The Experts below are selected from a list of 66 Experts worldwide ranked by ideXlab platform
Jianming Qiu - One of the best experts on this subject based on the ideXlab platform.
-
Molecular characterization of the small nonstructural proteins of parvovirus Aleutian mink disease virus (AMDV) during infection
Virology, 2014Co-Authors: Qinfeng Huang, Marshall E. Bloom, Yong Luo, Fang Cheng, Sonja M. Best, Jianming QiuAbstract:Aleutian mink disease virus (AMDV) is the only member in genus Amdovirus of the family Parvoviridae. During AMDV infection, six species of viral transcripts are generated from one precursor mRNA through alternative splicing and alternative polyadenylation. In addition to the large non-structural protein NS1, two small non-structural proteins, NS2 and NS3, are putatively encoded (Qiu J, et al., 2006. J. Virol. 80 654-662). However, these two proteins have not been experimentally demonstrated during virus infection, and nothing is known about their function. Here, we studied the nonstructural protein expression profile of AMDV, and for the first time, confirmed expression of NS2 and NS3 during infection, and identified their intracellular localization. More importantly, we provided evidence that both NS2 and NS3 are necessary for AMDV replication.
-
Internal polyadenylation of parvoviral precursor mRNA limits progeny virus production.
Virology, 2012Co-Authors: Qinfeng Huang, Marshall E. Bloom, Sonja M. Best, Xuefeng Deng, Jianming QiuAbstract:article i nfo Aleutian Mink Disease Virus (AMDV) is the only virus in the genus Amdovirus of family Parvoviridae. In adult mink, AMDV causes a persistent infection associated with severe dysfunction of the immune system. Cleav- age of AMDV capsid proteins has been previously shown to play a role in regulating progeny virus production (Fang Cheng et al., J. Virol. 84:2687-2696, 2010). The present study shows that AMDV has evolved a second strategy to limit expression of capsid proteins by preventing processing of the full-length capsid protein- encoding mRNA transcripts. Characterization of the cis-elements of the proximal polyadenylation site ((pA)p) in the infectious clone of AMDV revealed that polyadenylation at the (pA)p site is controlled by an upstream element (USE) of 200 nts in length, the AAUAAA signal, and a downstream element (DSE) of 40 nts. A decrease in polyadenylation at the (pA)p site, either by mutating the AAUAAA signal or the DSE, which does not affect the encoding of amino acids in the infectious clone, increased the expression of capsid protein VP1/VP2 and thereby increased progeny virus production approximately 2-3-fold. This increase was accompanied by enhanced replication of the AMDV genome. Thus, this study reveals correla- tions among internal polyadenylation, capsid production, viral DNA replication and progeny virus produc- tion of AMDV, indicating that internal polyadenylation is a limiting step for parvovirus replication and progeny virus production.
-
The Capsid Proteins of Aleutian Mink Disease Virus Activate Caspases and Are Specifically Cleaved during Infection
Journal of virology, 2009Co-Authors: Fang Cheng, Marshall E. Bloom, Sonja M. Best, Aaron Yun Chen, David J. Pintel, Jianming QiuAbstract:Aleutian mink disease virus (AMDV) is currently the only known member of the genus Amdovirus in the family Parvoviridae. It is the etiological agent of Aleutian disease of mink. We have previously shown that a small protein with a molecular mass of approximately 26 kDa was present during AMDV infection and following transfection of capsid expression constructs (J. Qiu, F. Cheng, L. R. Burger, and D. Pintel, J. Virol. 80:654-662, 2006). In this study, we report that the capsid proteins were specifically cleaved at aspartic acid residue 420 (D420) during virus infection, resulting in the previously observed cleavage product. Mutation of a single amino acid residue at D420 abolished the specific cleavage. Expression of the capsid proteins alone in Crandell feline kidney (CrFK) cells reproduced the cleavage of the capsid proteins in virus infection. More importantly, capsid protein expression alone induced active caspases, of which caspase-10 was the most active. Active caspases, in turn, cleaved capsid proteins in vivo. Our results also showed that active caspase-7 specifically cleaved capsid proteins at D420 in vitro. These results suggest that viral capsid proteins alone induce caspase activation, resulting in cleavage of capsid proteins. We also provide evidence that AMDV mutants resistant to caspase-mediated capsid cleavage increased virus production approximately 3- to 5-fold in CrFK cells compared to that produced from the parent virus AMDV-G at 37°C but not at 31.8°C. Collectively, our results indicate that caspase activity plays multiple roles in AMDV infection and that cleavage of the capsid proteins might have a role in regulating persistent infection of AMDV.
Qinfeng Huang - One of the best experts on this subject based on the ideXlab platform.
-
Molecular characterization of the small nonstructural proteins of parvovirus Aleutian mink disease virus (AMDV) during infection
Virology, 2014Co-Authors: Qinfeng Huang, Marshall E. Bloom, Yong Luo, Fang Cheng, Sonja M. Best, Jianming QiuAbstract:Aleutian mink disease virus (AMDV) is the only member in genus Amdovirus of the family Parvoviridae. During AMDV infection, six species of viral transcripts are generated from one precursor mRNA through alternative splicing and alternative polyadenylation. In addition to the large non-structural protein NS1, two small non-structural proteins, NS2 and NS3, are putatively encoded (Qiu J, et al., 2006. J. Virol. 80 654-662). However, these two proteins have not been experimentally demonstrated during virus infection, and nothing is known about their function. Here, we studied the nonstructural protein expression profile of AMDV, and for the first time, confirmed expression of NS2 and NS3 during infection, and identified their intracellular localization. More importantly, we provided evidence that both NS2 and NS3 are necessary for AMDV replication.
-
Internal polyadenylation of parvoviral precursor mRNA limits progeny virus production.
Virology, 2012Co-Authors: Qinfeng Huang, Marshall E. Bloom, Sonja M. Best, Xuefeng Deng, Jianming QiuAbstract:article i nfo Aleutian Mink Disease Virus (AMDV) is the only virus in the genus Amdovirus of family Parvoviridae. In adult mink, AMDV causes a persistent infection associated with severe dysfunction of the immune system. Cleav- age of AMDV capsid proteins has been previously shown to play a role in regulating progeny virus production (Fang Cheng et al., J. Virol. 84:2687-2696, 2010). The present study shows that AMDV has evolved a second strategy to limit expression of capsid proteins by preventing processing of the full-length capsid protein- encoding mRNA transcripts. Characterization of the cis-elements of the proximal polyadenylation site ((pA)p) in the infectious clone of AMDV revealed that polyadenylation at the (pA)p site is controlled by an upstream element (USE) of 200 nts in length, the AAUAAA signal, and a downstream element (DSE) of 40 nts. A decrease in polyadenylation at the (pA)p site, either by mutating the AAUAAA signal or the DSE, which does not affect the encoding of amino acids in the infectious clone, increased the expression of capsid protein VP1/VP2 and thereby increased progeny virus production approximately 2-3-fold. This increase was accompanied by enhanced replication of the AMDV genome. Thus, this study reveals correla- tions among internal polyadenylation, capsid production, viral DNA replication and progeny virus produc- tion of AMDV, indicating that internal polyadenylation is a limiting step for parvovirus replication and progeny virus production.
Marshall E. Bloom - One of the best experts on this subject based on the ideXlab platform.
-
Molecular characterization of the small nonstructural proteins of parvovirus Aleutian mink disease virus (AMDV) during infection
Virology, 2014Co-Authors: Qinfeng Huang, Marshall E. Bloom, Yong Luo, Fang Cheng, Sonja M. Best, Jianming QiuAbstract:Aleutian mink disease virus (AMDV) is the only member in genus Amdovirus of the family Parvoviridae. During AMDV infection, six species of viral transcripts are generated from one precursor mRNA through alternative splicing and alternative polyadenylation. In addition to the large non-structural protein NS1, two small non-structural proteins, NS2 and NS3, are putatively encoded (Qiu J, et al., 2006. J. Virol. 80 654-662). However, these two proteins have not been experimentally demonstrated during virus infection, and nothing is known about their function. Here, we studied the nonstructural protein expression profile of AMDV, and for the first time, confirmed expression of NS2 and NS3 during infection, and identified their intracellular localization. More importantly, we provided evidence that both NS2 and NS3 are necessary for AMDV replication.
-
Internal polyadenylation of parvoviral precursor mRNA limits progeny virus production.
