetically different subpopulations, and provided an indication of CAV's potential for genetic change.
-
Characterisation of a Chicken Anaemia Virus variant population that resists neutralisation with a group-specific monoclonal antibody.
Archives of virology, 2001Co-Authors: A. N. J. Scott, M. S. Mcnulty, Daniel ToddAbstract:A variant population of Chicken Anaemia Virus (CAV), termed P310 2A9-resist, that resists neutralisation by the monoclonal antibody (MAb) 2A9, was selected from Cux-1 Virus that had been passaged 310 times (P310) in MDCC-MSB1 cells. Substantially higher concentrations of MAb 2A9 were required to neutralise the selected Virus compared to those required to neutralise a low-passage (P13) Cux-1 isolate. Virus neutralisation tests showed that serum from Chickens infected with the P310 2A9-resist Virus neutralised P13 Virus and that serum from Chickens infected with P13 Virus conversely neutralised the P310 2A9-resist Virus. MDCC-MSB1 cells infected with the P310 2A9-resist Virus produced no staining with low dilutions (1:100) of Mab 2A9 in an indirect immunofluorescence (IF) test, whereas cells infected with P13 Virus reacted positively at high MAb dilutions (1:80,000). Experimental infections of 1-day-old SPF chicks showed that the P310 2A9-resist Virus was substantially attenuated. Chimaeric Viruses constructed using PCR-amplified regions from the P310 2A9-resist and a pathogenic low-passage cloned Cux-1 isolate showed that the reduced MAb reactivity and attenuation exhibited by the P310 2A9-resist Virus were mainly associated with a region encoding the N-terminal half of the 50 kDa capsid protein VP1 and C-terminal regions of VP2 and VP3. The nucleotide sequence of the protein-coding region of the P310 2A9-resist Virus is reported and the amino acid sequences of the 3 encoded proteins compared with those of other Cux-1 isolates.
Efstathios S. Giotis - One of the best experts on this subject based on the ideXlab platform.
-
Chicken Anaemia Virus evades host immune responses in transformed lymphocytes
The Journal of general virology, 2018Co-Authors: Efstathios S. Giotis, Daniel Todd, A. N. J. Scott, Lisa Rothwell, Richard Talbot, David W. Burt, Elizabeth Glass, Peter K. KaiserAbstract:Chicken Anaemia Virus (CAV) is a lymphotropic Virus that causes Anaemia and immunosuppression in Chickens. Previously, we proposed that CAV evades host antiviral responses in vivo by disrupting T-cell signalling, but the precise cellular targets and modes of action remain elusive. In this study, we examined gene expression in Marek’s disease Virus-transformed Chicken T-cell line MSB-1 after infection with CAV using both a custom 5K immune-focused microarray and quantitative real-time PCR at 24, 48 and 72 h post-infection. The data demonstrate an intricate equilibrium between CAV and the host gene expression, displaying subtle but significant modulation of transcripts involved in the T-cell, inflammation and NF-κB signalling cascades. CAV efficiently blocked the induction of type-I interferons and interferon-stimulated genes at 72 h. The cell expression pattern implies that CAV subverts host antiviral responses and that the transformed environment of MSB-1 cells offers an opportunistic advantage for Virus growth.
-
RESEARCH ARTICLE Transcriptomic Profiling of Virus-Host Cell Interactions following Chicken Anaemia Virus (CAV) Infection in an In VivoModel
2016Co-Authors: Efstathios S. Giotis, Alistair ScottAbstract:Chicken Anaemia Virus (CAV) is an economically important Virus that targets lymphoid and erythroblastoid progenitor cells leading to immunosuppression. This study aimed to investi-gate the interplay between viral infection and the host’s immune response to better under-stand the pathways that lead to CAV-induced immunosuppression. To mimic vertical transmission of CAV in the absence of maternally-derived antibody, day-old chicks were infected and their responses measured at various time-points post-infection by qRT-PCR and gene expression microarrays. The kinetics of mRNA expression levels of signature cytokines of innate and adaptive immune responses were determined by qRT-PCR. The global gene expression profiles of mock-infected (control) and CAV-infected Chickens at 14 dpi were also compared using a Chicken immune-related 5K microarray. Although in the thy-mus there was evidence of induction of an innate immune response following CAV infection, this was limited in magnitude. There was little evidence of a Th1 adaptive immune response in any lymphoid tissue, as would normally be expected in response to viral infection. Most cytokines associated with Th1, Th2 or Treg subsets were down-regulated, except IL-2, IL-13
-
Transcriptomic Profiling of Virus-Host Cell Interactions following Chicken Anaemia Virus (CAV) Infection in an In Vivo Model.
