Fusarium wilt caused by Fusarium oxysporum f. sp. momordicae (FoM) is an important fungal disease that affects the production of bitter gourd. Hypovirulence-associated mycoviruses have great potential and application prospects for controlling the fungal disease. In this study, a novel ourmia-like virus, named Fusarium oxysporum ourmia-like virus 1 (FoOuLV1), was isolated from FoM strain HuN8. The viral genomic RNA is 2,712 nucleotides (nt) in length and contains an open reading frame (ORF) encoding a putative RNA-dependent RNA polymerase (RdRp) using either standard or mitochondrial codes. In strain HuN8, there was also a FoOuLV1-associated RNA segment with 1,173 nt in length with no sequence homology. Phylogenetic analysis showed that FoOuLV1 is a member of the genus Magoulivirus of the family Botourmiaviridae. FoOuLV1 was found to be associated with hypovirulence in FoM. Moreover, FoOuLV1 and its hypovirulence trait can be transmitted horizontally to other FoM strains and also to other formae speciale strains of F. oxysporum. In addition, FoOuLV1 showed significant biological control effect against the bitter gourd Fusarium wilt. To our knowledge, this study reveals the first description of a hypovirulence-associated ourmia-like mycovirus, which has the potential to the biological control of Fusarium wilt.
Background: To investigate the therapeutic effect of total Astragalus saponins (AST) against viral myocarditis in animal and cell models. Methods: Primary myocardiocytes (PMCs) were stimulated by the coxsackie B (CVB) 3 virus to prepare the cell model of viral myocarditis. Cell viability, apoptosis and the mRNA expression of C-Myc, tumor necrosis factor (TNF)-α and Fas were detected to evaluate the protective effects of AST on CVB3-induced PMC damage. Results: AST could significantly increase survival and decrease the ratio of heart weight: body weight (P<0.05). The level of myocardial fibrosis in the AST group was significantly lower than that in the CVB3 group. Compared with the CVB3 group, the ejection fraction was increased significantly in the AST group. Levels of lactate dehydrogenase and creatine kinase-MB in the peripheral blood of the AST group were significantly lower than those in the control group. In vitro, AST could significantly decrease CVB3-induced PMC apoptosis. Expression of C-Myc, TNF-α, Fas in the AST group was significantly lower than that in the CVB3 group. Conclusions: It is demonstrated that AST was protective against CVB3-induced viral myocarditis, which may be associated with a decrease in CVB3-induced apoptosis and down-regulation of expression of C-Myc, TNF-α and Fas.
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