Virology, 2012Co-Authors: Qinfeng Huang, Marshall E. Bloom, Sonja M. Best, Xuefeng Deng, Jianming QiuAbstract:article i nfo Aleutian Mink Disease Virus (AMDV) is the only virus in the genus Amdovirus of family Parvoviridae. In adult mink, AMDV causes a persistent infection associated with severe dysfunction of the immune system. Cleav- age of AMDV capsid proteins has been previously shown to play a role in regulating progeny virus production (Fang Cheng et al., J. Virol. 84:2687-2696, 2010). The present study shows that AMDV has evolved a second strategy to limit expression of capsid proteins by preventing processing of the full-length capsid protein- encoding mRNA transcripts. Characterization of the cis-elements of the proximal polyadenylation site ((pA)p) in the infectious clone of AMDV revealed that polyadenylation at the (pA)p site is controlled by an upstream element (USE) of 200 nts in length, the AAUAAA signal, and a downstream element (DSE) of 40 nts. A decrease in polyadenylation at the (pA)p site, either by mutating the AAUAAA signal or the DSE, which does not affect the encoding of amino acids in the infectious clone, increased the expression of capsid protein VP1/VP2 and thereby increased progeny virus production approximately 2-3-fold. This increase was accompanied by enhanced replication of the AMDV genome. Thus, this study reveals correla- tions among internal polyadenylation, capsid production, viral DNA replication and progeny virus produc- tion of AMDV, indicating that internal polyadenylation is a limiting step for parvovirus replication and progeny virus production.
-
The Capsid Proteins of Aleutian Mink Disease Virus Activate Caspases and Are Specifically Cleaved during Infection
Journal of virology, 2009Co-Authors: Fang Cheng, Marshall E. Bloom, Sonja M. Best, Aaron Yun Chen, David J. Pintel, Jianming QiuAbstract:Aleutian mink disease virus (AMDV) is currently the only known member of the genus Amdovirus in the family Parvoviridae. It is the etiological agent of Aleutian disease of mink. We have previously shown that a small protein with a molecular mass of approximately 26 kDa was present during AMDV infection and following transfection of capsid expression constructs (J. Qiu, F. Cheng, L. R. Burger, and D. Pintel, J. Virol. 80:654-662, 2006). In this study, we report that the capsid proteins were specifically cleaved at aspartic acid residue 420 (D420) during virus infection, resulting in the previously observed cleavage product. Mutation of a single amino acid residue at D420 abolished the specific cleavage. Expression of the capsid proteins alone in Crandell feline kidney (CrFK) cells reproduced the cleavage of the capsid proteins in virus infection. More importantly, capsid protein expression alone induced active caspases, of which caspase-10 was the most active. Active caspases, in turn, cleaved capsid proteins in vivo. Our results also showed that active caspase-7 specifically cleaved capsid proteins at D420 in vitro. These results suggest that viral capsid proteins alone induce caspase activation, resulting in cleavage of capsid proteins. We also provide evidence that AMDV mutants resistant to caspase-mediated capsid cleavage increased virus production approximately 3- to 5-fold in CrFK cells compared to that produced from the parent virus AMDV-G at 37°C but not at 31.8°C. Collectively, our results indicate that caspase activity plays multiple roles in AMDV infection and that cleavage of the capsid proteins might have a role in regulating persistent infection of AMDV.
Sonja M. Best - One of the best experts on this subject based on the ideXlab platform.
-
Molecular characterization of the small nonstructural proteins of parvovirus Aleutian mink disease virus (AMDV) during infection
Virology, 2014Co-Authors: Qinfeng Huang, Marshall E. Bloom, Yong Luo, Fang Cheng, Sonja M. Best, Jianming QiuAbstract:Aleutian mink disease virus (AMDV) is the only member in genus Amdovirus of the family Parvoviridae. During AMDV infection, six species of viral transcripts are generated from one precursor mRNA through alternative splicing and alternative polyadenylation. In addition to the large non-structural protein NS1, two small non-structural proteins, NS2 and NS3, are putatively encoded (Qiu J, et al., 2006. J. Virol. 80 654-662). However, these two proteins have not been experimentally demonstrated during virus infection, and nothing is known about their function. Here, we studied the nonstructural protein expression profile of AMDV, and for the first time, confirmed expression of NS2 and NS3 during infection, and identified their intracellular localization. More importantly, we provided evidence that both NS2 and NS3 are necessary for AMDV replication.
