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Article: Active replication of middle east respiratory syndrome coronavirus and aberrant induction of inflammatory cytokines and chemokines in human macrophages: Implications for pathogenesis

TitleActive replication of middle east respiratory syndrome coronavirus and aberrant induction of inflammatory cytokines and chemokines in human macrophages: Implications for pathogenesis
Authors
Keywordspathogenesis
cytokine and chemokine response
SARS-CoV
viral replication
MERS-CoV
Issue Date2014
PublisherOxford University Press. The Journal's web site is located at http://www.oxfordjournals.org/our_journals/jid/
Citation
Journal of Infectious Diseases, 2014, v. 209, n. 9, p. 1331-1342 How to Cite?
AbstractMiddle East respiratory syndrome coronavirus (MERS-CoV) infection caused severe pneumonia and multiorgan dysfunction and had a higher crude fatality rate (around 50% vs. 10%) than SARS coronavirus (SARS-CoV) infection. To understand the pathogenesis, we studied viral replication, cytokine/chemokine response, and antigen presentation in MERS-CoV-infected human monocyte-derived macrophages (MDMs) versus SARS-CoV-infected MDMs. Only MERS-CoV can replicate in MDMs. Both viruses were unable to significantly stimulate the expression of antiviral cytokines (interferon alpha [IFN-alpha] and IFN-beta) but induced comparable levels of tumor necrosis factor alpha and interleukin 6. Notably, MERS-CoV induced significantly higher expression levels of interleukin 12, IFN-gamma, and chemokines (IP-10/CXCL-10, MCP-1/CCL-2, MIP-1alpha/CCL-3, RANTES/CCL-5, and interleukin 8) than SARS-CoV. The expression of major histocompatibility complex class I and costimulatory molecules were significantly higher in MERS-CoV-infected MDMs than in SARS-CoV-infected cells. MERS-CoV replication was validated by immunostaining of infected MDMs and ex vivo lung tissue. We conclusively showed that MERS-CoV can establish a productive infection in human macrophages. The aberrant induction of inflammatory cytokines/chemokines could be important in the disease pathogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/200730
ISSN
2015 Impact Factor: 6.344
2015 SCImago Journal Rankings: 4.000

 

DC FieldValueLanguage
dc.contributor.authorZhou, Jen_US
dc.contributor.authorChu, Hen_US
dc.contributor.authorLi, Cen_US
dc.contributor.authorWong, BHYen_US
dc.contributor.authorCheng, ZSen_US
dc.contributor.authorPoon, VKMen_US
dc.contributor.authorSun, Ten_US
dc.contributor.authorLau, CCYen_US
dc.contributor.authorWong, KKYen_US
dc.contributor.authorChan, JYWen_US
dc.contributor.authorChan, JFWen_US
dc.contributor.authorTo, KKWen_US
dc.contributor.authorChan, KHen_US
dc.contributor.authorZheng, BJen_US
dc.contributor.authorYuen, KYen_US
dc.date.accessioned2014-08-21T06:58:03Z-
dc.date.available2014-08-21T06:58:03Z-
dc.date.issued2014en_US
dc.identifier.citationJournal of Infectious Diseases, 2014, v. 209, n. 9, p. 1331-1342en_US
dc.identifier.issn0022-1899-
dc.identifier.urihttp://hdl.handle.net/10722/200730-
dc.description.abstractMiddle East respiratory syndrome coronavirus (MERS-CoV) infection caused severe pneumonia and multiorgan dysfunction and had a higher crude fatality rate (around 50% vs. 10%) than SARS coronavirus (SARS-CoV) infection. To understand the pathogenesis, we studied viral replication, cytokine/chemokine response, and antigen presentation in MERS-CoV-infected human monocyte-derived macrophages (MDMs) versus SARS-CoV-infected MDMs. Only MERS-CoV can replicate in MDMs. Both viruses were unable to significantly stimulate the expression of antiviral cytokines (interferon alpha [IFN-alpha] and IFN-beta) but induced comparable levels of tumor necrosis factor alpha and interleukin 6. Notably, MERS-CoV induced significantly higher expression levels of interleukin 12, IFN-gamma, and chemokines (IP-10/CXCL-10, MCP-1/CCL-2, MIP-1alpha/CCL-3, RANTES/CCL-5, and interleukin 8) than SARS-CoV. The expression of major histocompatibility complex class I and costimulatory molecules were significantly higher in MERS-CoV-infected MDMs than in SARS-CoV-infected cells. MERS-CoV replication was validated by immunostaining of infected MDMs and ex vivo lung tissue. We conclusively showed that MERS-CoV can establish a productive infection in human macrophages. The aberrant induction of inflammatory cytokines/chemokines could be important in the disease pathogenesis.-
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://www.oxfordjournals.org/our_journals/jid/-
dc.relation.ispartofJournal of Infectious Diseasesen_US
dc.subjectpathogenesis-
dc.subjectcytokine and chemokine response-
dc.subjectSARS-CoV-
dc.subjectviral replication-
dc.subjectMERS-CoV-
dc.subject.meshCoronavirus - immunology - pathogenicity - physiology-
dc.subject.meshCoronavirus Infections - immunology - virology-
dc.subject.meshCytokines - biosynthesis - immunology-
dc.subject.meshPneumonia, Viral - immunology - virology-
dc.subject.meshVirus Replication - physiology-
dc.titleActive replication of middle east respiratory syndrome coronavirus and aberrant induction of inflammatory cytokines and chemokines in human macrophages: Implications for pathogenesisen_US
dc.typeArticleen_US
dc.identifier.emailZhou, J: jiezhou@hku.hken_US
dc.identifier.emailChu, H: hinchu@hku.hken_US
dc.identifier.emailLi, C: licun@hku.hk-
dc.identifier.emailWong, BHY: boscowg@hku.hk-
dc.identifier.emailPoon, VKM: vinpoon@hku.hk-
dc.identifier.emailLau, CCY: candylau@graduate.hku.hk-
dc.identifier.emailWong, KKY: kkywong@hku.hk-
dc.identifier.emailChan, JYW: jywchan1@hku.hk-
dc.identifier.emailChan, JFW: jfwchan@hku.hk-
dc.identifier.emailTo, KKW: kelvinto@HKUCC.hku.hk-
dc.identifier.emailChan, KH: chankh2@hkucc.hku.hk-
dc.identifier.emailZheng, BJ: gpzheng@hkucc.hku.hk-
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hk-
dc.identifier.authorityZhou, J=rp01412en_US
dc.identifier.authorityWong, KKY=rp01392en_US
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/infdis/jit504-
dc.identifier.pmid24065148-
dc.identifier.scopuseid_2-s2.0-84898850857-
dc.identifier.hkuros234066en_US
dc.identifier.hkuros230921-
dc.identifier.hkuros242029-
dc.identifier.volume209en_US
dc.identifier.issue9-
dc.identifier.spage1331-
dc.identifier.epage1342-
dc.publisher.placeUnited States-

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