草莓白化相关病毒中国分离物全基因组分析

草莓白化相关病毒(strawberrypallidosis-associatedvirus,SPa V)属于长线形病毒科(Closteroviridae)毛形病毒属(Crinivirus),可引起草莓病害,2017年在中国首次报道。采用高通量测序、RACE和RT-PCR技术获得了SPa V中国分离物(FJ)的基因组全长。该病毒含有两条正单链基因组RNA1和RNA2。RNA1全长8 048 nt,5′和3′非编码区序列分别为264和197 nt,含有3个开放阅读框(ORF),分别编码ORF 1a/1b融合蛋白和p9蛋白。RNA2全长7 977 nt,5′和3′非编码区序列分别为248和186 nt,含有8个开放阅读框(ORF),分别编码HSP70h、CPh、CP、CPm、p7、p6、p9和p28等8个蛋白。RNA1和RNA2与美国M1分离物分别具有98.5%和99.0%的核苷酸一致性;系统发育分析结果表明,SPa V中国分离物(FJ)单独处在一个分支。对SPa V来源的小RNA的分析表明,来源于SPa V的小RAN长度以21和22 nt为主。

Effects of RIP3/CaMKII signaling pathway on cardiac function and survival curve in mice with severe viral myocarditis

AIM To investigate the effects of RIP3/CaMKII signaling pathway on Coxsaekie virus B3 （CVB3）-induced severe viral myocarditis and to explore the role of CaMKII specific inhibitor KN-93 in severe viral myocarditis. METHODS Male BALB/c mice （n=60） were divided into normal control group， CVB3 group， CVB3+KN-93 group and CVB3+KN-93+Ti （reactive oxygen species specific inhibitor） group. The myocardial necrosis markers were detected by double-antibody sandwich immunoassay. The structure and function of mouse heart were detected by echocardiography， and Kaplan-Meier survival curve was drawn to observe the protective effect of KN-93 on the mice with myocardial injury. RESULTS Compared with CVB3 group， significantly reduced myocardial cell necrosis， improved cardiac function and survival curve of the mice were observed in CVB3+KN-93 group （P<0.01）. The content of H₂O₂ in CVB3+KN-93 group was significantly lower than that in CVB3 group （P<0.01）. After adding Ti， H₂O₂ content in CVB3+KN-93+Ti group was slightly lower than that in CVB3+KN-93 group （P<0.05）， but the improvement of cardiac function and survival curve was not obvious. CONCLUSION RIP3/CaMKII signaling pathway plays a significant role in cardiomyocyte death induced by viral infection. KN-93 blocks this pathway and may serve as a new therapeutic option for the treatment of severe viral myocarditis. The mechanism may be related to the direct inhibition of CaMKII and the indirect inhibition of reactive oxygen species.