The Experts below are selected from a list of 26739 Experts worldwide ranked by ideXlab platform
Shijun J Zheng - One of the best experts on this subject based on the ideXlab platform.
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vp2 of infectious bursal Disease virus induces apoptosis via triggering oral cancer overexpressed 1 oraov1 protein degradation
2017Co-Authors: Yao Qin, Yongqiang Wang, Hong Cao, Shijun J ZhengAbstract:Infectious bursal Disease (IBD) is an acute, highly contagious and immunosuppressive Avian Disease caused by IBD virus (IBDV). Cell apoptosis triggered by IBD virus (IBDV) contributes to the dysfunction of immune system in host. VP2 of IBDV is known to induce cell death but the underlying mechanism remains unclear. Here we demonstrate that VP2 interacts with the oral cancer overexpressed 1 (ORAOV1), a potential oncoprotein. Infection by IBDV or ectopic expression of VP2 causes a reduction of cellular ORAOV1 and induction of apoptosis, so does knockdown of ORAOV1. In contrast, over-expression of ORAOV1 leads to the inhibition of VP2- or IBDV-induced apoptosis, accompanied with the decreased viral release (p<0.05). Thus, VP2-induced apoptosis during IBDV infection is mediated by interacting with and reducing ORAOV1, a protein that appears to act as an antiapoptotic molecule and restricts viral release early during IBDV infection.
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the association of receptor of activated protein kinase c 1 rack1 with infectious bursal Disease virus viral protein vp5 and voltage dependent anion channel 2 vdac2 inhibits apoptosis and enhances viral replication
2015Co-Authors: Zhiqiang Zhang, Yongqiang Wang, Zhichao Xu, Bin Wang, Xiaoqi Li, Shijun J ZhengAbstract:Infectious bursal Disease (IBD) is an acute, highly contagious, and immunosuppressive Avian Disease caused by IBD virus (IBDV). Our previous report indicates that IBDV VP5 induces apoptosis via interaction with voltage-dependent anion channel 2 (VDAC2). However, the underlying molecular mechanism is still unclear. We report here that receptor of activated protein kinase C 1 (RACK1) interacts with both VDAC2 and VP5 and that they could form a complex. We found that overexpression of RACK1 inhibited IBDV-induced apoptosis in DF-1 cells and that knockdown of RACK1 by small interfering RNA induced apoptosis associated with activation of caspases 9 and 3 and suppressed IBDV growth. These results indicate that RACK1 plays an antiapoptotic role during IBDV infection via interaction with VDAC2 and VP5, suggesting that VP5 sequesters RACK1 and VDAC2 in the apoptosis-inducing process.
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critical role for voltage dependent anion channel 2 in infectious bursal Disease virus induced apoptosis in host cells via interaction with vp5
2012Co-Authors: Yongqiang Wang, Yanfei Xue, Hong Cao, Shijun J ZhengAbstract:Infectious bursal Disease (IBD) is an acute, highly contagious, and immunosuppressive Avian Disease caused by IBD virus (IBDV). Although IBDV-induced host cell apoptosis has been established, the underlying molecular mechanism is still unclear. We report here that IBDV viral protein 5 (VP5) is a major apoptosis inducer in DF-1 cells by interacting with the voltage-dependent anion channel 2 (VDAC2) in the mitochondrion. We found that in DF-1 cells, VP5-induced apoptosis can be completely abolished by 4,4′-diisothiocyanatostibene-2,2′-disulfonic acid (DIDS), an inhibitor of VDAC. Furthermore, knockdown of VDAC2 by small interfering RNA markedly inhibits IBDV-induced apoptosis associated with decreased caspase-9 and -3 activation and cytochrome c release, leading to increased IBDV growth in host cells. Thus, VP5-induced apoptosis during IBDV infection is mediated by interacting with VDAC2, a protein that appears to restrict viral replication via induction of cell death.
Yongqiang Wang - One of the best experts on this subject based on the ideXlab platform.
