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Increased nucleoside diphosphate kinase activity induces white spot syndrome virus infection in Litopenaeus vannamei

机译:核苷二磷酸激酶活性增加导致凡纳滨对虾白斑综合症病毒感染

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摘要

Nucleoside diphosphate kinase (NDK), which has the same sequence as oncoprotein (OP) in humans, can induce nucleoside triphosphates in DNA replication by maintenance of the deoxynucleotide triphosphate (dNTP’s) and is known to be regulated by viral infection in the shrimp Litopenaeus vannamei. This paper describes the relationship between NDK and white spot syndrome virus (WSSV) infection. The recombinant NDK was produced by a prokaryotic expression system. WSSV copy numbers and mRNA levels of IE1 and VP28 were significantly increased in shrimp injected with recombinant NDK at 72 h after WSSV infection. After synthesizing dsRNA-NDK and confirming the efficacy of NDK silencing, we recorded the cumulative mortality of WSSV-infected shrimp injected with NDK and dsRNA-NDK. A comparison between the results demonstrated that silencing NDK delayed the death of shrimps. These findings indicate that NDK has an important role influencing the replication of WSSV replication in shrimp. Furthermore, NDK may have potential target as a new therapeutic strategy against WSSV infection in shrimp.
机译:核苷二磷酸激酶(NDK)在人类中与癌蛋白(OP)的序列相同,可通过维持脱氧核苷酸三磷酸(dNTP's)诱导DNA复制中的核苷三磷酸,并且已知其受到南美白对虾病毒感染的调节。 。本文介绍了NDK与白斑综合症病毒(WSSV)感染之间的关系。重组NDK是通过原核表达系统产生的。在WSSV感染后72小时,注射重组NDK的虾的WSSV拷贝数和IE1和VP28的mRNA水平显着增加。合成dsRNA-NDK并确认NDK沉默后,我们记录了注射NDK和dsRNA-NDK的WSSV感染虾的累积死亡率。结果之间的比较表明,沉默NDK可以延迟虾的死亡。这些发现表明NDK在影响虾中WSSV复制的复制中具有重要作用。此外,NDK作为针对虾WSSV感染的新治疗策略可能具有潜在的靶标。

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