File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

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
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/
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
ISSN
2023 Impact Factor: 3.1
2023 SCImago Journal Rankings: 0.261

 

DC FieldValueLanguage
dc.contributor.authorYip, MS-
dc.contributor.authorLeung, HL-
dc.contributor.authorLi, PH-
dc.contributor.authorCheung, CY-
dc.contributor.authorDutry, I-
dc.contributor.authorLi, D-
dc.contributor.authorDaëron, M-
dc.contributor.authorBruzzone, R-
dc.contributor.authorPeiris, JSM-
dc.contributor.authorJaume, M-
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.issn1024-2708-
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.publisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/-
dc.relation.ispartofHong Kong Medical Journal-
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
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.emailLeung, HL: leungnan@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, M: breizh@hku.hk-
dc.identifier.authorityLeung, HL=rp02637-
dc.identifier.authorityBruzzone, R=rp01442-
dc.identifier.authorityPeiris, JSM=rp00410-
dc.description.naturepublished_or_final_version-
dc.identifier.pmid27390007-
dc.identifier.scopuseid_2-s2.0-85040997097-
dc.identifier.hkuros267384-
dc.identifier.volume22-
dc.identifier.issue3, suppl. 4-
dc.identifier.spage25-
dc.identifier.epage31-
dc.publisher.placeHong Kong-
dc.identifier.issnl1024-2708-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats