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Article: Antibody-dependent enhancement of SARS coronavirus infection and its role in the pathogenesis of SARS

TitleAntibody-dependent enhancement of SARS coronavirus infection and its role in the pathogenesis of SARS
Authors
Issue Date2016
Citation
Hong Kong Medical Journal, 2016, v. 22 n. 3 Suppl 4, p. 25-31 How to Cite?
Abstract1. Anti-SARS-CoV spike antibodies promote infection of primary human immune cells by SARS-CoV. 2. The antibody-dependent enhancement (ADE) infection pathway grants SARS-CoV an opportunity to infect primary human macrophages, but it does not sustain productive viral replication in the infected cells. 3. ADE of SARS-CoV infection does not alter pro-inflammatory gene expression profile of primary human macrophages. 4. Infectivity of SARS-CoV does not rely solely on the potency of target cells to bind — via Fcγ receptor II (CD32) — infectious immune complexes, but depends on the properties of the intracellular domain of the FcγRII. 5. Occurrence of ADE of SARS-CoV infection into human primary macrophages, without alteration to their pro-inflammatory properties, advocates cautious development of SARS-CoV vaccine in humans, and provides new ways of investigation to understand the pathogenesis of SARS.
Persistent Identifierhttp://hdl.handle.net/10722/234335

 

DC FieldValueLanguage
dc.contributor.authorYip, MS-
dc.contributor.authorLEUNG, HL-
dc.contributor.authorLi, PH-
dc.contributor.authorCheung, CY-
dc.contributor.authorDutry, ICA-
dc.contributor.authorLi, D-
dc.contributor.authorDaëron, M-
dc.contributor.authorBruzzone, R-
dc.contributor.authorPeiris, JSM-
dc.contributor.authorJaume, MDA-
dc.date.accessioned2016-10-14T07:00:39Z-
dc.date.available2016-10-14T07:00:39Z-
dc.date.issued2016-
dc.identifier.citationHong Kong Medical Journal, 2016, v. 22 n. 3 Suppl 4, p. 25-31-
dc.identifier.urihttp://hdl.handle.net/10722/234335-
dc.description.abstract1. Anti-SARS-CoV spike antibodies promote infection of primary human immune cells by SARS-CoV. 2. The antibody-dependent enhancement (ADE) infection pathway grants SARS-CoV an opportunity to infect primary human macrophages, but it does not sustain productive viral replication in the infected cells. 3. ADE of SARS-CoV infection does not alter pro-inflammatory gene expression profile of primary human macrophages. 4. Infectivity of SARS-CoV does not rely solely on the potency of target cells to bind — via Fcγ receptor II (CD32) — infectious immune complexes, but depends on the properties of the intracellular domain of the FcγRII. 5. Occurrence of ADE of SARS-CoV infection into human primary macrophages, without alteration to their pro-inflammatory properties, advocates cautious development of SARS-CoV vaccine in humans, and provides new ways of investigation to understand the pathogenesis of SARS.-
dc.languageeng-
dc.relation.ispartofHong Kong Medical Journal-
dc.titleAntibody-dependent enhancement of SARS coronavirus infection and its role in the pathogenesis of SARS-
dc.typeArticle-
dc.identifier.emailYip, MS: amenyiu@hku.hk-
dc.identifier.emailLi, PH: phli@hkucc.hku.hk-
dc.identifier.emailBruzzone, R: bruzzone@hkucc.hku.hk-
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hk-
dc.identifier.emailJaume, MDA: breizh@hku.hk-
dc.identifier.authorityBruzzone, R=rp01442-
dc.identifier.authorityPeiris, JSM=rp00410-
dc.identifier.hkuros267384-
dc.identifier.volume22-
dc.identifier.issue3 Suppl 4-
dc.identifier.spage25-
dc.identifier.epage31-

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