PloS one, 2015Co-Authors: Efstathios S. Giotis, A. N. J. Scott, Lisa Rothwell, Richard Talbot, David W. Burt, Elizabeth Glass, Daniel A. Todd, Peter K. KaiserAbstract:Chicken Anaemia Virus (CAV) is an economically important Virus that targets lymphoid and erythroblastoid progenitor cells leading to immunosuppression. This study aimed to investigate the interplay between viral infection and the host's immune response to better understand the pathways that lead to CAV-induced immunosuppression. To mimic vertical transmission of CAV in the absence of maternally-derived antibody, day-old chicks were infected and their responses measured at various time-points post-infection by qRT-PCR and gene expression microarrays. The kinetics of mRNA expression levels of signature cytokines of innate and adaptive immune responses were determined by qRT-PCR. The global gene expression profiles of mock-infected (control) and CAV-infected Chickens at 14 dpi were also compared using a Chicken immune-related 5K microarray. Although in the thymus there was evidence of induction of an innate immune response following CAV infection, this was limited in magnitude. There was little evidence of a Th1 adaptive immune response in any lymphoid tissue, as would normally be expected in response to viral infection. Most cytokines associated with Th1, Th2 or Treg subsets were down-regulated, except IL-2, IL-13, IL-10 and IFNγ, which were all up-regulated in thymus and bone marrow. From the microarray studies, genes that exhibited significant (greater than 1.5-fold, false discovery rate
-
transcriptomic profiling of Virus host cell interactions following Chicken Anaemia Virus cav infection in an in vivo model
PLOS ONE, 2015Co-Authors: Efstathios S. Giotis, A. N. J. Scott, Lisa Rothwell, Richard Talbot, David W. Burt, Elizabeth Glass, Daniel A. Todd, Peter K. KaiserAbstract:Chicken Anaemia Virus (CAV) is an economically important Virus that targets lymphoid and erythroblastoid progenitor cells leading to immunosuppression. This study aimed to investigate the interplay between viral infection and the host's immune response to better understand the pathways that lead to CAV-induced immunosuppression. To mimic vertical transmission of CAV in the absence of maternally-derived antibody, day-old chicks were infected and their responses measured at various time-points post-infection by qRT-PCR and gene expression microarrays. The kinetics of mRNA expression levels of signature cytokines of innate and adaptive immune responses were determined by qRT-PCR. The global gene expression profiles of mock-infected (control) and CAV-infected Chickens at 14 dpi were also compared using a Chicken immune-related 5K microarray. Although in the thymus there was evidence of induction of an innate immune response following CAV infection, this was limited in magnitude. There was little evidence of a Th1 adaptive immune response in any lymphoid tissue, as would normally be expected in response to viral infection. Most cytokines associated with Th1, Th2 or Treg subsets were down-regulated, except IL-2, IL-13, IL-10 and IFNγ, which were all up-regulated in thymus and bone marrow. From the microarray studies, genes that exhibited significant (greater than 1.5-fold, false discovery rate <0.05) changes in expression in thymus and bone marrow on CAV infection were mainly associated with T-cell receptor signalling, immune response, transcriptional regulation, intracellular signalling and regulation of apoptosis. Expression levels of a number of adaptor proteins, such as src-like adaptor protein (SLA), a negative regulator of T-cell receptor signalling and the transcription factor Special AT-rich Binding Protein 1 (SATB1), were significantly down-regulated by CAV infection, suggesting potential roles for these genes as regulators of viral infection or cell defence. These results extend our understanding of CAV-induced immunosuppression and suggest a global immune dysregulation following CAV infection.