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vp2 of infectious bursal Disease virus induces apoptosis via triggering oral cancer overexpressed 1 oraov1 protein degradation
2017Co-Authors: Yao Qin, Yongqiang Wang, Hong Cao, Shijun J ZhengAbstract:Infectious bursal Disease (IBD) is an acute, highly contagious and immunosuppressive Avian Disease caused by IBD virus (IBDV). Cell apoptosis triggered by IBD virus (IBDV) contributes to the dysfunction of immune system in host. VP2 of IBDV is known to induce cell death but the underlying mechanism remains unclear. Here we demonstrate that VP2 interacts with the oral cancer overexpressed 1 (ORAOV1), a potential oncoprotein. Infection by IBDV or ectopic expression of VP2 causes a reduction of cellular ORAOV1 and induction of apoptosis, so does knockdown of ORAOV1. In contrast, over-expression of ORAOV1 leads to the inhibition of VP2- or IBDV-induced apoptosis, accompanied with the decreased viral release (p<0.05). Thus, VP2-induced apoptosis during IBDV infection is mediated by interacting with and reducing ORAOV1, a protein that appears to act as an antiapoptotic molecule and restricts viral release early during IBDV infection.
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the association of receptor of activated protein kinase c 1 rack1 with infectious bursal Disease virus viral protein vp5 and voltage dependent anion channel 2 vdac2 inhibits apoptosis and enhances viral replication
2015Co-Authors: Zhiqiang Zhang, Yongqiang Wang, Zhichao Xu, Bin Wang, Xiaoqi Li, Shijun J ZhengAbstract:Infectious bursal Disease (IBD) is an acute, highly contagious, and immunosuppressive Avian Disease caused by IBD virus (IBDV). Our previous report indicates that IBDV VP5 induces apoptosis via interaction with voltage-dependent anion channel 2 (VDAC2). However, the underlying molecular mechanism is still unclear. We report here that receptor of activated protein kinase C 1 (RACK1) interacts with both VDAC2 and VP5 and that they could form a complex. We found that overexpression of RACK1 inhibited IBDV-induced apoptosis in DF-1 cells and that knockdown of RACK1 by small interfering RNA induced apoptosis associated with activation of caspases 9 and 3 and suppressed IBDV growth. These results indicate that RACK1 plays an antiapoptotic role during IBDV infection via interaction with VDAC2 and VP5, suggesting that VP5 sequesters RACK1 and VDAC2 in the apoptosis-inducing process.
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critical role for voltage dependent anion channel 2 in infectious bursal Disease virus induced apoptosis in host cells via interaction with vp5
2012Co-Authors: Yongqiang Wang, Yanfei Xue, Hong Cao, Shijun J ZhengAbstract:Infectious bursal Disease (IBD) is an acute, highly contagious, and immunosuppressive Avian Disease caused by IBD virus (IBDV). Although IBDV-induced host cell apoptosis has been established, the underlying molecular mechanism is still unclear. We report here that IBDV viral protein 5 (VP5) is a major apoptosis inducer in DF-1 cells by interacting with the voltage-dependent anion channel 2 (VDAC2) in the mitochondrion. We found that in DF-1 cells, VP5-induced apoptosis can be completely abolished by 4,4′-diisothiocyanatostibene-2,2′-disulfonic acid (DIDS), an inhibitor of VDAC. Furthermore, knockdown of VDAC2 by small interfering RNA markedly inhibits IBDV-induced apoptosis associated with decreased caspase-9 and -3 activation and cytochrome c release, leading to increased IBDV growth in host cells. Thus, VP5-induced apoptosis during IBDV infection is mediated by interacting with VDAC2, a protein that appears to restrict viral replication via induction of cell death.
Huanmin Zhang - One of the best experts on this subject based on the ideXlab platform.
