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Infectious Disease: Enterovirus

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Total 22 results found since Jan 2013.

Inhibition of coxsackievirus infection in cardiomyocytes by small dsRNA targeting its cognate coxsackievirus adenovirus receptor.
Abstract Background & objectives: Coxsackievirus B (CVB), a member of human Enterovirus group, is the most common cause of viral myocarditis. Coxsackievirus adenovirus receptor (CAR) is identified as a key determinant for the entry of CVB in the target cells. Thus, blockade of receptor by RNA interference (RNAi) may inhibit the entry and pathogenesis of CVB in cardiac cells. The present study was aimed to determine the effect of CAR small dsRNA (siRNA) on coxsackieviral load and CAR expression in coxsackievirus-infected cardiomyocytes. Methods: Transfection efficiency in rat cardiomyocytes (H9c2) was dete...
Source: Indian J Med Res - October 1, 2017 Category: Research Authors: Sharma M, Mishra B, Saikia UN, Bahl A, Ratho RK Tags: Indian J Med Res Source Type: research

GSE99252 Human virus-derived small RNAs can confer antiviral immunity in mammals
Contributors : Yang Qiu ; Yanpeng Xu ; Yao Zhang ; Hui Zhou ; Yong-Qiang Deng ; Xiao-Feng Li ; Meng Miao ; Qiang Zhang ; Bo Zhong ; Yuanyang Hu ; Fu-Chun Zhang ; Ligang Wu ; Cheng-Feng Qin ; Xi ZhouSeries Type : Non-coding RNA profiling by high throughput sequencingOrganism : Homo sapiensRNA interference (RNAi) functions as a potent antiviral immunity in plants and invertebrates, however whether RNAi plays antiviral roles in mammals remains unclear. Here, using human enterovirus 71 (HEV71) as a model, we showed HEV71 3A protein as an authentic viral suppressor of RNAi during viral infection. When the 3A-mediated RNAi suppr...
Source: GEO: Gene Expression Omnibus - August 1, 2017 Category: Genetics & Stem Cells Tags: Non-coding RNA profiling by high throughput sequencing Homo sapiens Source Type: research

Enterovirus 71 suppresses interferon responses by blocking Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling through inducing karyopherin-{alpha}1 degradation Immunology
In this study, we found that in cells pretreated with IFN-β, EV71 infection could still lead to a cytopathic effect, and the viral replication was not affected. The mechanism by which EV71 antagonizes interferon signaling, however, has been controversial. Our study indicated that EV71 infection did not inhibit phosphorylation of STAT1/2 induced by IFN-β stimulation, but p-STAT1/2 transport into the nucleus was significantly blocked. We showed that EV71 infection reduced the formation of STAT/karyopherin-α1 (KPNA1) complex upon interferon stimulation and that the virus down-regulated the expression of KPNA1, a nuclear lo...
Source: Journal of Biological Chemistry - June 16, 2017 Category: Chemistry Authors: Chunyang Wang, Menghuai Sun, Xinhui Yuan, Lianfu Ji, Yu Jin, Carol J. Cardona, Zheng Xing Tags: Microbiology Source Type: research

Inhibition of iNOS protects cardiomyocytes against coxsackievirus B3-induced cell injury by suppressing autophagy.
CONCLUSION: The inhibition of iNOS protects cardiomyocytes against CVB3-induced cell injury by regulating autophagy and the JNK pathway, which may provide a novel therapeutic strategy for treating CVB3-induced myocarditis. PMID: 28499238 [PubMed - as supplied by publisher]
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - May 9, 2017 Category: Drugs & Pharmacology Authors: Qi L, Xin Q, Wenjun J Tags: Biomed Pharmacother Source Type: research

Antiviral screen identifies EV71 inhibitors and reveals camptothecin-target, DNA topoisomerase 1 as a novel EV71 host factor.
Abstract Enterovirus 71 (EV71) is one of the causative agents of hand, foot and mouth disease (HFMD) associated with severe neurological disease. EV71's pathogenesis remains poorly understood and the lack of approved antiviral has led to its emergence as a clinically important neurotropic virus. The goals of this study were to: (i) identify novel anti-EV71 compounds that may serve as lead molecules for therapeutics; and (ii) investigate their targets in downstream studies. We screened a 502-compound library of highly purified natural products for anti-EV71 activities in a cell-based immunofluorescence assay that w...
Source: Antiviral Research - April 17, 2017 Category: Virology Authors: Wu KX, Chu JJ Tags: Antiviral Res Source Type: research

Antiviral screen identifies EV71 inhibitors and reveals camptothecin-target, DNA topoisomerase 1 as a novel EV71 host factor
Publication date: Available online 17 April 2017 Source:Antiviral Research Author(s): Kan Xing Wu, Justin Jang-Hann Chu Enterovirus 71 (EV71) is one of the causative agents of hand, foot and mouth disease (HFMD) associated with severe neurological disease. EV71's pathogenesis remains poorly understood and the lack of approved antiviral has led to its emergence as a clinically important neurotropic virus. The goals of this study were to: (i) identify novel anti-EV71 compounds that may serve as lead molecules for therapeutics; and (ii) investigate their targets in downstream studies. We screened a 502-compound library of hi...
Source: Antiviral Therapy - April 17, 2017 Category: Virology Source Type: research

Viruses, Vol. 7, Pages 6689-6706: Glucose-6-Phosphate Dehydrogenase Enhances Antiviral Response through Downregulation of NADPH Sensor HSCARG and Upregulation of NF-κB Signaling
This study examined the mechanism underlying this phenomenon by measuring the expression of antiviral genes—tumor necrosis factor alpha (TNF-α) and GTPase myxovirus resistance 1 (MX1)—in G6PD-knockdown cells upon human coronavirus 229E (HCoV-229E) and enterovirus 71 (EV71) infection. Molecular analysis revealed that the promoter activities of TNF-α and MX1 were downregulated in G6PD-knockdown cells, and that the IκB degradation and DNA binding activity of NF-κB were decreased. The HSCARG protein, a nicotinamide adenine dinucleotide phosphate (NADPH) sensor and negative regulator of NF-κB, was upregulated in G6PD-k...
Source: Viruses - December 17, 2015 Category: Virology Authors: Yi-Hsuan WuDaniel ChiuHsin-Ru LinHsiang-Yu TangMei-Ling ChengHung-Yao Ho Tags: Article Source Type: research