Meng-shiou Lee - One of the best experts on this subject based on the ideXlab platform.
-
Tissue Tropism of Chicken Anaemia Virus in Naturally Infected Broiler Chickens.
Journal of Comparative Pathology, 2019Co-Authors: Pablo Castaño, Julio Benavides, Meng-shiou Lee, Miguel Fernández, Miguel A. Fuertes, M. Royo, J.m. Fernández, Valentín Pérez Pérez, M.c. FerrerasAbstract:Summary Chicken Anaemia Virus (CAV) causes Chicken infectious Anaemia, a severe disease characterized by Anaemia and immunosuppression and leading to serious economic losses in the poultry industry worldwide. Although CAV infection has been investigated under experimental conditions, information regarding natural infection is scarce. This report describes an outbreak of CAV infection in 18-day-old broiler Chickens and investigates Virus tropism in affected birds. Thymic atrophy, pale bone marrow, swelling of the legs and foot ulcers (gangrenous dermatitis) were the most common gross lesions. Severe lymphoid cell depletion in the thymic cortex and presence of intranuclear acidophilic inclusion bodies, depletion of haemopoietic cells in bone marrow and presence of lymphoid infiltrates in several organs were also observed. Immunohistochemical labelling demonstrated the CAV antigens VP1 and VP3 in several organs. The expression of both proteins was similar in the thymic cortex and in the bone marrow, the main target organs of CAV; however, VP3 expression was more abundant in the other organs. Labelling of serial sections showed that CD3+ T lymphocytes might be responsible for the dissemination of the Virus from the thymus and bone marrow to other organs and that Virus-induced apoptosis, mediated through caspase-3, occurred mainly in the thymus and bone marrow.
-
Characterization of the DNA binding activity of structural protein VP1 from Chicken Anaemia Virus
BMC Veterinary Research, 2018Co-Authors: Guan-hua Lai, Yi-yang Lien, Ming-kuem Lin, Hsi-jien Chen, Jai-hong Cheng, Fang-chun Sun, Meng-shiunn Lee, Meng-shiou LeeAbstract:Background Chicken Anaemia Virus (CAV) is commonly found in poultry. VP1 is the sole structural protein of CAV, which is the major component responsible for capsid assembly. The CAV virion consists of the VP1 protein and a viral genome. However, there is currently no information on the protein-nucleic acid interactions between VP1 and DNA molecules. Results In this study, the recombinant VP1 protein of CAV was expressed and purified to characterize its DNA binding activity. When VP1 protein was incubated with a DNA molecule, the DNA molecule exhibited retarded migration on an agarose gel. Regardless of whether the sequence of the viral genome was involved in the DNA molecule, DNA retardation was not significantly influenced. This outcome indicated VP1 is a DNA binding protein with no sequence specificity. Various DNA molecules with different conformations, such as circular dsDNA, linear dsDNA, linear ssDNA and circular ssDNA, interacted with VP1 proteins according to the results of a DNA retardation assay. Further quantification of the amount of VP1 protein required for DNA binding, the circular ssDNA demonstrated a high affinity for the VP1 protein. The preferences arranged in the order of affinity for the VP1 protein with DNA are circular ssDNA, linear ssDNA, supercoiled circular dsDNA, open circular DNA and linear dsDNA. Conclusions The results of this study demonstrated that the interaction between VP1 and DNA molecules exhibited various binding preferences that were dependent on the structural conformation of DNA. Taken together, the results of this report are the first to demonstrate that VP1 has no sequence-specific DNA binding activity. The particular binding preferences of VP1 might play multiple roles in DNA replication or encapsidation during the viral life cycle.
-
Characterization of the DNA binding activity of structural protein VP1 from Chicken Anaemia Virus.