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a premature stop codon within the tvb receptor gene results in decreased susceptibility to infection by Avian leukosis virus subgroups b d and e
2017Co-Authors: Weiguo Chen, Xinheng Zhang, Aijun Li, Xinjian Li, Hongxing Li, Huanmin ZhangAbstract:// WeiGuo Chen 1, 5, 6, * , Yang Liu 1, 5, * , Aijun Li 2 , Xinjian Li 1, 5 , Hongxing Li 1, 5 , Zhenkai Dai 1, 5 , Yiming Yan 1, 5 , Xinheng Zhang 1, 5 , Dingming Shu 3 , Huanmin Zhang 4 , Wencheng Lin 1, 5, 6 , Jingyun Ma 1, 5, 6 and Qingmei Xie 1, 5, 6 1 College of Animal Science, South China Agricultural University & Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding, Guangzhou 510642, P. R. China 2 College of Science and Engineering, Jinan University, Guangzhou 510632, P. R. China 3 Institute of Animal Science, Guangdong Academy of Agriculture Sciences, Guangzhou 510640, P. R. China 4 USDA, Agriculture Research Service, Avian Disease and Oncology Laboratory, East Lansing, MI 48823, USA 5 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou 510642, P. R. China 6 South China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou 510642, P. R. China * These authors have contributed equally to this work Correspondence to: Qingmei Xie, email: qmx@scau.edu.cn Keywords: Avian leukosis virus; tvb receptor gene; premature stop codon; host resistance; chicken Received: June 15, 2017 Accepted: November 03, 2017 Published: November 18, 2017 ABSTRACT Avian leukosis virus (ALV) is an oncogenic virus causing a variety of neoplasms in chickens. The group of Avian leukosis virus in chickens contains six closely related subgroups, A to E and J. The prevalence of ALVs in hosts may have imposed strong selective pressure toward resistance to ALVs infection. The tvb gene encodes Tvb receptor and determines susceptibility or resistance to the subgroups B, D, and E ALV. In this study, we characterized a novel resistant allele of the tvb receptor gene, tvb r3 , which carries a single-nucleotide substitution (c.298C>T) that constitutes a premature termination codon within the fourth exon and leads to the production of a truncated Tvb R3 receptor protein. As a result, we observed decreased susceptibility to infection by ALV-B, ALV-D and ALV-E both in vitro and in vivo , and decreased the binding affinity of the Tvb R3 receptor for the subgroups B, D, and E ALV envelope glycoproteins. Additionally, we found that the tvb r3 allele was prevalent in Chinese broiler lines. This study demonstrated that premature termination codon in the tvb receptor gene can confer genetic resistance to subgroups B, D, and E ALV in the host, and indicates that tvb r3 could potentially serve as a resistant target against ALV-B, ALV-D and ALV-E infection.
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circular rna alterations are involved in resistance to Avian leukosis virus subgroup j induced tumor formation in chickens
2017Co-Authors: Xinheng Zhang, Aijun Li, Huanmin Zhang, Xinjian Li, Weiguo Chen, Feng ChenAbstract:// Xinheng Zhang 1, 2, 5, 6 , Yiming Yan 1, 2, 5 , Xiaoya Lei 1, 2, 5 , Aijun Li 3 , Huanmin Zhang 4 , Zhenkai Dai 1, 2, 5 , Xinjian Li 1, 2, 5 , Weiguo Chen 1, 2, 5, 6 , Wencheng Lin 1, 2, 5, 6 , Feng Chen 1, 2, 5, 6 , Jingyun Ma 1, 2, 5, 6 and Qingmei Xie 1, 2, 5, 6 1 College of Animal Science, South China Agricultural University, Guangzhou, 510642, P.R. China 2 Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding, Guangzhou, 510642, P.R. China 3 College of Science and Engineering, Jinan University, Guangzhou, 510632, P.R. China 4 USDA, Agriculture Research Service, Avian Disease and Oncology Laboratory, East Lansing, MI, 48823, USA 5 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou, 510642, P.R. China 6 South China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou, 510642, P.R. China Correspondence to: Qingmei Xie, email: qmx@scau.edu.cn Keywords: circular RNA, ALV-J-resistant chickens, circular-seq, tumor Received: November 25, 2016 Accepted: March 08, 2017 Published: March 22, 2017 ABSTRACT Avian leukosis virus subgroup (ALV-J) is an oncogenic neoplasm-inducing retrovirus that causes significant economic losses in the poultry industry. Recent studies have demonstrated circular RNAs (circRNAs) are implicated in pathogenic processes; however, no research has indicated circRNAs are involved in resistance to Disease. In this study, over 1800 circRNAs were detected by circRNA sequencing of liver tissues from ALV-J-resistant ( n = 3) and ALV-J-susceptible chickens ( n = 3). 32 differentially expressed circRNAs were selected for analyzing including 12 upregulated in ALV-J-resistant chickens and 20 upregulated in ALV-J-susceptible chickens, besides, the top five microRNAs (miRNAs) for 12 upregulated circRNAs in ALV-J-resistant chickens were analyzed. Gene ontology and KEGG pathway analyses were performed for miRNA target genes, the predicted genes were mainly involved in immune pathways. This study provides the first evidence that circRNA alterations are involved in resistance to ALV-J-induced tumor formation. We propose circRNAs may help to mediate tumor induction and development in chickens.
