Deletion of the small RNA chaperone protein Hfq down regulates genes related to virulence and confers protection against wild-type Brucella challenge in mice
Brucellosis is one of the most common zoonotic epidemics worldwide. Brucella, the etiological pathogen of brucellosis, has unique virulence characteristics, including the ability to survive within the host cell. Hfq is a bacterial chaperone protein that is involved in the survival of the pathogen un...
Ausführliche Beschreibung
Autor*in: |
Shuangshuang eLei [verfasserIn] Zhijun eZhong [verfasserIn] Yuehua eKe [verfasserIn] Mingjuan eYang [verfasserIn] Xiaoyang eXu [verfasserIn] Hang eRen [verfasserIn] Chang eAn [verfasserIn] Jiuyun eYuan [verfasserIn] Jiuxuan eYu [verfasserIn] Jie eXu [verfasserIn] Yanchun eShi [verfasserIn] Yefeng eQiu [verfasserIn] Yufei eWang [verfasserIn] Guangneng ePeng [verfasserIn] Zeliang eChen [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2016 |
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Übergeordnetes Werk: |
In: Frontiers in Microbiology - Frontiers Media S.A., 2011, 6(2016) |
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Übergeordnetes Werk: |
volume:6 ; year:2016 |
Links: |
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DOI / URN: |
10.3389/fmicb.2015.01570 |
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Katalog-ID: |
DOAJ005126711 |
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520 | |a Brucellosis is one of the most common zoonotic epidemics worldwide. Brucella, the etiological pathogen of brucellosis, has unique virulence characteristics, including the ability to survive within the host cell. Hfq is a bacterial chaperone protein that is involved in the survival of the pathogen under stress conditions. Moreover, hfq affects the expression of a large number of target genes. In the present study, we characterized the expression and regulatory patterns of the target genes of Hfq during brucellosis. The results revealed that hfq expression is highly induced in macrophages at the early infection stage and at the late stage of mouse infection. Several genes related to virulence, including omp25, omp31, vjbR, htrA, gntR, and dnaK, were found to be regulated by hfq during infection in BALB/c mice. Gene expression and cytokine secretion analysis revealed that an hfq-deletion mutant induced different cytokine profiles compared with that induced by 16M. Infection with the hfq-deletion mutant induced protective immune responses against 16M challenge. Together, these results suggest that hfq is induced during infection and its deletion results in significant attenuation which affects the host immune response caused by Brucella infection. By regulating genes related to virulence, hfq promotes the virulence of Brucella. The unique characteristics of the hfq-deletion mutant, including its decreased virulence and the ability to induce protective immune response upon infection, suggest that it represents an attractive candidate for the design of a live attenuated vaccine against Brucella. | ||
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10.3389/fmicb.2015.01570 doi (DE-627)DOAJ005126711 (DE-599)DOAJfc4c7a0938f3497389e63aa2bcc5ccdf DE-627 ger DE-627 rakwb eng QR1-502 Shuangshuang eLei verfasserin aut Deletion of the small RNA chaperone protein Hfq down regulates genes related to virulence and confers protection against wild-type Brucella challenge in mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Brucellosis is one of the most common zoonotic epidemics worldwide. Brucella, the etiological pathogen of brucellosis, has unique virulence characteristics, including the ability to survive within the host cell. Hfq is a bacterial chaperone protein that is involved in the survival of the pathogen under stress conditions. Moreover, hfq affects the expression of a large number of target genes. In the present study, we characterized the expression and regulatory patterns of the target genes of Hfq during brucellosis. The results revealed that hfq expression is highly induced in macrophages at the early infection stage and at the late stage of mouse infection. Several genes related to virulence, including omp25, omp31, vjbR, htrA, gntR, and dnaK, were found to be regulated by hfq during infection in BALB/c mice. Gene expression and cytokine secretion analysis revealed that an hfq-deletion mutant induced different cytokine profiles compared with that induced by 16M. Infection with the hfq-deletion mutant induced protective immune responses against 16M challenge. Together, these results suggest that hfq is induced during infection and its deletion results in significant attenuation which affects the host immune response caused by Brucella infection. By regulating genes related to virulence, hfq promotes the virulence of Brucella. The unique characteristics of the hfq-deletion mutant, including its decreased virulence and the ability to induce protective immune response upon infection, suggest that it represents an attractive candidate for the design of a live attenuated vaccine against Brucella. Brucellosis Hfq protective immunity Host immune response Virulence-related genes Microbiology Zhijun eZhong verfasserin aut Yuehua eKe verfasserin aut Mingjuan eYang verfasserin aut Xiaoyang eXu verfasserin aut Hang eRen verfasserin aut Chang eAn verfasserin aut Jiuyun eYuan verfasserin aut Jiuxuan eYu verfasserin aut Jie eXu verfasserin aut Yanchun eShi verfasserin aut Yefeng eQiu verfasserin aut Yufei eWang verfasserin aut Guangneng ePeng verfasserin aut Zeliang eChen verfasserin aut Zeliang eChen verfasserin aut In Frontiers in Microbiology Frontiers Media S.A., 2011 6(2016) (DE-627)642889384 (DE-600)2587354-4 1664302X nnns volume:6 year:2016 https://doi.org/10.3389/fmicb.2015.01570 kostenfrei https://doaj.org/article/fc4c7a0938f3497389e63aa2bcc5ccdf kostenfrei http://journal.frontiersin.org/Journal/10.3389/fmicb.2015.01570/full kostenfrei https://doaj.org/toc/1664-302X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2016 |
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10.3389/fmicb.2015.01570 doi (DE-627)DOAJ005126711 (DE-599)DOAJfc4c7a0938f3497389e63aa2bcc5ccdf DE-627 ger DE-627 rakwb eng QR1-502 Shuangshuang eLei verfasserin aut Deletion of the small RNA chaperone protein Hfq down regulates genes related to virulence and confers protection against wild-type Brucella challenge in mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Brucellosis is one of the most common zoonotic epidemics worldwide. Brucella, the etiological pathogen of brucellosis, has unique virulence characteristics, including the ability to survive within the host cell. Hfq is a bacterial chaperone protein that is involved in the survival of the pathogen under stress conditions. Moreover, hfq affects the expression of a large number of target genes. In the present study, we characterized the expression and regulatory patterns of the target genes of Hfq during brucellosis. The results revealed that hfq expression is highly induced in macrophages at the early infection stage and at the late stage of mouse infection. Several genes related to virulence, including omp25, omp31, vjbR, htrA, gntR, and dnaK, were found to be regulated by hfq during infection in BALB/c mice. Gene expression and cytokine secretion analysis revealed that an hfq-deletion mutant induced different cytokine profiles compared with that induced by 16M. Infection with the hfq-deletion mutant induced protective immune responses against 16M challenge. Together, these results suggest that hfq is induced during infection and its deletion results in significant attenuation which affects the host immune response caused by Brucella infection. By regulating genes related to virulence, hfq promotes the virulence of Brucella. The unique characteristics of the hfq-deletion mutant, including its decreased virulence and the ability to induce protective immune response upon infection, suggest that it represents an attractive candidate for the design of a live attenuated vaccine against Brucella. Brucellosis Hfq protective immunity Host immune response Virulence-related genes Microbiology Zhijun eZhong verfasserin aut Yuehua eKe verfasserin aut Mingjuan eYang verfasserin aut Xiaoyang eXu verfasserin aut Hang eRen verfasserin aut Chang eAn verfasserin aut Jiuyun eYuan verfasserin aut Jiuxuan eYu verfasserin aut Jie eXu verfasserin aut Yanchun eShi verfasserin aut Yefeng eQiu verfasserin aut Yufei eWang verfasserin aut Guangneng ePeng verfasserin aut Zeliang eChen verfasserin aut Zeliang eChen verfasserin aut In Frontiers in Microbiology Frontiers Media S.A., 2011 6(2016) (DE-627)642889384 (DE-600)2587354-4 1664302X nnns volume:6 year:2016 https://doi.org/10.3389/fmicb.2015.01570 kostenfrei https://doaj.org/article/fc4c7a0938f3497389e63aa2bcc5ccdf kostenfrei http://journal.frontiersin.org/Journal/10.3389/fmicb.2015.01570/full kostenfrei https://doaj.org/toc/1664-302X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2016 |
