Role for Nonstructural Protein 1 of Severe Acute Respiratory Syndrome Coronavirus in Chemokine Dysregulation

Law, Anna H.Y.; Lee, Davy C. W.; Cheung, Benny K. W.; Yim, Howard Chi Ho; Lau, Andy K. S.

doi:10.1128/jvi.02336-05

Cited by 64 publications

(63 citation statements)

References 25 publications

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“…SARS-CoV up-regulates pro-inflammatory cytokines like IFN-γ, IL-18, TGF-β1, TNF-α, IL-6, IP-10, MCP-1, MIG, and IL-8 (Huang et al, 2005;He et al, 2006), in which recruits immune responder cells into the lungs, triggers acute respiratory distress syndrome (ARDS), and even causes lung fibrosis in the late phase (Huang et al, 2005;He et al, 2006). Among SARS-CoV proteins, the nucleocapsid induces a Smad3dependent induction of TGF-β1 expression (Zhao et al, 2008); spike protein stimulates the IL-8 up-regulation in lung cells (Chang et al, 2004); NSP1 provokes the expression of CCL5, CXVL10, and CCL3 (Law et al, 2007); PLpro elavates the production of TGF-β1 and pro-fibrotic markers via ubiquitin proteasome, p38 MAPK, and ERK1/2-mediated signaling (Li et al, 2012). Recently, SARS-CoV PLpro notably initiates ROS/p38 MAPK/STAT3 pathway to activate Egr-1 dependent expression of TSP-1, TGF-β1 and vimentin in vitro and in vivo (Li et al, 2016b).…”

Section: Introductionmentioning

confidence: 99%

SARS coronavirus papain-like protease up-regulates the collagen expression through non-Samd TGF-β1 signaling

Wang

et al. 2017

Virus Research

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SARS coronavirus (CoV) papain-like protease (PLpro) reportedly induced the production of TGF-β1 through p38 MAPK/STAT3-meidated Egr-1-dependent activation (Sci. Rep. 6, 25754). This study investigated the correlation of PLpro-induced TGF-β1 with the expression of Type I collagen in human lung epithelial cells and mouse pulmonary tissues. Specific inhibitors for TGF-βRI, p38 MAPK, MEK, and STAT3 proved that SARS-CoV PLpro induced TGF-β1-dependent up-regulation of Type I collagen in vitro and in vivo. Subcellular localization analysis of SMAD3 and SMAD7 indicated that non-SMAD pathways in TGF-β1 signaling involved in the production of Type I collagen in transfected cells with pSARS-PLpro. Comprehensive analysis of ubiquitin-conjugated proteins using immunoprecipitation and nanoLC-MS/MS indicated that SARS-CoV PLpro caused the change in the ubiquitination profile of Rho GTPase family proteins, in which linked with the increase of Rho-like GTPase family proteins. Moreover, selective inhibitors TGF-βRI and STAT6 (AS1517499) ascertained that STAT6 activation was required for PLpro-induced TGF-β1-dependent up-regulation of Type I collagen in human lung epithelial cells. The results showed that SARS-CoV PLpro stimulated TGF-β1-dependent expression of Type I collagen via activating STAT6 pathway.

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Section: Introductionmentioning

confidence: 99%

SARS coronavirus papain-like protease up-regulates the collagen expression through non-Samd TGF-β1 signaling

Wang

et al. 2017

Virus Research

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“…nsp1 and nsp2 are rather variable in sequence, and possibly subgroup-specific replicase subunits Ziebuhr et al, 2001). SARS-CoV nsp1 (20 kDa) was implicated in suppression of cellular gene expression by promoting host cell mRNA degradation (Kamitani et al, 2006) and in chemokine dysregulation (Law et al, 2007). SARS-CoV nsp2 (70 kDa) is dispensable for replication in cell culture, but its deletion attenuates viral replication (Graham et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

The SARS-Coronavirus PLnc domain of nsp3 as a replication/transcription scaffolding protein

et al. 2008

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Many genetic and mechanistic features distinguish the coronavirus replication machinery from that encoded by most other RNA viruses. The coronavirus replication/transcription complex is an assembly of viral and, most probably, cellular proteins that mediate the synthesis of both the unusually large (approximately 30 kb) RNA genome and an extensive set of subgenomic mRNAs. The viral components of the complex are encoded by the giant replicase gene, which is expressed in the form of two polyproteins (pp1a and pp1ab) that are processed into 16 cleavage products (nonstructural proteins 1-16). Using the combination of yeast two-hybrid screening and GST pull-down assays, we have now analyzed all potential interactions between SARS-Coronavirus nonstructural proteins, which may contribute to the structure and/or function of the viral replication/transcription complex. We demonstrate the existence of a complex network of interactions involving all 16 nonstructural proteins. Our results both confirmed previously described associations and identified novel heterodimerizations. The interaction map thus provides a sum of the interactions that may occur at some point during coronavirus RNA synthesis and provides a framework for future research.

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“…Moreover, it was found that spike protein induces innate immune response through the activation of the nuclear factor-kappaB (NF-kB) pathway [75]. In addition, Law et al found that SARS-CoV NSP1 induces CCL5, CXVL10, and CCL3 mRNA expression via the activation of NF-kB [76]. The 3a DNA vaccine is reported to stimulate IFN-g production mainly by stimulating the production of CD8þ T cells, and IL-2 mainly by stimulating the production of CD4þ T cells [77].…”

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confidence: 99%

Human coronaviruses: Clinical features and phylogenetic analysis

Lin

2013

BioMedicine

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Keywords: human betacoronavirus 2c EMC2012 human coronavirus phylogenetic tree severe acute respiratory syndrome coronavirus (SARS-CoV) a b s t r a c t Strains of human coronavirus (HCoV), namely HCoV-OC43, HCoV-229E, HCoV-NL63, and HCoV-HKU1, primarily infect the upper respiratory and gastrointestinal tracts and are the most common cause of non-rhinovirus-induced common cold in humans. Although the manifestations of coronavirus infection (i.e., rhinorrhea, sneezing, cough, nasal obstruction, and bronchitis) are generally self-limiting in healthy adults, certain strains such as HCoV-NL63 and HCoV-HKU1 can cause severe lower respiratory tract infection and febrile seizure, especially in infants, people of advanced age, and immunocompromised hosts. In 2003, a novel HCoV strain was identified as the causative agent of the severe acute respiratory syndrome (SARS) epidemic that began in Asia in 2002. The strain has hence been referred to as SARS-CoV. In addition, as recently as September 2012, another novel HCoV, human betacoronavirus 2c EMC2012, was identified as being the cause of fever, renal failure, pneumonia, and severe respiratory distress in two patients in the Middle East.Phylogenetic analysis has revealed highly conserved sequences of ORF1ab, spike, nucleocapsid, and envelope protein genes, but not membrane protein genes, between human betacoronavirus 2c EMC2012 and SARS-CoV. This review focuses on the differences in the genomes of certain HCoV strains, the pathogenesis of said strains, and recent developments in the establishment of therapeutic agents that might aid in the treatment of patients with such infections.

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Role for Nonstructural Protein 1 of Severe Acute Respiratory Syndrome Coronavirus in Chemokine Dysregulation

Cited by 64 publications

References 25 publications

SARS coronavirus papain-like protease up-regulates the collagen expression through non-Samd TGF-β1 signaling

SARS coronavirus papain-like protease up-regulates the collagen expression through non-Samd TGF-β1 signaling

The SARS-Coronavirus PLnc domain of nsp3 as a replication/transcription scaffolding protein

Human coronaviruses: Clinical features and phylogenetic analysis

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