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comparative evaluation of vaccine efficacy of recombinant marek s Disease virus vaccine lacking meq oncogene in commercial chickens
2010Co-Authors: Lucy F Lee, Aly M. Fadly, Huanmin Zhang, Blanca Lupiani, K S Kreager, J Arango, A Paraguassu, B Beckman, Sanjay M ReddyAbstract:Abstract Marek's Disease virus (MDV) oncogene meq has been identified as the gene involved in tumorigenesis in chickens. We have recently developed a Meq-null virus, rMd5ΔMeq, in which the oncogene meq was deleted. Vaccine efficacy experiments conducted in Avian Disease and Oncology Laboratory (ADOL) 15I 5 × 7 1 chickens vaccinated with rMd5ΔMeq virus or an ADOL preparation of CVI988/Rispens indicated that rMd5ΔMeq provided superior protection than CVI988/Rispens when challenged with the very virulent plus MDV 648A strain. In the present study we set to investigate the vaccine efficacy of rMd5ΔMeq in the field compared to several commercial preparations of CVI988/Rispens. Three large-scale field experiments, in which seeder chickens were inoculated with a very virulent plus strain of 686, vv+ MDV, were conducted in a model developed by Hy-Line International. In addition, comparisons were made with bivalent vaccine (HVT + SB-1), HVT alone and several serotype 3 HVT-vectored vaccines individually or in combination with CVI988/Rispens. Experimental results showed that addition of HVT to either of the two commercial CVI988/Rispens preparations tested (A or B) did not enhance protection conferred by CVI988/Rispens alone and that rMd5ΔMeq was a better or equal vaccine compared to any of the CVI988/Rispens vaccines tested under the conditions of the field trials presented herein. Our results also emphasized the complexity of factors affecting vaccine efficacy and the importance of challenge dose in protection.
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comparative evaluation of vaccine efficacy of recombinant marek s Disease virus vaccine lacking meq oncogene in commercial chickens
2010Co-Authors: Lucy F Lee, Aly M. Fadly, Huanmin Zhang, Blanca Lupiani, K S Kreager, J Arango, A Paraguassu, B Beckman, Sanjay M ReddyAbstract:Marek's Disease virus (MDV) oncogene meq has been identified as the gene involved in tumorigenesis in chickens. We have recently developed a Meq-null virus, rMd5 Delta Meq, in which the oncogene meq was deleted. Vaccine efficacy experiments conducted in Avian Disease and Oncology Laboratory (ADOL) 15I(5) x 7(1) chickens vaccinated with rMd5 Delta Meq virus or an ADOL preparation of CVI988/Rispens indicated that rMd5 Delta Meq provided superior protection than CVI988/Rispens when challenged with the very virulent plus MDV 648A strain. In the present study we set to investigate the vaccine efficacy of rMd5 Delta Meq in the field compared to several commercial preparations of CVI988/Rispens. Three large-scale field experiments, in which seeder chickens were inoculated with a very virulent plus strain of 686, vv+ MDV, were conducted in a model developed by Hy-Line International. In addition, comparisons were made with bivalent vaccine (HVT+SB-1), HVT alone and several serotype 3 HVT-vectored vaccines individually or in combination with CVI988/Rispens. Experimental results showed that addition of HVT to either of the two commercial CVI988/Rispens preparations tested (A or B) did not enhance protection conferred by CVI988/Rispens alone and that rMd5 Delta Meq was a better or equal vaccine compared to any of the CVI988/Rispens vaccines tested under the conditions of the field trials presented herein. Our results also emphasized the complexity of factors affecting vaccine efficacy and the importance of challenge dose in protection.
