Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice
Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individua...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Costa, Vivian V. [verfasserIn] Fagundes, Caio T. [verfasserIn] Valadão, Deborah F. [verfasserIn] Ávila, Thiago V. [verfasserIn] Cisalpino, Daniel [verfasserIn] Rocha, Rebeca F. [verfasserIn] Ribeiro, Lucas S. [verfasserIn] Ascenção, Fernando R. [verfasserIn] Kangussu, Lucas M. [verfasserIn] Junior, Celso M. Q. [verfasserIn] Astigarraga, Ruiz G. [verfasserIn] Gouveia, Frederico L. [verfasserIn] Silva, Tarcília A. [verfasserIn] Bonaventura, Daniela [verfasserIn] de Almeida Sampaio, Divaldo [verfasserIn] Leite, Ana Cristina L. [verfasserIn] Teixeira, Mauro M. [verfasserIn] Souza, Danielle G. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2014 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Medical microbiology and immunology - Berlin : Springer, 1886, 203(2014), 4 vom: 11. Apr., Seite 231-250 |
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| Übergeordnetes Werk: |
volume:203 ; year:2014 ; number:4 ; day:11 ; month:04 ; pages:231-250 |
| Links: |
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| DOI / URN: |
10.1007/s00430-014-0334-5 |
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| Katalog-ID: |
SPR005748887 |
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| 100 | 1 | |a Costa, Vivian V. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice |
| 264 | 1 | |c 2014 | |
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| 520 | |a Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary DENV infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B cells play a pivotal role in host responses against primary DENV infection in mice. After infection, $ μMT^{−/−} $ mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-DENV-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/DSS. Finally, treatment with intravenous immunoglobulin containing anti-DENV antibodies confirmed the potential enhancing capacity of subneutralizing antibodies to mediate virus infection and replication and induce severe disease manifestation of DENV-infected mice. Thus, our results show that humoral responses unleashed during DENV infections can exert protective or pathological outcomes and provide insight into the pathogenesis of this important human pathogen. | ||
| 650 | 4 | |a Antibody-dependent enhancement |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a DHF/DSS |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Type I interferons |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Humoral response against DENV |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Fagundes, Caio T. |e verfasserin |4 aut | |
| 700 | 1 | |a Valadão, Deborah F. |e verfasserin |4 aut | |
| 700 | 1 | |a Ávila, Thiago V. |e verfasserin |4 aut | |
| 700 | 1 | |a Cisalpino, Daniel |e verfasserin |4 aut | |
| 700 | 1 | |a Rocha, Rebeca F. |e verfasserin |4 aut | |
| 700 | 1 | |a Ribeiro, Lucas S. |e verfasserin |4 aut | |
| 700 | 1 | |a Ascenção, Fernando R. |e verfasserin |4 aut | |
| 700 | 1 | |a Kangussu, Lucas M. |e verfasserin |4 aut | |
| 700 | 1 | |a Junior, Celso M. Q. |e verfasserin |4 aut | |
| 700 | 1 | |a Astigarraga, Ruiz G. |e verfasserin |4 aut | |
| 700 | 1 | |a Gouveia, Frederico L. |e verfasserin |4 aut | |
| 700 | 1 | |a Silva, Tarcília A. |e verfasserin |4 aut | |
| 700 | 1 | |a Bonaventura, Daniela |e verfasserin |4 aut | |
| 700 | 1 | |a de Almeida Sampaio, Divaldo |e verfasserin |4 aut | |
| 700 | 1 | |a Leite, Ana Cristina L. |e verfasserin |4 aut | |
| 700 | 1 | |a Teixeira, Mauro M. |e verfasserin |4 aut | |
| 700 | 1 | |a Souza, Danielle G. |e verfasserin |4 aut | |
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10.1007/s00430-014-0334-5 doi (DE-627)SPR005748887 (SPR)s00430-014-0334-5-e DE-627 ger DE-627 rakwb eng 570 610 ASE 44.75 bkl Costa, Vivian V. verfasserin aut Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary DENV infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B cells play a pivotal role in host responses against primary DENV infection in mice. After infection, $ μMT^{−/−} $ mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-DENV-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/DSS. Finally, treatment with intravenous immunoglobulin containing anti-DENV antibodies confirmed the potential enhancing capacity of subneutralizing antibodies to mediate virus infection and replication and induce severe disease manifestation of DENV-infected mice. Thus, our results