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Metal-Free Cascade Enhancement involving Intermolecular C-N Bonds Being able to access Tried Isoindolinones underneath Cathodic Reduction.
To investigate the occurrence of little cherry virus 1 (LChV-1), little cherry virus 2 (LChV-2), cherry green ring mottle virus (CGRMV), cherry necrotic rusty mottle virus (CNRMV), and cherry virus A (CVA) in stone fruit trees in Poland, leaf samples were collected from sweet and sour cherry, peach, and apricot trees. Two sets of primers were used to increase the effectiveness of virus detection. The RT-PCR results indicated that the most frequently detected virus in all of the tested samples was CVA (60%), followed by CGRMV (13%), CNRMV (12%), LChV-1 (11%), and LChV-2 (4%). CVA and CNRMV were not detected in peaches. Mixed infections of these viruses were frequently detected. Keywords little- cherry virus 1; little cherry virus 2; cherry green ring mottle virus; cherry necrotic rusty mottle virus; cherry virus A; RT-PCR.Epstein-Barr virus (EBV), a B lymphotrophic herpesvirus associated with various forms of tumors, exhibits several latency phases with expressed EBV nuclear antigen 1 (EBNA-1). In the search of novel EBV-inhibiting targets, to curb the menace of EBV-borne lymphotropic transformations, EBNA-1 protein might serve as a best target for novel antiviral natural compounds. This study is thus aimed to explore the inhibitory potential of Muuraya koengii bioactive compounds isomahanine, murrayanol and mahanimbine against the EBNA-1 of EBV. 3D structure of EBNA-1 was retrieved from the PDB data bank with further optimization of both the protein and ligands. In-silico inhibitory potential of the selected M. koengii bio-compounds against EBNA-1 as well as the molecular properties of the derivatives against EBNA-1 were assessed. Murrayanol seems to be a potent inhibitory drug to target EBNA-1 with a promising binding energy of -7.21 with two hydrogen bonds. Drug likeliness parameters recorded murrayanol to be the most promising of the tested compounds, followed by isomahanine. Molecular docking evaluations show that EBNA-1 might be inhibited with M. koengii biocompounds. Keywords EBV; EBNA; M. koengii; in-silico.Tomato spotted wilt virus (TSWV) is an economically important pathogen of many crops worldwide. However, prior to this study, only one complete genome sequence of an African TSWV isolate was available in public databases. Selleckchem 666-15 inhibitor This limits genetic diversity and evolutionary studies of the pathogen on the continent. TSWV was detected in symptomatic Zimbabwean chrysanthemum plants using late-ral flow kits. The presence of the pathogen was subsequently confirmed by double antibody sandwich enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction (RT-PCR). Total RNAs for RT-PCR and next-generation sequencing (NGS) were extracted using an RNA extraction kit. NGS performed on an Illumina HiSeq platform was used to recover the full TSWV genome and analyzed by different software packages. The tripartite genome of the Zimbabwe TSWV isolate consisted of L, M and S RNAs of 8914, 4824 and 2968 nucleotides, respectively. This isolate shared highest protein and nucleotide sequence identities with the isolate LK-1 from neighboring South Africa. The Zimbabwe TSWV isolate was found to be a non-recombinant and non-resistance-breaking. This study provides the first full genome of TSWV from Zimbabwe. It also adds useful information towards understanding the evolution of the pathogen. Keywords Africa; tospovirus; phylogenetic analysis; recombination; virus identification.Non-structural NS1 protein of influenza A virus counters host antiviral defences by antagonizing the interferon response. The C-terminal effector domain suppresses the host response and is associated with the pathogenicity of the virus. To better understand the regulatory role of the C-terminal domain, we used reverse genetics system to generate NS1-truncated virus (NS80) and compared the cytokine profiles in the lungs of mice infected with the NS80 mutant and with the control virus A/WSN/33 (WSN). The NS80 virus was attenuated and the viral titer in the lungs was about 25 times lower than viral titer of control A/WSN/33. Mice infected with NS80 virus exhibited more severe clinical symptoms and 2 mice died 6 days post infection. NS80 virus activated retinoic-inducible gene (RIG)-1-like receptor signaling pathway more strongly than control WSN virus and mice infected with NS80 virus exhibited a greater abundance and more diverse cytokine profile. Infection with NS80 virus induced the expression of the following factors pro-inflammatory cytokines (IL-1α, IL-1β, TNF-α, IL-16), interferons (IFN-α and IFN-ε), chemokines (CCL2, CCL11, CXCL1, CXCL5, CXCL10, CXCL11 and CXCL13), matrix metallopeptidase 9 (MMP-9), metallopeptidase inhibitor 1 (TIMP-1), macrophage colony-stimulating factor (M-CSF), and vascular cell adhesion protein 1 (VCAM-1). All these cytokines are associated with viral pathogenicity. Our data show that attenuation of the virus should not be directly linked with pathogenicity. Keywords influenza virus; NS1 protein; cytokines; interferon; pathogenicity.The H9N2 influenza virus has been frequently endemic in poultry, infected mammals and humans and has threatened public health. It is therefore imperative to understand the molecular mechanism enabling this virus to jump from avian to mammalian species. In this study, two H9N2 influenza viruses were isolated from the same region in eastern China but from different hosts; one was isolated from mink and named A/Mink/Shandong/WM01/2014(H9N2)(WM01), while the other was isolated from chicken and named A/Chicken/Shandong/LX830/2014(H9N2)(LX830). Sequencing and phylogenetic analysis showed that both H9N2 influenza viruses had similar genetic backgrounds. The results of infection in minks suggested that both viruses caused significant weight loss and pathological changes in the lungs. Mouse infection showed that LX830 was nonpathogenic in mice, but WM01 resulted in 25% mortality and pathological changes in the lungs, such as severe edema and diffused inflammation of the interalveolar septa. Comparison of the full genomes of both H9N2 influenza viruses showed 52-nucleotide-synonym mutations in 8 gene segments and 7-nucleotide-antonym mutations, resulting in 7 amino acid (AA) substitutions distributed in the PB1, PA, NA and M gene segments. None of these mutations did affect splicing of the M and NS gene segments at the nucleotide level or minor open reading frames (ORFs), such as PB1-F2 and PA-X. Phylogenetic analysis showed that both H9N2 influenza viruses belong to the prevalent epidemic genotype in Asia. Keywords H9N2 influenza virus; chicken; minks; pathogenicity; phylogenetic.
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