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Article: Fc receptors in antibody-dependent enhancement of viral infections

TitleFc receptors in antibody-dependent enhancement of viral infections
Authors
Issue Date2015
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/IMR
Citation
Immunological Reviews, 2015, v. 268 n. 1, p. 340-64 How to Cite?
AbstractSensitization of the humoral immune response to invading viruses and production of antiviral antibodies forms part of the host antiviral repertoire. Paradoxically, for a number of viral pathogens, under certain conditions, antibodies provide an attractive means of enhanced virus entry and replication in a number of cell types. Known as antibody-dependent enhancement (ADE) of infection, the phenomenon occurs when virus-antibody immunocomplexes interact with cells bearing complement or Fc receptors, promoting internalization of the virus and increasing infection. Frequently associated with exacerbation of viral disease, ADE of infection presents a major obstacle to the prevention of viral disease by vaccination and is thought to be partly responsible for the adverse effects of novel antiviral therapeutics such as intravenous immunoglobulins. There is a growing body of work examining the intracellular signaling pathways and epitopes responsible for mediating ADE, with a view to aiding rational design of antiviral strategies. With in vitro studies also confirming ADE as a feature of infection for a growing number of viruses, challenges remain in understanding the multilayered molecular mechanisms of ADE and its effect on viral pathogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/223371
ISSN
2015 Impact Factor: 9.542
2015 SCImago Journal Rankings: 7.059

 

DC FieldValueLanguage
dc.contributor.authorTaylor, A-
dc.contributor.authorFoo, SS-
dc.contributor.authorBruzzone, R-
dc.contributor.authorDinh, LV-
dc.contributor.authorKing, NJC-
dc.contributor.authorMahalingam, S-
dc.date.accessioned2016-02-23T01:57:33Z-
dc.date.available2016-02-23T01:57:33Z-
dc.date.issued2015-
dc.identifier.citationImmunological Reviews, 2015, v. 268 n. 1, p. 340-64-
dc.identifier.issn0105-2896-
dc.identifier.urihttp://hdl.handle.net/10722/223371-
dc.description.abstractSensitization of the humoral immune response to invading viruses and production of antiviral antibodies forms part of the host antiviral repertoire. Paradoxically, for a number of viral pathogens, under certain conditions, antibodies provide an attractive means of enhanced virus entry and replication in a number of cell types. Known as antibody-dependent enhancement (ADE) of infection, the phenomenon occurs when virus-antibody immunocomplexes interact with cells bearing complement or Fc receptors, promoting internalization of the virus and increasing infection. Frequently associated with exacerbation of viral disease, ADE of infection presents a major obstacle to the prevention of viral disease by vaccination and is thought to be partly responsible for the adverse effects of novel antiviral therapeutics such as intravenous immunoglobulins. There is a growing body of work examining the intracellular signaling pathways and epitopes responsible for mediating ADE, with a view to aiding rational design of antiviral strategies. With in vitro studies also confirming ADE as a feature of infection for a growing number of viruses, challenges remain in understanding the multilayered molecular mechanisms of ADE and its effect on viral pathogenesis.-
dc.languageeng-
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/IMR-
dc.relation.ispartofImmunological Reviews-
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.titleFc receptors in antibody-dependent enhancement of viral infections-
dc.typeArticle-
dc.identifier.emailBruzzone, R: bruzzone@hkucc.hku.hk-
dc.identifier.authorityBruzzone, R=rp01442-
dc.identifier.doi10.1111/imr.12367-
dc.identifier.pmid26497532-
dc.identifier.hkuros256978-
dc.identifier.volume268-
dc.identifier.issue1-
dc.identifier.spage340-
dc.identifier.epage64-
dc.publisher.placeDenmark-

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