-
Internal polyadenylation of parvoviral precursor mRNA limits progeny virus production.
Virology, 2012Co-Authors: Qinfeng Huang, Marshall E. Bloom, Sonja M. Best, Xuefeng Deng, Jianming QiuAbstract:article i nfo Aleutian Mink Disease Virus (AMDV) is the only virus in the genus Amdovirus of family Parvoviridae. In adult mink, AMDV causes a persistent infection associated with severe dysfunction of the immune system. Cleav- age of AMDV capsid proteins has been previously shown to play a role in regulating progeny virus production (Fang Cheng et al., J. Virol. 84:2687-2696, 2010). The present study shows that AMDV has evolved a second strategy to limit expression of capsid proteins by preventing processing of the full-length capsid protein- encoding mRNA transcripts. Characterization of the cis-elements of the proximal polyadenylation site ((pA)p) in the infectious clone of AMDV revealed that polyadenylation at the (pA)p site is controlled by an upstream element (USE) of 200 nts in length, the AAUAAA signal, and a downstream element (DSE) of 40 nts. A decrease in polyadenylation at the (pA)p site, either by mutating the AAUAAA signal or the DSE, which does not affect the encoding of amino acids in the infectious clone, increased the expression of capsid protein VP1/VP2 and thereby increased progeny virus production approximately 2-3-fold. This increase was accompanied by enhanced replication of the AMDV genome. Thus, this study reveals correla- tions among internal polyadenylation, capsid production, viral DNA replication and progeny virus produc- tion of AMDV, indicating that internal polyadenylation is a limiting step for parvovirus replication and progeny virus production.
-
The Capsid Proteins of Aleutian Mink Disease Virus Activate Caspases and Are Specifically Cleaved during Infection
Journal of virology, 2009Co-Authors: Fang Cheng, Marshall E. Bloom, Sonja M. Best, Aaron Yun Chen, David J. Pintel, Jianming QiuAbstract:Aleutian mink disease virus (AMDV) is currently the only known member of the genus Amdovirus in the family Parvoviridae. It is the etiological agent of Aleutian disease of mink. We have previously shown that a small protein with a molecular mass of approximately 26 kDa was present during AMDV infection and following transfection of capsid expression constructs (J. Qiu, F. Cheng, L. R. Burger, and D. Pintel, J. Virol. 80:654-662, 2006). In this study, we report that the capsid proteins were specifically cleaved at aspartic acid residue 420 (D420) during virus infection, resulting in the previously observed cleavage product. Mutation of a single amino acid residue at D420 abolished the specific cleavage. Expression of the capsid proteins alone in Crandell feline kidney (CrFK) cells reproduced the cleavage of the capsid proteins in virus infection. More importantly, capsid protein expression alone induced active caspases, of which caspase-10 was the most active. Active caspases, in turn, cleaved capsid proteins in vivo. Our results also showed that active caspase-7 specifically cleaved capsid proteins at D420 in vitro. These results suggest that viral capsid proteins alone induce caspase activation, resulting in cleavage of capsid proteins. We also provide evidence that AMDV mutants resistant to caspase-mediated capsid cleavage increased virus production approximately 3- to 5-fold in CrFK cells compared to that produced from the parent virus AMDV-G at 37°C but not at 31.8°C. Collectively, our results indicate that caspase activity plays multiple roles in AMDV infection and that cleavage of the capsid proteins might have a role in regulating persistent infection of AMDV.
Deana L. Clifford - One of the best experts on this subject based on the ideXlab platform.