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behavioral and physiological features of chickens diversely selected for resistance to Avian Disease 1 selected inbred lines differ in behavioral and physical responses to social stress
2004Co-Authors: R L Dennis, Inma Estevez, L D Bacon, Huanmin Zhang, H W ChengAbstract:Abstract To test the hypothesis that genetic variations in response to social stress modulate susceptibility to Disease in poultry, aggressive behaviors induced by social stress were measured in chickens of different inbred lines selected for Disease resistance (line 63) or susceptibility (lines 72 and 15I5), as well as 2 recombinant congenic strains (B and X). At 15 wk of age, roosters from each genetic line or strain were randomly assigned to pairs for intraline male-male aggression tests (n = 8 per line). Based on the results of the intraline aggression tests, the roosters were divided into 2 groups, winners and losers. At 16 wk of age, the roosters were randomly paired as winners vs. winners and losers vs. losers for interline aggression tests, i.e., line 63 vs. 72 and 15I5; line 73 vs. line 15I5; and strain X vs. strain B. Similarly, at 17 wk of age, line 63 vs. strains X and B, and line 72 vs. strains X and B were tested. The tests were conducted in a novel cage that was similar to their home cages, to provide a neutral space for both roosters being tested. Each pair was videotaped for 15 min. Male-male interaction-induced aggressive behaviors were markedly different among the genetic lines. Compared with roosters of lines 15I5 and 72, line 63 roosters generally showed fewer aggressive behaviors, including aggressive pecks and fights, as well as durations (P
Hong Cao - One of the best experts on this subject based on the ideXlab platform.
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vp2 of infectious bursal Disease virus induces apoptosis via triggering oral cancer overexpressed 1 oraov1 protein degradation
2017Co-Authors: Yao Qin, Yongqiang Wang, Hong Cao, Shijun J ZhengAbstract:Infectious bursal Disease (IBD) is an acute, highly contagious and immunosuppressive Avian Disease caused by IBD virus (IBDV). Cell apoptosis triggered by IBD virus (IBDV) contributes to the dysfunction of immune system in host. VP2 of IBDV is known to induce cell death but the underlying mechanism remains unclear. Here we demonstrate that VP2 interacts with the oral cancer overexpressed 1 (ORAOV1), a potential oncoprotein. Infection by IBDV or ectopic expression of VP2 causes a reduction of cellular ORAOV1 and induction of apoptosis, so does knockdown of ORAOV1. In contrast, over-expression of ORAOV1 leads to the inhibition of VP2- or IBDV-induced apoptosis, accompanied with the decreased viral release (p<0.05). Thus, VP2-induced apoptosis during IBDV infection is mediated by interacting with and reducing ORAOV1, a protein that appears to act as an antiapoptotic molecule and restricts viral release early during IBDV infection.
