SrasV1, PubMed, Checkpoint, bibRecord, 001050

Active replication of Middle East respiratory syndrome coronavirus and aberrant induction of inflammatory cytokines and chemokines in human macrophages: implications for pathogenesis.

Identifieur interne : 001050 ( PubMed/Checkpoint ); précédent : 001049; suivant : 001051

Active replication of Middle East respiratory syndrome coronavirus and aberrant induction of inflammatory cytokines and chemokines in human macrophages: implications for pathogenesis.

Auteurs : Jie Zhou ; Hin Chu ; Cun Li ; Bosco Ho-Yin Wong ; Zhong-Shan Cheng ; Vincent Kwok-Man Poon ; Tianhao Sun ; Candy Choi-Yi Lau ; Kenneth Kak-Yuen Wong ; Jimmy Yu-Wai Chan ; Jasper Fuk-Woo Chan ; Kelvin Kai-Wang To ; Kwok-Hung Chan ; Bo-Jian Zheng ; Kwok-Yung Yuen

Source :

The Journal of infectious diseases [ 1537-6613 ] ; 2014.

RBID : pubmed:24065148

Descripteurs français

KwdFr :
- Animaux, Cellules Vero, Cellules cultivées, Coronavirus (immunologie), Coronavirus (pathogénicité), Coronavirus (physiologie), Cytokines (biosynthèse), Cytokines (immunologie), Humains, Infections à coronavirus (immunologie), Infections à coronavirus (virologie), Macrophages (immunologie), Macrophages (virologie), Pneumopathie virale (immunologie), Pneumopathie virale (virologie), Poumon (virologie), Présentation d'antigène, Réplication virale (physiologie), Survie cellulaire (immunologie).
MESH :
- biosynthèse : Cytokines.
- immunologie : Coronavirus, Cytokines, Infections à coronavirus, Macrophages, Pneumopathie virale, Survie cellulaire.
- pathogénicité : Coronavirus.
- physiologie : Coronavirus, Réplication virale.
- virologie : Infections à coronavirus, Macrophages, Pneumopathie virale, Poumon.
- Animaux, Cellules Vero, Cellules cultivées, Humains, Présentation d'antigène.

English descriptors

KwdEn :
- Animals, Antigen Presentation, Cell Survival (immunology), Cells, Cultured, Chlorocebus aethiops, Coronavirus (immunology), Coronavirus (pathogenicity), Coronavirus (physiology), Coronavirus Infections (immunology), Coronavirus Infections (virology), Cytokines (biosynthesis), Cytokines (immunology), Humans, Lung (virology), Macrophages (immunology), Macrophages (virology), Pneumonia, Viral (immunology), Pneumonia, Viral (virology), Vero Cells, Virus Replication (physiology).
MESH :
- chemical , biosynthesis : Cytokines.
- immunology : Cell Survival, Coronavirus, Coronavirus Infections, Cytokines, Macrophages, Pneumonia, Viral.
- pathogenicity : Coronavirus.
- physiology : Coronavirus, Virus Replication.
- virology : Coronavirus Infections, Lung, Macrophages, Pneumonia, Viral.
- Animals, Antigen Presentation, Cells, Cultured, Chlorocebus aethiops, Humans, Vero Cells.

Abstract

Middle 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 α [IFN-α] and IFN-β) but induced comparable levels of tumor necrosis factor α and interleukin 6. Notably, MERS-CoV induced significantly higher expression levels of interleukin 12, IFN-γ, and chemokines (IP-10/CXCL-10, MCP-1/CCL-2, MIP-1α/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.

DOI: 10.1093/infdis/jit504
PubMed: 24065148

Affiliations:

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Le document en format XML

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<front><div type="abstract" xml:lang="en">Middle 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 α [IFN-α] and IFN-β) but induced comparable levels of tumor necrosis factor α and interleukin 6. Notably, MERS-CoV induced significantly higher expression levels of interleukin 12, IFN-γ, and chemokines (IP-10/CXCL-10, MCP-1/CCL-2, MIP-1α/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.</div>
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<Abstract><AbstractText>Middle 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 α [IFN-α] and IFN-β) but induced comparable levels of tumor necrosis factor α and interleukin 6. Notably, MERS-CoV induced significantly higher expression levels of interleukin 12, IFN-γ, and chemokines (IP-10/CXCL-10, MCP-1/CCL-2, MIP-1α/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.</AbstractText>
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<tree><noCountry><name sortKey="Chan, Jasper Fuk Woo" sort="Chan, Jasper Fuk Woo" uniqKey="Chan J" first="Jasper Fuk-Woo" last="Chan">Jasper Fuk-Woo Chan</name>
<name sortKey="Chan, Jimmy Yu Wai" sort="Chan, Jimmy Yu Wai" uniqKey="Chan J" first="Jimmy Yu-Wai" last="Chan">Jimmy Yu-Wai Chan</name>
<name sortKey="Chan, Kwok Hung" sort="Chan, Kwok Hung" uniqKey="Chan K" first="Kwok-Hung" last="Chan">Kwok-Hung Chan</name>
<name sortKey="Cheng, Zhong Shan" sort="Cheng, Zhong Shan" uniqKey="Cheng Z" first="Zhong-Shan" last="Cheng">Zhong-Shan Cheng</name>
<name sortKey="Chu, Hin" sort="Chu, Hin" uniqKey="Chu H" first="Hin" last="Chu">Hin Chu</name>
<name sortKey="Lau, Candy Choi Yi" sort="Lau, Candy Choi Yi" uniqKey="Lau C" first="Candy Choi-Yi" last="Lau">Candy Choi-Yi Lau</name>
<name sortKey="Li, Cun" sort="Li, Cun" uniqKey="Li C" first="Cun" last="Li">Cun Li</name>
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Active replication of Middle East respiratory syndrome coronavirus and aberrant induction of inflammatory cytokines and chemokines in human macrophages: implications for pathogenesis.

Active replication of Middle East respiratory syndrome coronavirus and aberrant induction of inflammatory cytokines and chemokines in human macrophages: implications for pathogenesis.

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