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10.3389/fmicb.2015.01570 doi (DE-627)DOAJ005126711 (DE-599)DOAJfc4c7a0938f3497389e63aa2bcc5ccdf DE-627 ger DE-627 rakwb eng QR1-502 Shuangshuang eLei verfasserin aut Deletion of the small RNA chaperone protein Hfq down regulates genes related to virulence and confers protection against wild-type Brucella challenge in mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Brucellosis is one of the most common zoonotic epidemics worldwide. Brucella, the etiological pathogen of brucellosis, has unique virulence characteristics, including the ability to survive within the host cell. Hfq is a bacterial chaperone protein that is involved in the survival of the pathogen under stress conditions. Moreover, hfq affects the expression of a large number of target genes. In the present study, we characterized the expression and regulatory patterns of the target genes of Hfq during brucellosis. The results revealed that hfq expression is highly induced in macrophages at the early infection stage and at the late stage of mouse infection. Several genes related to virulence, including omp25, omp31, vjbR, htrA, gntR, and dnaK, were found to be regulated by hfq during infection in BALB/c mice. Gene expression and cytokine secretion analysis revealed that an hfq-deletion mutant induced different cytokine profiles compared with that induced by 16M. Infection with the hfq-deletion mutant induced protective immune responses against 16M challenge. Together, these results suggest that hfq is induced during infection and its deletion results in significant attenuation which affects the host immune response caused by Brucella infection. By regulating genes related to virulence, hfq promotes the virulence of Brucella. The unique characteristics of the hfq-deletion mutant, including its decreased virulence and the ability to induce protective immune response upon infection, suggest that it represents an attractive candidate for the design of a live attenuated vaccine against Brucella. Brucellosis Hfq protective immunity Host immune response Virulence-related genes Microbiology Zhijun eZhong verfasserin aut Yuehua eKe verfasserin aut Mingjuan eYang verfasserin aut Xiaoyang eXu verfasserin aut Hang eRen verfasserin aut Chang eAn verfasserin aut Jiuyun eYuan verfasserin aut Jiuxuan eYu verfasserin aut Jie eXu verfasserin aut Yanchun eShi verfasserin aut Yefeng eQiu verfasserin aut Yufei eWang verfasserin aut Guangneng ePeng verfasserin aut Zeliang eChen verfasserin aut Zeliang eChen verfasserin aut In Frontiers in Microbiology Frontiers Media S.A., 2011 6(2016) (DE-627)642889384 (DE-600)2587354-4 1664302X nnns volume:6 year:2016 https://doi.org/10.3389/fmicb.2015.01570 kostenfrei https://doaj.org/article/fc4c7a0938f3497389e63aa2bcc5ccdf kostenfrei http://journal.frontiersin.org/Journal/10.3389/fmicb.2015.01570/full kostenfrei https://doaj.org/toc/1664-302X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2016 |
allfieldsGer |
10.3389/fmicb.2015.01570 doi (DE-627)DOAJ005126711 (DE-599)DOAJfc4c7a0938f3497389e63aa2bcc5ccdf DE-627 ger DE-627 rakwb eng QR1-502 Shuangshuang eLei verfasserin aut Deletion of the small RNA chaperone protein Hfq down regulates genes related to virulence and confers protection against wild-type Brucella challenge in mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Brucellosis is one of the most common zoonotic epidemics worldwide. Brucella, the etiological pathogen of brucellosis, has unique virulence characteristics, including the ability to survive within the host cell. Hfq is a bacterial chaperone protein that is involved in the survival of the pathogen under stress conditions. Moreover, hfq affects the expression of a large number of target genes. In the present study, we