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【病毒外文文獻(xiàn)】2011 Investigation of Antibody-Dependent Enhancement (ADE) of SARS coronavirus infection and its role in pathogenesis of

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【病毒外文文獻(xiàn)】2011 Investigation of Antibody-Dependent Enhancement (ADE) of SARS coronavirus infection and its role in pathogenesis of

POSTER PRESENTATION Open Access Investigation of Antibody Dependent Enhancement ADE of SARS coronavirus infection and its role in pathogenesis of SARS Ming S Yip 1 Chung Y Cheung 2 Ping H Li 1 Roberto Bruzzone 1 JS Malik Peiris 1 2 Martial Jaume 1 From Institut Pasteur International Network Annual Scientific Meeting Hong Kong 22 23 November 2010 Antibody dependent enhancement ADE is a mechanism by which viruses such as dengue HIV and Ebola gain entry into some target cells through the use of host anti viral humoral immune responses 1 Here we studied the ability of severe acute respiratory syndrome coronavirus SARS CoV 2 to use ADE mechanisms to enhance its infectivity towards cells of the hematopoietic lineage We found that heat inactivated immune serum from rodents vaccinated with recombinant native full length Spike protein trimers 3 triggered infection of human immune cells monocytic and B cell lines by SARS CoV Spike pseudotyped particle SARS CoVpp The occur rence of antibody mediated infection of human Raji B cells was further investigated by using live SARS CoV Similarly to results obtained with the SARS CoVpp only anti SARS CoV Spike serum but not mock immune serum induced a massive increase of SARS CoV viral genes ORF1b and Nucleocapsid and viral proteins Membrane and Nucleocapsid in Raji B cells As revealed by immunostaining only a relatively low how ever significant percentage of the Raji cells get infected by antibody mediated infection and did not allow direct assessment of productive replication by conventional cytopathic assays and TCID50 titration Taken together our data suggested that SARS CoV is able to enter human immune cells via an antibody mediated pathway and immunological consequences of such infection are under investigation productive replication cytokines secretion profile and cell death etc Our data raise reasonable concerns regarding the useofSARS CoVvaccineinhumansandpave the way to further studies focusing on the role of immune mediated infection phenomenon during SARS pathogenesis Author details 1 HKU Pasteur Research Centre Hong Kong Hong Kong SAR 2 Department of Microbiology The University of Hong Kong Hong Kong SAR Published 10 January 2011 References 1 Takada A Kawaoka Y Antibody dependent enhancement of viral infection molecular mechanisms and in vivo implications Rev Med Virol 2003 13 387 398 2 Du L He Y Zhou Y Liu S Zheng BJ Jiang S The spike protein of SARS CoV a target for vaccine and therapeutic development Nat Rev Microbiol 2009 3 226 236 3 Kam YW Kien F Roberts A Cheung YC Lamirande EW Vogel L Chu SL Tse J Guarner J Zaki SR Subbarao K Peiris M Nal B Altmeyer R Antibodies against trimeric S glycoprotein protect hamsters against SARS CoV challenge despite their capacity to mediate FcgammaRII dependent entry into B cells in vitro Vaccine 2007 25 729 740 doi 10 1002 rmv 405 Cite this article as Yip et al Investigation of Antibody Dependent Enhancement ADE of SARS coronavirus infection and its role in pathogenesis of SARS BMC Proceedings 2011 5 Suppl 1 P80 Submit your next manuscript to BioMed Central and take full advantage of Convenient online submission Thorough peer review No space constraints or color figure charges Immediate publication on acceptance Inclusion in PubMed CAS Scopus and Google Scholar Research which is freely available for redistribution Submit your manuscript at Correspondence simonyms hkusua hku hk 1 HKU Pasteur Research Centre Hong Kong Hong Kong SAR Full list of author information is available at the end of the article Yip et al BMC Proceedings 2011 5 Suppl 1 P80 2011 Yip et al licensee BioMed Central Ltd This is an open access article distributed under the terms of the Creative Commons Attribution License http creativecommons org licenses by 2 0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited

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