The objectives of this research were to assess the genetic diversity, population structure, linkage disequilibrium and perform a genome-wide association study (GWAS) to search for single nucleotide polymorphisms (SNPs) that associate with the resistance of Pacific white shrimp (Litopenaeus vannamei) to White Spot Syndrome Virus (WSSV). The line here analyzed was formerly founded with animals originated from different origins (Ecuador, Panama, and United States of America), with a history of resistance to WSSV and they have undergone a selection process, currently reaching up to F6 generation. In a controlled challenge to WSSV, this line showed a binary survival (39.0% ± 1.1%) and time to death (109.7 ± 0.9 h post-infection) (n = 1944). The population was genotyped using a commercially available 50 K SNP chip and ∼32 K SNPs remained after quality control of genotypes. Population structure, extent and decay of linkage disequilibrium (LD), and genetic variability in the population were evaluated. The principal component analysis (PCA) did not show apparent genetic stratification in the population. The LD decay estimated, revealed a rapid decrease in r² as the physical distance between markers increased. The most significant decrease was observed in the first 30Kb of distance, suggesting the need to use a higher density of informative markers to meet the requirement of a genome-wide association study in L. vannamei. The observed and expected heterozygosities were both = 0.38, which indicates that the population presents acceptable genetic variability for WSSV resistance. Two SNPs were significantly associated to WSSV resistance at a genome-wide level, which in turn together explained 0.17% of the genetic variance for the trait. One identified SNP surpassing the genome-wide significance threshold (chromosome 1 at 51207389 bp) is located near potential candidate genes, such as Arylsulfatase B-like (ARSB), and D-beta-hydroxybutyrate dehydrogenase mitochondrial-like (βhyD); which was linked to the humoral immune response to WSSV, in addition to the Putative mediator of RNA polymerase II transcription subunit 26 (PMed26); which are associated with the hepatopancreas immune response against infection of WSSV and acute hepatopancreatic necrosis disease (AHPND). Our results indicate a polygenic architecture for WSSV resistance in L. vannamei, suggesting that incorporating genome-wide SNP information, through genomic selection, might be the most appropriate approach to accelerate the genetic progress for this trait.

本研究的目的是评估遗传多样性、种群结构、连锁不平衡，并进行全基因组关联研究 (GWAS)，以寻找与太平洋白对虾 ( Litopenaeus vannamei ) 抗性相关的单核苷酸多态性 (SNP)白斑综合症病毒 (WSSV)。这里分析的品系以前是用来自不同来源（厄瓜多尔、巴拿马和美利坚合众国）的动物建立的，具有对 WSSV 的抗性历史，它们经历了选择过程，目前达到 F6 代。在对 WSSV 的受控挑战中，该品系显示出二元存活率（39.0% ± 1.1%）和死亡时间（感染后 109.7 ± 0.9 小时）（n = 1944）。使用市售的 50 K SNP 芯片对群体进行基因分型，在基因型质量控制后剩余约 32 K SNP。评估了种群结构、连锁不平衡 (LD) 的范围和衰减以及种群中的遗传变异性。主成分分析（PCA）未显示人群中明显的遗传分层。估计的 LD 衰减表明，随着标记之间物理距离的增加， r ²迅速下降。在前 30Kb 的距离中观察到最显着的下降，表明需要使用更高密度的信息标记来满足南美白对虾全基因组关联研究的要求. 观察到的和预期的杂合度均为 = 0.38，这表明该群体呈现出可接受的 WSSV 抗性遗传变异性。两个 SNP 在全基因组水平上与 WSSV 抗性显着相关，这反过来又共同解释了该性状遗传变异的 0.17%。一个超过全基因组显着性阈值（51207389 bp 的染色体 1）的 SNP 位于潜在的候选基因附近，例如芳基硫酸酯酶 B 样 (ARSB) 和 D-β-羟基丁酸脱氢酶线粒体样 (βhyD)；除了推定的 RNA 聚合酶 II 转录亚基 26 (PMed26) 的介质外，这与对 WSSV 的体液免疫反应有关；这与肝胰腺对 WSSV 感染和急性肝胰腺坏死病 (AHPND) 的免疫反应有关。vannamei提出通过基因组选择整合全基因组 SNP 信息可能是加速该性状遗传进展的最合适方法。