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  • To respond to the need for QNAT commercial assays

    2021-03-04

    To respond to the need for QNAT, commercial assays have been developed on automated systems. The first reagents for CMV and EBV VLs in whole blood were Abbott RealTime kits on the m2000 SP/RT system (Abbott Molecular Inc, Des plaines, USA) (M2000) [4,5] and Artus QS-RGQ kits on the QIAsymphony RGQ system (Qiagen S.A.S., France) (QS/RGQ) [6]. Recently two new systems have been commercialized: i) the eMAG/eSTREAM system (Biomerieux, Marcy-l'Etoile, France) (EMAG) coupled with R-gene kits whose performance seems equivalent to the previous Nuclisens Easy Mag system [7] and ii) the Versant kPCR system (Siemens Healthcare n-acetyl-l-cysteine Diagnostics, Saint Denis, France) with kPCR PLX kits (KPCR) [8]. A comparison of these systems is necessary to evaluate their performances.
    Objectives
    Study design
    Results
    Discussion
    Acknowledgments
    Introduction Cucumber mosaic virus (CMV) is a member of the genus Cucumovirus, family Bromoviridae (Di et al., 2010a). CMV has a wide plant host range. It causes huge economic losses to crop production (Jacquemond, 2012). This virus contains three essential single-stranded RNA, namely, RNA1, RNA2, and RNA3 (Kang et al., 2012; Moyle et al., 2018; Revathy and Bhat, 2017; Yamaguchi et al., 2005). CMV RNA encodes viral helicase, replicase, movement, and coat n-acetyl-l-cysteine (Kang et al., 2012; Shen et al., 2014). The replicase of CMV is responsible for plant defense pathways (Mochizuki and Ohki, 2012). Meanwhile, the coat and movement proteins of CMV are important for viral transmission (Zhang et al., 2017a; Nemes et al., 2014; Guiu-Aragonés and Díaz-Pendón, 2015; Salánki et al., 2004). In a virus–host system, the host can produce self-defense substances to resist pathogenic bacteria (Di et al., 2012; Di et al., 2010b; Elena and Rodrigo, 2012; Alazem and Lin, 2015). However, the self-defense substances cannot inhibit the invasion of pathogenic bacteria if no allogenic materials are present, such as antiviral compounds ningnanmycin (NNM), chitosan oligosaccharide, cytosinpeptidemycin, salicylic acid, and dufulin (DFL). NNM is a commonly used antimicrobial agent that exhibits antiviral activity against tobacco mosaic virus (TMV) (Wang et al., 2012; Xiang et al., 1995; Li et al., 2017; Li et al., 2016). NNM strengthens the defensive enzyme activities and promotes the systemic accumulation of pathogenesis-related proteins in TMV-inoculated tobacco (Han et al., 2014). Chitosan oligosaccharide strengthens defensive enzyme activities to enhance rice disease resistance by the mitogen-activated protein kinase signaling cascade pathway (Jones and Dangl, 2006). Cytosinpeptidemycin up-regulates serine and threonine protein kinase SAPK7 induce ABA response and can up-regulate some resistance genes (Shi et al., 2018; Yang et al., 2017a). Salicylic acid (SA) activates reactive oxygen species and temperature stress signals (Zipfel, 2014). DFL activates the SA signaling pathway to induce host plants to generate antiviral responses (Chen et al., 2012). Xiangcaoliusuobingmi triggers the abscisic acid (ABA) pathway to induce host plants to generate antiviral responses (Yu et al., 2017). The innovation of new compounds and new mechanisms for studying the role of highly active antiviral compounds has become the focus of research attention (Gao et al., 2012; Li et al., 2007; Long et al., 2015; Chen et al., 2016; Zhang et al., 2016; Xie et al., 2018; Wu et al., 2017; Zhang et al., 2017b; Lan et al., 2017; Wang et al., 2018). The traditional antiviral compound screening method is mainly inoculation by the half leaf method performed on Nicotiana glutinosa in the laboratory (Ma et al., 2014). However, this screening method cannot clarify the specific single target of drug action. In our previous studies, NNM was screened with antiviral activity against CMV using CMV inoculated by half leaf methods (Ma et al., 2014; Long et al., 2015b). However, the underlying mechanism of NNM on CMV-infected tobacco remains unclear. Therefore, we must study the specific mechanism of action of antiviral drugs and guide the innovation of new pesticides.