% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Costa:284095,
      author       = {Costa, Vivian V. and Fagundes, Caio T. and Valadão,
                      Deborah F. and Ávila, Thiago V. and Cisalpino, Daniel and
                      Rocha, Rebeca F. and Secchim Ribeiro, Lucas and Ascenção,
                      Fernando R. and Kangussu, Lucas M. and Junior, Celso M. Q.
                      and Astigarraga, Ruiz G. and Gouveia, Frederico L. and
                      Silva, Tarcília A. and Bonaventura, Daniela and de Almeida
                      Sampaio, Divaldo and Leite, Ana Cristina L. and Teixeira,
                      Mauro M. and Souza, Danielle G.},
      title        = {{S}ubversion of early innate antiviral responses during
                      antibody-dependent enhancement of {D}engue virus infection
                      induces severe disease in immunocompetent mice},
      journal      = {Medical microbiology and immunology},
      volume       = {203},
      number       = {4},
      issn         = {0300-8584},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DZNE-2026-00103},
      pages        = {231 - 250},
      year         = {2014},
      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.},
      keywords     = {Animals / Antibody-Dependent Enhancement / B-Lymphocytes:
                      immunology / Cytokines: blood / Death / Dengue: immunology /
                      Dengue: pathology / Dengue Virus: immunology / Immunity,
                      Innate / Liver: pathology / Mice, Inbred C57BL / Mice,
                      Knockout / Thrombocytopenia / Viral Load / Cytokines (NLM
                      Chemicals)},
      ddc          = {610},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1007/s00430-014-0334-5},
      url          = {https://pub.dzne.de/record/284095},
}