show that humoral responses unleashed during DENV infections can exert protective or pathological outcomes and provide insight into the pathogenesis of this important human pathogen. Antibody-dependent enhancement (dpeaa)DE-He213 DHF/DSS (dpeaa)DE-He213 Type I interferons (dpeaa)DE-He213 Humoral response against DENV (dpeaa)DE-He213 Fagundes, Caio T. verfasserin aut Valadão, Deborah F. verfasserin aut Ávila, Thiago V. verfasserin aut Cisalpino, Daniel verfasserin aut Rocha, Rebeca F. verfasserin aut Ribeiro, Lucas S. verfasserin aut Ascenção, Fernando R. verfasserin aut Kangussu, Lucas M. verfasserin aut Junior, Celso M. Q. verfasserin aut Astigarraga, Ruiz G. verfasserin aut Gouveia, Frederico L. verfasserin aut Silva, Tarcília A. verfasserin aut Bonaventura, Daniela verfasserin aut de Almeida Sampaio, Divaldo verfasserin aut Leite, Ana Cristina L. verfasserin aut Teixeira, Mauro M. verfasserin aut Souza, Danielle G. verfasserin aut Enthalten in Medical microbiology and immunology Berlin : Springer, 1886 203(2014), 4 vom: 11. Apr., Seite 231-250 (DE-627)254630871 (DE-600)1462140-X 1432-1831 nnns volume:203 year:2014 number:4 day:11 month:04 pages:231-250 https://dx.doi.org/10.1007/s00430-014-0334-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_252 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2110 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.75 ASE AR 203 2014 4 11 04 231-250 |
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10.1007/s00430-014-0334-5 doi (DE-627)SPR005748887 (SPR)s00430-014-0334-5-e DE-627 ger DE-627 rakwb eng 570 610 ASE 44.75 bkl Costa, Vivian V. verfasserin aut Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary DENV infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B cells play a pivotal role in host responses against primary DENV infection in mice. After infection, $ μMT^{−/−} $ mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-DENV-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/DSS. Finally, treatment with intravenous immunoglobulin containing anti-DENV antibodies confirmed the potential enhancing capacity of subneutralizing antibodies to mediate virus infection and replication and induce severe disease manifestation of DENV-infected mice. Thus, our results show that humoral responses unleashed during DENV infections can exert protective or pathological outcomes and provide insight into the pathogenesis of this important human pathogen. Antibody-dependent enhancement (dpeaa)DE-He213 DHF/DSS (dpeaa)DE-He213 Type I interferons (dpeaa)DE-He213 Humoral response against DENV (dpeaa)DE-He213 Fagundes, Caio T. verfasserin aut Valadão, Deborah F. verfasserin aut Ávila, Thiago V. verfasserin aut Cisalpino, Daniel verfasserin aut Rocha, Rebeca F. verfasserin aut Ribeiro, Lucas S. verfasserin aut Ascenção, Fernando R. verfasserin aut Kangussu, Lucas M. verfasserin aut Junior, Celso M. Q. verfasserin aut Astigarraga, Ruiz G. verfasserin aut Gouveia, Frederico L. verfasserin aut Silva, Tarcília A. verfasserin aut Bonaventura, Daniela verfasserin aut de Almeida Sampaio, Divaldo verfasserin aut Leite, Ana Cristina L. verfasserin aut Teixeira, Mauro M. verfasserin aut Souza, Danielle G. verfasserin aut Enthalten in Medical microbiology and immunology Berlin : Springer, 1886 203(2014), 4 vom: 11. Apr., Seite 231-250 (DE-627)254630871 (DE-600)1462140-X 1432-1831 nnns volume:203 year:2014 number:4 day:11 month:04 pages:231-250 https://dx.doi.org/10.1007/s00430-014-0334-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_252 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2110 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.75 ASE AR 203 2014 4 11 04 231-250 |
| allfields_unstemmed |
10.1007/s00430-014-0334-5 doi (DE-627)SPR005748887 (SPR)s00430-014-0334-5-e DE-627 ger DE-627 rakwb eng 570 610 ASE 44.75 bkl Costa, Vivian V. verfasserin aut Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary DENV infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B cells play a pivotal role in host responses against primary DENV infection in mice. After infection, $ μMT^{−/−} $ mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-DENV-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/DSS. Finally, treatment with intravenous immunoglobulin containing anti-DENV antibodies confirmed the potential enhancing capacity of subneutralizing antibodies to mediate virus infection and replication and induce severe disease manifestation of DENV-infected mice. Thus, our results show that humoral responses unleashed during DENV infections