Abstract：
Acute hepatopancreatic necrosis disease (AHPND) is a highly contagious and lethal disease of shrimp caused by Vibrio strains carrying the virulence plasmid (pAHPND) containing the pirAB virulence genes. Through analysis of plasmid sequence similarity, clustering, and phylogeny, a horizontal transfer element similar to IS91 was discovered within the pAHPND plasmid. Additionally, two distinct clades of plasmids related to pAHPND (designated as pAHPND-r1 and pAHPND-r2) were identified, which may serve as potential parental plasmids for pAHPND. The available evidence, including the difference in G+C content between the plasmid and its host, codon usage preference, and plasmid recombination event prediction, suggests that the formation of the pAHPND plasmid in the Vibrio owensii strain was likely due to the synergistic effect of the recombinase RecA and the associated proteins RecBCD on the pAHPND-r1 and pAHPND-r2, resulting in the recombination and formation of the precursor plasmid for pAHPND (pre-pAHPND). The emergence of pAHPND was found to be a result of successive insertions of the horizontal transfer elements of pirAB-Tn903 and IS91-like segment, which led to the deletion of one third of the pre-pAHPND. This plasmid was then able to spread horizontally to other Vibrio strains, contributing to the epidemics of AHPND. These findings shed light on previously unknown mechanisms involved in the emergence of pAHPND and improve our understanding of the disease\'s spread.
摘要：
急性肝胰腺坏死病（AHPND）是由携带含pirAB毒力基因的毒力质粒（pAHPND）的弧菌菌株引起的一种高度传染性和致死性虾疾病。通过质粒序列相似性分析,聚类，和系统发育，在pAHPND质粒中发现了类似于IS91的水平转移元件。此外,鉴定了与pAHPND相关的两个不同的质粒进化枝（称为pAHPND-r1和pAHPND-r2），它可以作为pAHPND的潜在亲本质粒。现有的证据,包括质粒和宿主之间G+C含量的差异，密码子使用偏好，和质粒重组事件预测，表明，在弧菌弧菌菌株中pAHPND质粒的形成可能是由于重组酶RecA和相关蛋白RecBCD对pAHPND-r1和pAHPND-r2的协同作用，导致pAHPND前体质粒的重组和形成（pre-pAPND）。发现pAHPND的出现是pirAB-Tn903和IS91样片段的水平转移元件连续插入的结果，这导致pAHPND前的三分之一的缺失。然后该质粒能够水平传播到其他弧菌菌株，有助于AHPND的流行。这些发现揭示了以前未知的pAHPND出现的机制，并提高了我们对疾病传播的理解。