characterized the expression and regulatory patterns of the target genes of Hfq during brucellosis. The results revealed that hfq expression is highly induced in macrophages at the early infection stage and at the late stage of mouse infection. Several genes related to virulence, including omp25, omp31, vjbR, htrA, gntR, and dnaK, were found to be regulated by hfq during infection in BALB/c mice. Gene expression and cytokine secretion analysis revealed that an hfq-deletion mutant induced different cytokine profiles compared with that induced by 16M. Infection with the hfq-deletion mutant induced protective immune responses against 16M challenge. Together, these results suggest that hfq is induced during infection and its deletion results in significant attenuation which affects the host immune response caused by Brucella infection. By regulating genes related to virulence, hfq promotes the virulence of Brucella. The unique characteristics of the hfq-deletion mutant, including its decreased virulence and the ability to induce protective immune response upon infection, suggest that it represents an attractive candidate for the design of a live attenuated vaccine against Brucella. Brucellosis Hfq protective immunity Host immune response Virulence-related genes Microbiology Zhijun eZhong verfasserin aut Yuehua eKe verfasserin aut Mingjuan eYang verfasserin aut Xiaoyang eXu verfasserin aut Hang eRen verfasserin aut Chang eAn verfasserin aut Jiuyun eYuan verfasserin aut Jiuxuan eYu verfasserin aut Jie eXu verfasserin aut Yanchun eShi verfasserin aut Yefeng eQiu verfasserin aut Yufei eWang verfasserin aut Guangneng ePeng verfasserin aut Zeliang eChen verfasserin aut Zeliang eChen verfasserin aut In Frontiers in Microbiology Frontiers Media S.A., 2011 6(2016) (DE-627)642889384 (DE-600)2587354-4 1664302X nnns volume:6 year:2016 https://doi.org/10.3389/fmicb.2015.01570 kostenfrei https://doaj.org/article/fc4c7a0938f3497389e63aa2bcc5ccdf kostenfrei http://journal.frontiersin.org/Journal/10.3389/fmicb.2015.01570/full kostenfrei https://doaj.org/toc/1664-302X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2016 |
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Deletion of the small RNA chaperone protein Hfq down regulates genes related to virulence and confers protection against wild-type Brucella challenge in mice |
abstract |
Brucellosis is one of the most common zoonotic epidemics worldwide. Brucella, the etiological pathogen of brucellosis, has unique virulence characteristics, including the ability to survive within the host cell. Hfq is a bacterial chaperone protein that is involved in the survival of the pathogen under stress conditions. Moreover, hfq affects the expression of a large number of target genes. In the present study, we characterized the expression and regulatory patterns of the target genes of Hfq during brucellosis. The results revealed that hfq expression is highly induced in macrophages at the early infection stage and at the late stage of mouse infection. Several genes related to virulence, including omp25, omp31, vjbR, htrA, gntR, and dnaK, were found to be regulated by hfq during infection in BALB/c mice. Gene expression and cytokine secretion analysis revealed that an hfq-deletion mutant induced different cytokine profiles compared with that induced by 16M. Infection with the hfq-deletion mutant induced protective immune responses against 16M challenge. Together, these results suggest that hfq is induced during infection and its deletion results in significant attenuation which affects the host immune response caused by Brucella infection. By regulating genes related to virulence, hfq promotes the virulence of Brucella. The unique characteristics of the hfq-deletion mutant, including its decreased virulence and the ability to induce protective immune response upon infection, suggest that it represents an attractive candidate for the design of a live attenuated vaccine against Brucella. |
abstractGer |