-
Brief Communication Aleutian Disease: An Emerging Disease in Free-Ranging Striped Skunks (Mephitis mephitis) From California
2016Co-Authors: Elise E B Ladouceur, Paula G. Ciembor, Guillermo Rimoldi, Melanie Piazza, Branson W Ritchie, Denise Pesti, Deana L. Clifford, M. Anderson, Federico GiannittiAbstract:Aleutian disease virus (ADV, Amdovirus, Parvoviridae) primarily infects farmed mustelids (mink and ferrets) but also other fur-bearing animals and humans. Three Aleutian disease (AD) cases have been described in captive striped skunks; however, little is known about the relevance of AD in free-ranging carnivores. This work describes the pathological findings and temporospatial distribution in 7 cases of AD in free-ranging striped skunks. All cases showed neurologic disease and were found in a 46-month period (2010–2013) within a localized geographical region in California. Lesions included multisystemic plasmacytic and lymphocytic inflammation (ie, interstitial nephritis, myocarditis, hepatitis, meningoencephalitis, pneumonia, and splenitis), glomer-ulonephritis, arteritis with or without fibrinoid necrosis in several organs (ie, kidney, heart, brain, and spleen), splenomegaly, ascites/hydrothorax, and/or encephalomalacia with cerebral microangiopathy. ADV infection was confirmed in all cases by specific polymerase chain reaction and/or in situ hybridization. The results suggest that AD is an emerging disease in free-ranging striped skunks in California
-
Aleutian Disease: An Emerging Disease in Free-Ranging Striped Skunks (Mephitis mephitis) From California
Veterinary Pathology, 2014Co-Authors: Elise E B Ladouceur, Paula G. Ciembor, Guillermo Rimoldi, Melanie Piazza, Branson W Ritchie, Denise Pesti, Deana L. Clifford, Mark L Anderson, Federico GiannittiAbstract:Aleutian disease virus (ADV, Amdovirus, Parvoviridae) primarily infects farmed mustelids (mink and ferrets) but also other fur-bearing animals and humans. Three Aleutian disease (AD) cases have bee...
-
Aleutian Disease: An Emerging Disease in Free-Ranging Striped Skunks (Mephitis mephitis) From California
Veterinary pathology, 2014Co-Authors: Elise E B Ladouceur, Paula G. Ciembor, Guillermo Rimoldi, Melanie Piazza, Branson W Ritchie, Denise Pesti, Deana L. Clifford, Mark L Anderson, Federico GiannittiAbstract:Aleutian disease virus (ADV, Amdovirus, Parvoviridae) primarily infects farmed mustelids (mink and ferrets) but also other fur-bearing animals and humans. Three Aleutian disease (AD) cases have been described in captive striped skunks; however, little is known about the relevance of AD in free-ranging carnivores. This work describes the pathological findings and temporospatial distribution in 7 cases of AD in free-ranging striped skunks. All cases showed neurologic disease and were found in a 46-month period (2010-2013) within a localized geographical region in California. Lesions included multisystemic plasmacytic and lymphocytic inflammation (ie, interstitial nephritis, myocarditis, hepatitis, meningoencephalitis, pneumonia, and splenitis), glomerulonephritis, arteritis with or without fibrinoid necrosis in several organs (ie, kidney, heart, brain, and spleen), splenomegaly, ascites/hydrothorax, and/or encephalomalacia with cerebral microangiopathy. ADV infection was confirmed in all cases by specific polymerase chain reaction and/or in situ hybridization. The results suggest that AD is an emerging disease in free-ranging striped skunks in California.
-
DISPATCHES Novel Amdovirus in Gray Foxes
2013Co-Authors: Patricia A. Pesavento, Deana L. Clifford, Jennifer A. Luff, Chunlin Wang, Leslie Woods, Eric DelwartAbstract:We used viral metagenomics to identify a novel parvovirus in tissues of a gray fox (Urocyon cinereoargenteus). Nearly full genome characterization and phylogenetic analyses showed this parvovirus (provisionally named gray fox Amdovirus) to be distantly related to Aleutian mink disease virus, representing the second viral species in the Amdovirus genus. Aleutian mink disease virus (AMDV) is currently the only member of the genus Amdovirus in the family Parvoviridae; it can infect diverse breeds of farmed and feral mink, in addition to other mustelids (e.g., ferrets, otters), raccoons, and foxes (1,2). AMDV has an ≈5-kb single-stranded DNA genome and, like other parvoviruses, replicates through a rolling-hairpin mechanism (3). The viral genome has 2 large open reading frames (ORFs)
-
Novel Amdovirus in Gray Foxes
Emerging Infectious Diseases, 2011Co-Authors: Patricia A. Pesavento, Deana L. Clifford, Leslie W. Woods, Jennifer A. Luff, Chunlin Wang, Eric DelwartAbstract:We used viral metagenomics to identify a novel parvovirus in tissues of a gray fox (Urocyon cinereoargenteus). Nearly full genome characterization and phylogenetic analyses showed this parvovirus (provisionally named gray fox Amdovirus) to be distantly related to Aleutian mink disease virus, representing the second viral species in the Amdovirus genus.