can exert protective or pathological outcomes and provide insight into the pathogenesis of this important human pathogen. Antibody-dependent enhancement (dpeaa)DE-He213 DHF/DSS (dpeaa)DE-He213 Type I interferons (dpeaa)DE-He213 Humoral response against DENV (dpeaa)DE-He213 Fagundes, Caio T. verfasserin aut Valadão, Deborah F. verfasserin aut Ávila, Thiago V. verfasserin aut Cisalpino, Daniel verfasserin aut Rocha, Rebeca F. verfasserin aut Ribeiro, Lucas S. verfasserin aut Ascenção, Fernando R. verfasserin aut Kangussu, Lucas M. verfasserin aut Junior, Celso M. Q. verfasserin aut Astigarraga, Ruiz G. verfasserin aut Gouveia, Frederico L. verfasserin aut Silva, Tarcília A. verfasserin aut Bonaventura, Daniela verfasserin aut de Almeida Sampaio, Divaldo verfasserin aut Leite, Ana Cristina L. verfasserin aut Teixeira, Mauro M. verfasserin aut Souza, Danielle G. verfasserin aut Enthalten in Medical microbiology and immunology Berlin : Springer, 1886 203(2014), 4 vom: 11. Apr., Seite 231-250 (DE-627)254630871 (DE-600)1462140-X 1432-1831 nnns volume:203 year:2014 number:4 day:11 month:04 pages:231-250 https://dx.doi.org/10.1007/s00430-014-0334-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_252 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2110 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.75 ASE AR 203 2014 4 11 04 231-250 |
| allfieldsGer |
10.1007/s00430-014-0334-5 doi (DE-627)SPR005748887 (SPR)s00430-014-0334-5-e DE-627 ger DE-627 rakwb eng 570 610 ASE 44.75 bkl Costa, Vivian V. verfasserin aut Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary DENV infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B cells play a pivotal role in host responses against primary DENV infection in mice. After infection, $ μMT^{−/−} $ mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-DENV-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/DSS. Finally, treatment with intravenous immunoglobulin containing anti-DENV antibodies confirmed the potential enhancing capacity of subneutralizing antibodies to mediate virus infection and replication and induce severe disease manifestation of DENV-infected mice. Thus, our results show that humoral responses unleashed during DENV infections can exert protective or pathological outcomes and provide insight into the pathogenesis of this important human pathogen. Antibody-dependent enhancement (dpeaa)DE-He213 DHF/DSS (dpeaa)DE-He213 Type I interferons (dpeaa)DE-He213 Humoral response against DENV (dpeaa)DE-He213 Fagundes, Caio T. verfasserin aut Valadão, Deborah F. verfasserin aut Ávila, Thiago V. verfasserin aut Cisalpino, Daniel verfasserin aut Rocha, Rebeca F. verfasserin aut Ribeiro, Lucas S. verfasserin aut Ascenção, Fernando R. verfasserin aut Kangussu, Lucas M. verfasserin aut Junior, Celso M. Q. verfasserin aut Astigarraga, Ruiz G. verfasserin aut Gouveia, Frederico L. verfasserin aut Silva, Tarcília A. verfasserin aut Bonaventura, Daniela verfasserin aut de Almeida Sampaio, Divaldo verfasserin aut Leite, Ana Cristina L. verfasserin aut Teixeira, Mauro M. verfasserin aut Souza, Danielle G. verfasserin aut Enthalten in Medical microbiology and immunology Berlin : Springer, 1886 203(2014), 4 vom: 11. Apr., Seite 231-250 (DE-627)254630871 (DE-600)1462140-X 1432-1831 nnns volume:203 year:2014 number:4 day:11 month:04 pages:231-250 https://dx.doi.org/10.1007/s00430-014-0334-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_252 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2110 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.75 ASE AR 203 2014 4 11 04 231-250 |
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10.1007/s00430-014-0334-5 doi (DE-627)SPR005748887 (SPR)s00430-014-0334-5-e DE-627 ger DE-627 rakwb eng 570 610 ASE 44.75 bkl Costa, Vivian V. verfasserin aut Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary DENV infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B cells play a pivotal role in host responses against primary DENV infection in mice. After infection, $ μMT^{−/−} $ mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-DENV-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/DSS. Finally, treatment with intravenous immunoglobulin containing anti-DENV antibodies confirmed the potential enhancing capacity of subneutralizing antibodies to mediate virus infection and replication and induce severe disease manifestation of DENV-infected mice. Thus, our results show that humoral responses unleashed during DENV infections can exert protective or pathological outcomes and provide insight