Brucellosis is one of the most common zoonotic epidemics worldwide. Brucella, the etiological pathogen of brucellosis, has unique virulence characteristics, including the ability to survive within the host cell. Hfq is a bacterial chaperone protein that is involved in the survival of the pathogen under stress conditions. Moreover, hfq affects the expression of a large number of target genes. In the present study, we characterized the expression and regulatory patterns of the target genes of Hfq during brucellosis. The results revealed that hfq expression is highly induced in macrophages at the early infection stage and at the late stage of mouse infection. Several genes related to virulence, including omp25, omp31, vjbR, htrA, gntR, and dnaK, were found to be regulated by hfq during infection in BALB/c mice. Gene expression and cytokine secretion analysis revealed that an hfq-deletion mutant induced different cytokine profiles compared with that induced by 16M. Infection with the hfq-deletion mutant induced protective immune responses against 16M challenge. Together, these results suggest that hfq is induced during infection and its deletion results in significant attenuation which affects the host immune response caused by Brucella infection. By regulating genes related to virulence, hfq promotes the virulence of Brucella. The unique characteristics of the hfq-deletion mutant, including its decreased virulence and the ability to induce protective immune response upon infection, suggest that it represents an attractive candidate for the design of a live attenuated vaccine against Brucella. |
abstract_unstemmed |
Brucellosis is one of the most common zoonotic epidemics worldwide. Brucella, the etiological pathogen of brucellosis, has unique virulence characteristics, including the ability to survive within the host cell. Hfq is a bacterial chaperone protein that is involved in the survival of the pathogen under stress conditions. Moreover, hfq affects the expression of a large number of target genes. In the present study, we characterized the expression and regulatory patterns of the target genes of Hfq during brucellosis. The results revealed that hfq expression is highly induced in macrophages at the early infection stage and at the late stage of mouse infection. Several genes related to virulence, including omp25, omp31, vjbR, htrA, gntR, and dnaK, were found to be regulated by hfq during infection in BALB/c mice. Gene expression and cytokine secretion analysis revealed that an hfq-deletion mutant induced different cytokine profiles compared with that induced by 16M. Infection with the hfq-deletion mutant induced protective immune responses against 16M challenge. Together, these results suggest that hfq is induced during infection and its deletion results in significant attenuation which affects the host immune response caused by Brucella infection. By regulating genes related to virulence, hfq promotes the virulence of Brucella. The unique characteristics of the hfq-deletion mutant, including its decreased virulence and the ability to induce protective immune response upon infection, suggest that it represents an attractive candidate for the design of a live attenuated vaccine against Brucella. |
collection_details |
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title_short |
Deletion of the small RNA chaperone protein Hfq down regulates genes related to virulence and confers protection against wild-type Brucella challenge in mice |
url |
https://doi.org/10.3389/fmicb.2015.01570 https://doaj.org/article/fc4c7a0938f3497389e63aa2bcc5ccdf http://journal.frontiersin.org/Journal/10.3389/fmicb.2015.01570/full https://doaj.org/toc/1664-302X |
remote_bool |
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author2 |
Zhijun eZhong Yuehua eKe Mingjuan eYang Xiaoyang eXu Hang eRen Chang eAn Jiuyun eYuan Jiuxuan eYu Jie eXu Yanchun eShi Yefeng eQiu Yufei eWang Guangneng ePeng Zeliang eChen |
author2Str |
Zhijun eZhong Yuehua eKe Mingjuan eYang Xiaoyang eXu Hang eRen Chang eAn Jiuyun eYuan Jiuxuan eYu Jie eXu Yanchun eShi Yefeng eQiu Yufei eWang Guangneng ePeng Zeliang eChen |
ppnlink |
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callnumber-subject |
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hochschulschrift_bool |
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doi_str |
10.3389/fmicb.2015.01570 |
callnumber-a |
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up_date |
2024-07-04T02:24:17.064Z |
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