About: Antibody-dependent infection of human macrophages by severe acute respiratory syndrome coronavirus

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About: Antibody-dependent infection of human macrophages by severe acute respiratory syndrome coronavirus Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Antibody-dependent infection of human macrophages by severe acute respiratory syndrome coronavirus
Creator	Peiris, Malik Li, Ping Bruzzone, Roberto Jaume, Martial Daëron, Marc Cheung, Chung Hiu, Nancy Hok, Horace Lee, Yeung Leung, Lan Shum Yip, Ming Sriyal, Joseph
Source	Medline; PMC
abstract	BACKGROUND: Public health risks associated to infection by human coronaviruses remain considerable and vaccination is a key option for preventing the resurgence of severe acute respiratory syndrome coronavirus (SARS-CoV). We have previously reported that antibodies elicited by a SARS-CoV vaccine candidate based on recombinant, full-length SARS-CoV Spike-protein trimers, trigger infection of immune cell lines. These observations prompted us to investigate the molecular mechanisms and responses to antibody-mediated infection in human macrophages. METHODS: We have used primary human immune cells to evaluate their susceptibility to infection by SARS-CoV in the presence of anti-Spike antibodies. Fluorescence microscopy and real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR) were utilized to assess occurrence and consequences of infection. To gain insight into the underlying molecular mechanism, we performed mutational analysis with a series of truncated and chimeric constructs of fragment crystallizable γ receptors (FcγR), which bind antibody-coated pathogens. RESULTS: We show here that anti-Spike immune serum increased infection of human monocyte-derived macrophages by replication-competent SARS-CoV as well as Spike-pseudotyped lentiviral particles (SARS-CoVpp). Macrophages infected with SARS-CoV, however, did not support productive replication of the virus. Purified anti-viral IgGs, but not other soluble factor(s) from heat-inactivated mouse immune serum, were sufficient to enhance infection. Antibody-mediated infection was dependent on signaling-competent members of the human FcγRII family, which were shown to confer susceptibility to otherwise naïve ST486 cells, as binding of immune complexes to cell surface FcγRII was necessary but not sufficient to trigger antibody-dependent enhancement (ADE) of infection. Furthermore, only FcγRII with intact cytoplasmic signaling domains were competent to sustain ADE of SARS-CoVpp infection, thus providing additional information on the role of downstream signaling by FcγRII. CONCLUSIONS: These results demonstrate that human macrophages can be infected by SARS-CoV as a result of IgG-mediated ADE and indicate that this infection route requires signaling pathways activated downstream of binding to FcγRII receptors.
has issue date	2014-05-06(xsd:dateTime)
bibo:doi	10.1186/1743-422x-11-82
bibo:pmid	24885320
has license	cc-by
sha1sum (hex)	4930fc9d9e3cb5bea0a97320187aca766f07493d
schema:url	https://doi.org/10.1186/1743-422x-11-82
resource representing a document's title	Antibody-dependent infection of human macrophages by severe acute respiratory syndrome coronavirus
has PubMed Central identifier	PMC4018502
has PubMed identifier	24885320
schema:publication	Virol J
resource representing a document's body	covid:4930fc9d9e3cb5bea0a97320187aca766f07493d#body_text
is schema:about of	named entity 'human coronaviruses' named entity 'trimers' named entity 'ADE' named entity 'reverse transcriptase' named entity 'series' named entity 'lentiviral' named entity 'immune complexes' named entity 'Macrophages' named entity 'RECOMBINANT' named entity 'PREVIOUSLY' named entity 'INFECTION' named entity 'DEPENDENT' named entity 'DID' named entity 'LENGTH' named entity 'DEPENDENT' named entity 'FAMILY' named entity 'INFECTION ROUTE' named entity 'CELL SURFACE' named entity 'INACTIVATED' named entity 'RESULTS' named entity 'IMMUNE CELLS' named entity 'ANTIBODY' named entity 'VACCINATION' named entity 'MOLECULAR' covid:arg/4930fc9d9e3cb5bea0a97320187aca766f07493d named entity 'RISKS' named entity 'PRESENCE OF' named entity 'ST486' named entity 'MECHANISMS' named entity 'SUPPORT' named entity 'OPTION' named entity 'SUSCEPTIBILITY TO INFECTION' named entity 'ADE' named entity 'HERE' named entity 'TRUNCATED' named entity 'SIGNALING' named entity 'SIGNALING PATHWAYS' named entity 'ENHANCE' named entity 'QUANTITATIVE REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION' named entity 'HUMAN' named entity 'COATED' named entity 'PROTEIN ' named entity 'INSIGHT' named entity 'AS A RESULT OF' named entity 'SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS' named entity 'ELICITED BY' named entity 'ROLE' named entity 'PERFORMED' named entity 'INFECTED' named entity 'BIND' named entity 'PUBLIC HEALTH' named entity 'PATHOGENS' named entity 'SOLUBLE' named entity 'USED' named entity 'TRIGGER' named entity 'HUMAN' named entity 'CHIMERIC' named entity 'REPORTED' named entity 'OCCURRENCE' named entity 'BUT' named entity 'FLUORESCENCE MICROSCOPY' named entity '28S' named entity 'MOUSE' named entity 'CONSIDERABLE' named entity 'IGG' named entity 'SARS' named entity 'COMPETENT' named entity 'MACROPHAGES' named entity 'PROVIDING' named entity 'CYTOPLASMIC'

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