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Article: Attenuated Interferon and Proinflammatory Response in SARS-CoV-2-Infected Human Dendritic Cells Is Associated With Viral Antagonism of STAT1 Phosphorylation

TitleAttenuated Interferon and Proinflammatory Response in SARS-CoV-2-Infected Human Dendritic Cells Is Associated With Viral Antagonism of STAT1 Phosphorylation
Authors
KeywordsCOVID-19
SARS-CoV-2
Coronavirus
Dendritic cells
Macrophages
moDCs
MDMs
Issue Date2020
PublisherOxford University Press. The Journal's web site is located at http://www.oxfordjournals.org/our_journals/jid/
Citation
Journal of Infectious Diseases, 2020, v. 222 n. 5, p. 734-745 How to Cite?
AbstractClinical manifestations of coronavirus disease 2019 (COVID-19) vary from asymptomatic virus shedding, nonspecific pharyngitis, to pneumonia with silent hypoxia and respiratory failure. Dendritic cells and macrophages are sentinel cells for innate and adaptive immunity that affect the pathogenesis of severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). The interplay between SARS-CoV-2 and these cell types remains unknown. We investigated infection and host responses of monocyte-derived dendritic cells (moDCs) and macrophages (MDMs) infected by SARS-CoV-2. MoDCs and MDMs were permissive to SARS-CoV-2 infection and protein expression but did not support productive virus replication. Importantly, SARS-CoV-2 launched an attenuated interferon response in both cell types and triggered significant proinflammatory cytokine/chemokine expression in MDMs but not moDCs. Investigations suggested that this attenuated immune response to SARS-CoV-2 in moDCs was associated with viral antagonism of STAT1 phosphorylation. These findings may explain the mild and insidious course of COVID-19 until late deterioration.
Persistent Identifierhttp://hdl.handle.net/10722/286253
ISSN
2019 Impact Factor: 5.022
2015 SCImago Journal Rankings: 4.000
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorYang, D-
dc.contributor.authorChu, H-
dc.contributor.authorHou, Y-
dc.contributor.authorChai, Y-
dc.contributor.authorShuai, H-
dc.contributor.authorLee, ACY-
dc.contributor.authorZhang, X-
dc.contributor.authorWang, Y-
dc.contributor.authorHu, B-
dc.contributor.authorHuang, X-
dc.contributor.authorYuen, TTT-
dc.contributor.authorCai, JP-
dc.contributor.authorZhou, J-
dc.contributor.authorYuan, S-
dc.contributor.authorZhang, AJ-
dc.contributor.authorChan, JFW-
dc.contributor.authorYuen, KY-
dc.date.accessioned2020-08-31T07:01:20Z-
dc.date.available2020-08-31T07:01:20Z-
dc.date.issued2020-
dc.identifier.citationJournal of Infectious Diseases, 2020, v. 222 n. 5, p. 734-745-
dc.identifier.issn0022-1899-
dc.identifier.urihttp://hdl.handle.net/10722/286253-
dc.description.abstractClinical manifestations of coronavirus disease 2019 (COVID-19) vary from asymptomatic virus shedding, nonspecific pharyngitis, to pneumonia with silent hypoxia and respiratory failure. Dendritic cells and macrophages are sentinel cells for innate and adaptive immunity that affect the pathogenesis of severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). The interplay between SARS-CoV-2 and these cell types remains unknown. We investigated infection and host responses of monocyte-derived dendritic cells (moDCs) and macrophages (MDMs) infected by SARS-CoV-2. MoDCs and MDMs were permissive to SARS-CoV-2 infection and protein expression but did not support productive virus replication. Importantly, SARS-CoV-2 launched an attenuated interferon response in both cell types and triggered significant proinflammatory cytokine/chemokine expression in MDMs but not moDCs. Investigations suggested that this attenuated immune response to SARS-CoV-2 in moDCs was associated with viral antagonism of STAT1 phosphorylation. These findings may explain the mild and insidious course of COVID-19 until late deterioration.-
dc.languageeng-
dc.publisherOxford University Press. The Journal's web site is located at http://www.oxfordjournals.org/our_journals/jid/-
dc.relation.ispartofJournal of Infectious Diseases-
dc.subjectCOVID-19-
dc.subjectSARS-CoV-2-
dc.subjectCoronavirus-
dc.subjectDendritic cells-
dc.subjectMacrophages-
dc.subjectmoDCs-
dc.subjectMDMs-
dc.titleAttenuated Interferon and Proinflammatory Response in SARS-CoV-2-Infected Human Dendritic Cells Is Associated With Viral Antagonism of STAT1 Phosphorylation-
dc.typeArticle-
dc.identifier.emailChu, H: hinchu@hku.hk-
dc.identifier.emailChai, Y: chaiyue@hku.hk-
dc.identifier.emailShuai, H: shuaihp@connect.hku.hk-
dc.identifier.emailLee, ACY: cyalee@hku.hk-
dc.identifier.emailHu, B: bingjie@hku.hk-
dc.identifier.emailCai, JP: caijuice@hku.hk-
dc.identifier.emailZhou, J: jiezhou@hku.hk-
dc.identifier.emailYuan, S: yuansf@hku.hk-
dc.identifier.emailZhang, AJ: zhangajx@hkucc.hku.hk-
dc.identifier.emailChan, JFW: jfwchan@hku.hk-
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hk-
dc.identifier.authorityChu, H=rp02125-
dc.identifier.authorityZhou, J=rp01412-
dc.identifier.authorityYuan, S=rp02640-
dc.identifier.authorityZhang, AJ=rp00413-
dc.identifier.authorityChan, JFW=rp01736-
dc.identifier.authorityYuen, KY=rp00366-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/infdis/jiaa356-
dc.identifier.pmid32563187-
dc.identifier.pmcidPMC7337793-
dc.identifier.scopuseid_2-s2.0-85089129573-
dc.identifier.hkuros313103-
dc.identifier.volume222-
dc.identifier.issue5-
dc.identifier.spage734-
dc.identifier.epage745-
dc.publisher.placeUnited States-

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