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critical role for voltage dependent anion channel 2 in infectious bursal Disease virus induced apoptosis in host cells via interaction with vp5
2012Co-Authors: Yongqiang Wang, Yanfei Xue, Hong Cao, Shijun J ZhengAbstract:Infectious bursal Disease (IBD) is an acute, highly contagious, and immunosuppressive Avian Disease caused by IBD virus (IBDV). Although IBDV-induced host cell apoptosis has been established, the underlying molecular mechanism is still unclear. We report here that IBDV viral protein 5 (VP5) is a major apoptosis inducer in DF-1 cells by interacting with the voltage-dependent anion channel 2 (VDAC2) in the mitochondrion. We found that in DF-1 cells, VP5-induced apoptosis can be completely abolished by 4,4′-diisothiocyanatostibene-2,2′-disulfonic acid (DIDS), an inhibitor of VDAC. Furthermore, knockdown of VDAC2 by small interfering RNA markedly inhibits IBDV-induced apoptosis associated with decreased caspase-9 and -3 activation and cytochrome c release, leading to increased IBDV growth in host cells. Thus, VP5-induced apoptosis during IBDV infection is mediated by interacting with VDAC2, a protein that appears to restrict viral replication via induction of cell death.
Xinheng Zhang - One of the best experts on this subject based on the ideXlab platform.
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a premature stop codon within the tvb receptor gene results in decreased susceptibility to infection by Avian leukosis virus subgroups b d and e
2017Co-Authors: Weiguo Chen, Xinheng Zhang, Aijun Li, Xinjian Li, Hongxing Li, Huanmin ZhangAbstract:// WeiGuo Chen 1, 5, 6, * , Yang Liu 1, 5, * , Aijun Li 2 , Xinjian Li 1, 5 , Hongxing Li 1, 5 , Zhenkai Dai 1, 5 , Yiming Yan 1, 5 , Xinheng Zhang 1, 5 , Dingming Shu 3 , Huanmin Zhang 4 , Wencheng Lin 1, 5, 6 , Jingyun Ma 1, 5, 6 and Qingmei Xie 1, 5, 6 1 College of Animal Science, South China Agricultural University & Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding, Guangzhou 510642, P. R. China 2 College of Science and Engineering, Jinan University, Guangzhou 510632, P. R. China 3 Institute of Animal Science, Guangdong Academy of Agriculture Sciences, Guangzhou 510640, P. R. China 4 USDA, Agriculture Research Service, Avian Disease and Oncology Laboratory, East Lansing, MI 48823, USA 5 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou 510642, P. R. China 6 South China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou 510642, P. R. China * These authors have contributed equally to this work Correspondence to: Qingmei Xie, email: qmx@scau.edu.cn Keywords: Avian leukosis virus; tvb receptor gene; premature stop codon; host resistance; chicken Received: June 15, 2017 Accepted: November 03, 2017 Published: November 18, 2017 ABSTRACT Avian leukosis virus (ALV) is an oncogenic virus causing a variety of neoplasms in chickens. The group of Avian leukosis virus in chickens contains six closely related subgroups, A to E and J. The prevalence of ALVs in hosts may have imposed strong selective pressure toward resistance to ALVs infection. The tvb gene encodes Tvb receptor and determines susceptibility or resistance to the subgroups B, D, and E ALV. In this study, we characterized a novel resistant allele of the tvb receptor gene, tvb r3 , which carries a single-nucleotide substitution (c.298C>T) that constitutes a premature termination codon within the fourth exon and leads to the production of a truncated Tvb R3 receptor protein. As a result, we observed decreased susceptibility to infection by ALV-B, ALV-D and ALV-E both in vitro and in vivo , and decreased the binding affinity of the Tvb R3 receptor for the subgroups B, D, and E ALV envelope glycoproteins. Additionally, we found that the tvb r3 allele was prevalent in Chinese broiler lines. This study demonstrated that premature termination codon in the tvb receptor gene can confer genetic resistance to subgroups B, D, and E ALV in the host, and indicates that tvb r3 could potentially serve as a resistant target against ALV-B, ALV-D and ALV-E infection.
