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Article: Productive replication of Middle East respiratory syndrome coronavirus in monocyte-derived dendritic cells modulates innate immune response.

TitleProductive replication of Middle East respiratory syndrome coronavirus in monocyte-derived dendritic cells modulates innate immune response.
Authors
Issue Date2014
Citation
Virology, 2014, v. 454-455, p. 197-205. How to Cite?
AbstractThe Middle East respiratory syndrome coronavirus (MERS-CoV) closely resembled severe acute respiratory syndrome coronavirus (SARS-CoV) in disease manifestation as rapidly progressive acute pneumonia with multi-organ dysfunction. Using monocyte-derived-dendritic cells (Mo-DCs), we discovered fundamental discrepancies in the outcome of MERS-CoV- and SARS-CoV-infection. First, MERS-CoV productively infected Mo-DCs while SARS-CoV-infection was abortive. Second, MERS-CoV induced significantly higher levels of IFN-γ, IP-10, IL-12, and RANTES expression than SARS-CoV. Third, MERS-CoV-infection induced higher surface expression of MHC class II (HLA-DR) and the co-stimulatory molecule CD86 than SARS-CoV-infection. Overall, our data suggests that the dendritic cell can serve as an important target of viral replication and a vehicle for dissemination. MERS-CoV-infection in DCs results in the production of a rich combination of cytokines and chemokines, and modulates innate immune response differently from that of SARS-CoV-infection. Our findings may help to explain the apparent discrepancy in the pathogenicity between MERS-CoV and SARS-CoV.
Persistent Identifierhttp://hdl.handle.net/10722/199184
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChu, Hen_US
dc.contributor.authorZhou, Jen_US
dc.contributor.authorWong, HYBen_US
dc.contributor.authorLi, Cen_US
dc.contributor.authorCheng, Zen_US
dc.contributor.authorLin, Xen_US
dc.contributor.authorPoon, KMen_US
dc.contributor.authorSun, Ten_US
dc.contributor.authorLau, CYen_US
dc.contributor.authorChan, JFWen_US
dc.contributor.authorTo, KKWen_US
dc.contributor.authorChan, KHen_US
dc.contributor.authorLu, Len_US
dc.contributor.authorZheng, Ben_US
dc.contributor.authorYuen, KYen_US
dc.date.accessioned2014-07-22T01:06:18Z-
dc.date.available2014-07-22T01:06:18Z-
dc.date.issued2014en_US
dc.identifier.citationVirology, 2014, v. 454-455, p. 197-205.en_US
dc.identifier.urihttp://hdl.handle.net/10722/199184-
dc.description.abstractThe Middle East respiratory syndrome coronavirus (MERS-CoV) closely resembled severe acute respiratory syndrome coronavirus (SARS-CoV) in disease manifestation as rapidly progressive acute pneumonia with multi-organ dysfunction. Using monocyte-derived-dendritic cells (Mo-DCs), we discovered fundamental discrepancies in the outcome of MERS-CoV- and SARS-CoV-infection. First, MERS-CoV productively infected Mo-DCs while SARS-CoV-infection was abortive. Second, MERS-CoV induced significantly higher levels of IFN-γ, IP-10, IL-12, and RANTES expression than SARS-CoV. Third, MERS-CoV-infection induced higher surface expression of MHC class II (HLA-DR) and the co-stimulatory molecule CD86 than SARS-CoV-infection. Overall, our data suggests that the dendritic cell can serve as an important target of viral replication and a vehicle for dissemination. MERS-CoV-infection in DCs results in the production of a rich combination of cytokines and chemokines, and modulates innate immune response differently from that of SARS-CoV-infection. Our findings may help to explain the apparent discrepancy in the pathogenicity between MERS-CoV and SARS-CoV.en_US
dc.languageengen_US
dc.relation.ispartofVirologyen_US
dc.titleProductive replication of Middle East respiratory syndrome coronavirus in monocyte-derived dendritic cells modulates innate immune response.en_US
dc.typeArticleen_US
dc.identifier.emailChu, H: hinchu@hku.hken_US
dc.identifier.emailZhou, J: jiezhou@hku.hken_US
dc.identifier.emailWong, HYB: boscowg@hku.hken_US
dc.identifier.emailLi, C: licun@hku.hken_US
dc.identifier.emailCheng, Z: chzhshan@hku.hken_US
dc.identifier.emailLin, X: linxiang@hku.hken_US
dc.identifier.emailPoon, KM: vinpoon@hku.hken_US
dc.identifier.emailSun, T: sunth@hku.hken_US
dc.identifier.emailLau, CY: candylau@graduate.hku.hken_US
dc.identifier.emailChan, JFW: jfwchan@hku.hken_US
dc.identifier.emailTo, KKW: kelvinto@hkucc.hku.hken_US
dc.identifier.emailChan, KH: chankh2@hkucc.hku.hken_US
dc.identifier.emailLu, L: liweilu@hkucc.hku.hken_US
dc.identifier.emailZheng, B: bzheng@hkucc.hku.hken_US
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hken_US
dc.identifier.authorityZhou, J=rp01412en_US
dc.identifier.authorityChan, JFW=rp01736en_US
dc.identifier.authorityTo, KKW=rp01384en_US
dc.identifier.authorityLu, L=rp00477en_US
dc.identifier.authorityZheng, B=rp00353en_US
dc.identifier.authorityYuen, KY=rp00366en_US
dc.identifier.doi10.1016/j.virol.2014.02.018en_US
dc.identifier.pmid24725946-
dc.identifier.scopuseid_2-s2.0-84895742275-
dc.identifier.hkuros230917en_US
dc.identifier.volume454-455en_US
dc.identifier.spage197en_US
dc.identifier.epage205en_US
dc.identifier.isiWOS:000334655000021-

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