BMC veterinary research, 2018Co-Authors: Guan-hua Lai, Yi-yang Lien, Ming-kuem Lin, Hsi-jien Chen, Jai-hong Cheng, Fang-chun Sun, Meng-shiunn Lee, Meng-shiou LeeAbstract:Chicken Anaemia Virus (CAV) is commonly found in poultry. VP1 is the sole structural protein of CAV, which is the major component responsible for capsid assembly. The CAV virion consists of the VP1 protein and a viral genome. However, there is currently no information on the protein-nucleic acid interactions between VP1 and DNA molecules. In this study, the recombinant VP1 protein of CAV was expressed and purified to characterize its DNA binding activity. When VP1 protein was incubated with a DNA molecule, the DNA molecule exhibited retarded migration on an agarose gel. Regardless of whether the sequence of the viral genome was involved in the DNA molecule, DNA retardation was not significantly influenced. This outcome indicated VP1 is a DNA binding protein with no sequence specificity. Various DNA molecules with different conformations, such as circular dsDNA, linear dsDNA, linear ssDNA and circular ssDNA, interacted with VP1 proteins according to the results of a DNA retardation assay. Further quantification of the amount of VP1 protein required for DNA binding, the circular ssDNA demonstrated a high affinity for the VP1 protein. The preferences arranged in the order of affinity for the VP1 protein with DNA are circular ssDNA, linear ssDNA, supercoiled circular dsDNA, open circular DNA and linear dsDNA. The results of this study demonstrated that the interaction between VP1 and DNA molecules exhibited various binding preferences that were dependent on the structural conformation of DNA. Taken together, the results of this report are the first to demonstrate that VP1 has no sequence-specific DNA binding activity. The particular binding preferences of VP1 might play multiple roles in DNA replication or encapsidation during the viral life cycle.
-
VP2 of Chicken Anaemia Virus Interacts with Apoptin for Down-regulation of Apoptosis through De-phosphorylated Threonine 108 on Apoptin
Scientific Reports, 2017Co-Authors: Guan-hua Lai, Yi-yang Lien, Ming-kuem Lin, Hsi-jien Chen, Jai-hong Cheng, Fang-chun Sun, Meng-shiunn Lee, Jason Tc Tzen, Meng-shiou LeeAbstract:Chicken Anaemia Virus (CAV) is an important contagious agent that causes immunosuppressive disease in Chickens. CAV Apoptin is a nucleoplasmic shuffling protein that induces apoptosis in Chicken lymphoblastoid cells. In the present study, confocal microscopy revealed co-localisation of expressed CAV non-structural protein VP2 with Apoptin in the nucleus of MDCC-MSB1 cells and the nucleoplasmic compartment of CHO-K1 cells. In vitro pull-down and ex vivo biomolecular fluorescent complementation (BiFC) assays further showed that the VP2 protein directly interacts with Apoptin. Transient co-expression of VP2 and Apoptin in MDCC-MSB1 cells significantly decreased the rate of apoptosis compared with that in cells transfected with the Apoptin gene alone. In addition, the phosphorylation status of threonine 108 (Thr108) of Apoptin was found to decrease upon interaction with VP2. Although dephosphorylated Thr108 did not alter the subcellular distribution of Apoptin in the nucleus of MDCC-MSB1 cells, it did suppress apoptosis. These findings provide the first evidence that VP2 directly interacts with Apoptin in the nucleus to down-regulate apoptosis through alterations in the phosphorylation status of the latter. This information will be useful to further elucidate the underlying mechanism of viral replication in the CAV life cycle.
-
Production and Diagnostic Application of a Purified, E. coli‐Expressed, Serological‐Specific Chicken Anaemia Virus Antigen VP3
Transboundary and emerging diseases, 2011Co-Authors: Meng-shiou Lee, Yu-mei Chou, Yi-yang Lien, Ming-kuem Lin, Wen-te Chang, Hong-zin Lee, Guan-hua Lai, Hsi-jien Chen, C.-h. Huang, Wen-hsin LinAbstract:The aim of this study was to evaluate the production of Chicken Anaemia Virus VP3 protein in different Escherichia coli strains and to address the diagnostic application of purified E. coli-expressed VP3 protein for the detection of Chicken Anaemia Virus (CAV) infection and the development of an ELISA kit. Three E. coli strains, BL21, BL21 codonplus RP and BL21 pLysS, each harbouring a VP3 protein expressing plasmid, were investigated after induction to produce recombinant VP3 protein. After isopropyl-β-D-thiogalactoside (IPTG) induction, VP3 protein was successfully expressed in all three E. coli strains. The BL21 pLysS strain gave the best performance in terms of protein productivity and growth profile. In addition, the optimal culture temperature and IPTG concentration were found to be 0.25 mM and 20 °C, respectively. Using Ni-NTA-purified VP3 protein as an ELISA coating antigen, the purified VP3 was shown to be highly antigenic and able to discriminate sera from Chickens infected with CAV from those that were uninfected during an evaluation of CAV infection serodiagnosis. A VP3-based ELISA demonstrated 100% (6/6 x 100%) specificity and sensitivities of 91.3% (21/23 x 100%) and 82.6% (19/23 x 100%) using cut-off values of the mean plus 2 SD and the mean plus 3 SD, respectively.
Mahmoud M. Naguib - One of the best experts on this subject based on the ideXlab platform.
-
Chicken Anaemia Virus enhances and prolongs subsequent avian influenza h9n2 and infectious bronchitis viral infections
Veterinary Microbiology, 2019Co-Authors: Ahmed M. Erfan, Abdullah Selim, Shawky A. Helmy, Per Eriksson, Mahmoud M. NaguibAbstract:Immunosuppressive viral diseases have a great economic importance in the poultry industry due to the increased susceptibility to secondary infections. Chicken Anaemia Virus (CAV) is one of the major immunosuppressive diseases in Chickens. In addition, low pathogenic avian influenza (LPAI) of subtype H9N2 and infectious bronchitis (IB) Viruses are among the most frequently reported respiratory viral diseases in poultry worldwide. In the present study, specific pathogen free Chickens were used to understand the impact of CAV on secondary infection with LPAI-H9N2 or IB Viruses. Clinical outcomes, viral shedding dynamics, and cytokine levels wereassessed. The results exhibit that Chickens previously infected with CAV produceconsiderablyhigher titresof LPAI-H9N2 or IB Viruses in the oropharyngeal swabs (P < 0.05), tracheas and kidneys. In addition, the immunologic effect of CAV provokedthe development of clinical signs of LPAI-H9N2 and IB Virus infections. Moreover, results suggested that pre-infection with CAV directly correlated with elevated levels of IL-6 and IFNγ. These findings underline the importance of CAV pre-infection on LPAI-H9N2 or IB infection in Chickens, and indicate that co-circulation of CAV can contribute to the spread and evolution of LPAI H9N2 and IB Viruses.
-
Chicken Anaemia Virus enhances and prolongs subsequent avian influenza (H9N2) and infectious bronchitis viral infections.
Veterinary microbiology, 2019Co-Authors: Ahmed M. Erfan, Abdullah Selim, Shawky A. Helmy, Per Eriksson, Mahmoud M. NaguibAbstract:Immunosuppressive viral diseases have a great economic importance in the poultry industry due to the increased susceptibility to secondary infections. Chicken Anaemia Virus (CAV) is one of the major immunosuppressive diseases in Chickens. In addition, low pathogenic avian influenza (LPAI) of subtype H9N2 and infectious bronchitis (IB) Viruses are among the most frequently reported respiratory viral diseases in poultry worldwide. In the present study, specific pathogen free Chickens were used to understand the impact of CAV on secondary infection with LPAI-H9N2 or IB Viruses. Clinical outcomes, viral shedding dynamics, and cytokine levels wereassessed. The results exhibit that Chickens previously infected with CAV produceconsiderablyhigher titresof LPAI-H9N2 or IB Viruses in the oropharyngeal swabs (P