into the pathogenesis of this important human pathogen. Antibody-dependent enhancement (dpeaa)DE-He213 DHF/DSS (dpeaa)DE-He213 Type I interferons (dpeaa)DE-He213 Humoral response against DENV (dpeaa)DE-He213 Fagundes, Caio T. verfasserin aut Valadão, Deborah F. verfasserin aut Ávila, Thiago V. verfasserin aut Cisalpino, Daniel verfasserin aut Rocha, Rebeca F. verfasserin aut Ribeiro, Lucas S. verfasserin aut Ascenção, Fernando R. verfasserin aut Kangussu, Lucas M. verfasserin aut Junior, Celso M. Q. verfasserin aut Astigarraga, Ruiz G. verfasserin aut Gouveia, Frederico L. verfasserin aut Silva, Tarcília A. verfasserin aut Bonaventura, Daniela verfasserin aut de Almeida Sampaio, Divaldo verfasserin aut Leite, Ana Cristina L. verfasserin aut Teixeira, Mauro M. verfasserin aut Souza, Danielle G. verfasserin aut Enthalten in Medical microbiology and immunology Berlin : Springer, 1886 203(2014), 4 vom: 11. Apr., Seite 231-250 (DE-627)254630871 (DE-600)1462140-X 1432-1831 nnns volume:203 year:2014 number:4 day:11 month:04 pages:231-250 https://dx.doi.org/10.1007/s00430-014-0334-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_252 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2110 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.75 ASE AR 203 2014 4 11 04 231-250 |
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Enthalten in Medical microbiology and immunology 203(2014), 4 vom: 11. Apr., Seite 231-250 volume:203 year:2014 number:4 day:11 month:04 pages:231-250 |
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Enthalten in Medical microbiology and immunology 203(2014), 4 vom: 11. Apr., Seite 231-250 volume:203 year:2014 number:4 day:11 month:04 pages:231-250 |
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Antibody-dependent enhancement DHF/DSS Type I interferons Humoral response against DENV |
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Costa, Vivian V. @@aut@@ Fagundes, Caio T. @@aut@@ Valadão, Deborah F. @@aut@@ Ávila, Thiago V. @@aut@@ Cisalpino, Daniel @@aut@@ Rocha, Rebeca F. @@aut@@ Ribeiro, Lucas S. @@aut@@ Ascenção, Fernando R. @@aut@@ Kangussu, Lucas M. @@aut@@ Junior, Celso M. Q. @@aut@@ Astigarraga, Ruiz G. @@aut@@ Gouveia, Frederico L. @@aut@@ Silva, Tarcília A. @@aut@@ Bonaventura, Daniela @@aut@@ de Almeida Sampaio, Divaldo @@aut@@ Leite, Ana Cristina L. @@aut@@ Teixeira, Mauro M. @@aut@@ Souza, Danielle G. @@aut@@ |
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2014-04-11T00:00:00Z |
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Costa, Vivian V. |
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Costa, Vivian V. ddc 570 bkl 44.75 misc Antibody-dependent enhancement misc DHF/DSS misc Type I interferons misc Humoral response against DENV Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice |
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570 610 ASE 44.75 bkl Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice Antibody-dependent enhancement (dpeaa)DE-He213 DHF/DSS (dpeaa)DE-He213 Type I interferons (dpeaa)DE-He213 Humoral response against DENV (dpeaa)DE-He213 |
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ddc 570 bkl 44.75 misc Antibody-dependent enhancement misc DHF/DSS misc Type I interferons misc Humoral response against DENV |
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ddc 570 bkl 44.75 misc Antibody-dependent enhancement misc DHF/DSS misc Type I interferons misc Humoral response against DENV |
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ddc 570 bkl 44.75 misc Antibody-dependent enhancement misc DHF/DSS misc Type I interferons misc Humoral response against DENV |
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Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice |
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Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice |
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Costa, Vivian V. |
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Medical microbiology and immunology |
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Costa, Vivian V. Fagundes, Caio T. Valadão, Deborah F. Ávila, Thiago V. Cisalpino, Daniel Rocha, Rebeca F. Ribeiro, Lucas S. Ascenção, Fernando R. Kangussu, Lucas M. Junior, Celso M. Q. Astigarraga, Ruiz G. Gouveia, Frederico L. Silva, Tarcília A. Bonaventura, Daniela de Almeida Sampaio, Divaldo Leite, Ana Cristina L. Teixeira, Mauro M. Souza, Danielle G. |
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Costa, Vivian V. |