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circular rna alterations are involved in resistance to Avian leukosis virus subgroup j induced tumor formation in chickens
2017Co-Authors: Xinheng Zhang, Aijun Li, Huanmin Zhang, Xinjian Li, Weiguo Chen, Feng ChenAbstract:// Xinheng Zhang 1, 2, 5, 6 , Yiming Yan 1, 2, 5 , Xiaoya Lei 1, 2, 5 , Aijun Li 3 , Huanmin Zhang 4 , Zhenkai Dai 1, 2, 5 , Xinjian Li 1, 2, 5 , Weiguo Chen 1, 2, 5, 6 , Wencheng Lin 1, 2, 5, 6 , Feng Chen 1, 2, 5, 6 , Jingyun Ma 1, 2, 5, 6 and Qingmei Xie 1, 2, 5, 6 1 College of Animal Science, South China Agricultural University, Guangzhou, 510642, P.R. China 2 Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding, Guangzhou, 510642, P.R. China 3 College of Science and Engineering, Jinan University, Guangzhou, 510632, P.R. China 4 USDA, Agriculture Research Service, Avian Disease and Oncology Laboratory, East Lansing, MI, 48823, USA 5 Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou, 510642, P.R. China 6 South China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou, 510642, P.R. China Correspondence to: Qingmei Xie, email: qmx@scau.edu.cn Keywords: circular RNA, ALV-J-resistant chickens, circular-seq, tumor Received: November 25, 2016 Accepted: March 08, 2017 Published: March 22, 2017 ABSTRACT Avian leukosis virus subgroup (ALV-J) is an oncogenic neoplasm-inducing retrovirus that causes significant economic losses in the poultry industry. Recent studies have demonstrated circular RNAs (circRNAs) are implicated in pathogenic processes; however, no research has indicated circRNAs are involved in resistance to Disease. In this study, over 1800 circRNAs were detected by circRNA sequencing of liver tissues from ALV-J-resistant ( n = 3) and ALV-J-susceptible chickens ( n = 3). 32 differentially expressed circRNAs were selected for analyzing including 12 upregulated in ALV-J-resistant chickens and 20 upregulated in ALV-J-susceptible chickens, besides, the top five microRNAs (miRNAs) for 12 upregulated circRNAs in ALV-J-resistant chickens were analyzed. Gene ontology and KEGG pathway analyses were performed for miRNA target genes, the predicted genes were mainly involved in immune pathways. This study provides the first evidence that circRNA alterations are involved in resistance to ALV-J-induced tumor formation. We propose circRNAs may help to mediate tumor induction and development in chickens.
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Assessing the efficacy of an inactivated chicken anemia virus vaccine
2015Co-Authors: Xinheng Zhang, Zhenkai Dai, Yuanjia Liu, Weiguo Chen, Qingmei XieAbstract:Abstract Background Chicken anemia virus (CAV) is an immunosuppressive virus that causes chicken infectious anemia (CIA) which is a highly contagious Avian Disease. CAV causes major economic losses in the poultry industry worldwide. The current CAV vaccine is a live attenuated strain administered in the drinking water that risks horizontal infection of other chickens. The purpose of this study was to develop a novel vaccine against CAV that can be administered safely using a highly pathogenic isolate inactivated with β-propiolactone hydrolysis that would protect chicks from CAV. Methods Hens were vaccinated twice intramuscularly with a novel CAV GD-G-12 inactivated vaccine and the humoral immune responses of the hens and offspring were monitored by ELISA. A heterologous intramuscular challenge using the CAV strain GD-E-12 was conducted in the chicks hatched from vaccinated or unvaccinated hens. Results The vaccine strain, GD-G-12, was shown to be highly pathogenic prior to inactivation evidenced by thymic atrophy and bleeding, and weight loss. The inactivated vaccine was considered safe and showed no signs of pathogenicity. High titers of CAV specific antibodies were detected in the vaccinated hens and in their chicks, indicating vertical transfer of maternal antibodies. Furthermore, the chicks hatched from vaccinated hens were resistant to a heterologous CAV challenge and showed no signs of weight loss and thymic atrophy and bleeding. Conclusion Our studies are proof of principle that inactivated GD-G-12 might be a novel vaccine candidate to prevent CAV infection, and highlight the utility of using an inactivated virus for this vaccine.