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subversion of early innate antiviral responses during antibody-dependent enhancement of dengue virus infection induces severe disease in immunocompetent mice |
| title_auth |
Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice |
| abstract |
Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary DENV infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B cells play a pivotal role in host responses against primary DENV infection in mice. After infection, $ μMT^{−/−} $ mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-DENV-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/DSS. Finally, treatment with intravenous immunoglobulin containing anti-DENV antibodies confirmed the potential enhancing capacity of subneutralizing antibodies to mediate virus infection and replication and induce severe disease manifestation of DENV-infected mice. Thus, our results show that humoral responses unleashed during DENV infections can exert protective or pathological outcomes and provide insight into the pathogenesis of this important human pathogen. |
| abstractGer |
Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary DENV infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B cells play a pivotal role in host responses against primary DENV infection in mice. After infection, $ μMT^{−/−} $ mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-DENV-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/DSS. Finally, treatment with intravenous immunoglobulin containing anti-DENV antibodies confirmed the potential enhancing capacity of subneutralizing antibodies to mediate virus infection and replication and induce severe disease manifestation of DENV-infected mice. Thus, our results show that humoral responses unleashed during DENV infections can exert protective or pathological outcomes and provide insight into the pathogenesis of this important human pathogen. |
| abstract_unstemmed |
Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary DENV infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B cells play a pivotal role in host responses against primary DENV infection in mice. After infection, $ μMT^{−/−} $ mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-DENV-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/DSS. Finally, treatment with intravenous immunoglobulin containing anti-DENV antibodies confirmed the potential enhancing capacity of subneutralizing antibodies to mediate virus infection and replication and induce severe disease manifestation of DENV-infected mice. Thus, our results show that humoral responses unleashed during DENV infections can exert protective or pathological outcomes and provide insight into the pathogenesis of this important human pathogen. |
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Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice |
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Fagundes, Caio T. Valadão, Deborah F. Ávila, Thiago V. Cisalpino, Daniel Rocha, Rebeca F. Ribeiro, Lucas S. Ascenção, Fernando R. Kangussu, Lucas M. Junior, Celso M. Q. Astigarraga, Ruiz G. Gouveia, Frederico L. Silva, Tarcília A. Bonaventura, Daniela de Almeida Sampaio, Divaldo Leite, Ana Cristina L. Teixeira, Mauro M. Souza, Danielle G. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR005748887</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519162636.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201002s2014 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s00430-014-0334-5</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR005748887</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s00430-014-0334-5-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.75</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Costa, Vivian V.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2014</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (DENV-1–4). Epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary DENV infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B cells play a pivotal role in host responses against primary DENV infection in mice. After infection, $ μMT^{−/−} $ mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-DENV-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/DSS. Finally, treatment with intravenous immunoglobulin containing anti-DENV antibodies confirmed the potential enhancing capacity of subneutralizing antibodies to mediate virus infection and replication and induce severe disease manifestation of DENV-infected mice. 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