Shen Zeen, Kumar Dhiraj, Liu Xunmeng, Yan Bingyu, Fang Ping, Gu Yuchao, Li Manyun, Xie Meiping, Yuan Rui, Feng Yongjie, Hu Xiaolong, Cao Guangli, Xue Renyu, Chen Hui, Liu Xiaohan, Gong Chengliang
School of Biology and Basic Medical Science, Soochow University, Suzhou 215123, China.
School of Studies in Zoology, Jiwaji University, Gwalior 474011, India.
Biology (Basel). 2021 May 23;10(6):462. doi: 10.3390/biology10060462.
Hepatopancreas necrosis disease (HPND) of the Chinese mitten crab Eriocheir sinensis causes huge economic loss in China. However, the pathogenic factors and pathogenesis are still a matter of dissension. To search for potential pathogens, the hepatopancreatic flora of diseased crabs with mild symptoms, diseased crabs with severe symptoms, and crabs without visible symptoms were investigated using metatranscriptomics sequencing. The prevalence of Absidia glauca and Candidatus Synechococcus spongiarum decreased, whereas the prevalence of Spiroplasma eriocheiris increased in the hepatopancreatic flora of crabs with HPND. Homologous sequences of 34 viral species and 4 Microsporidian species were found in the crab hepatopancreas without any significant differences between crabs with and without HPND. Moreover, DEGs in the hepatopancreatic flora between crabs with severe symptoms and without visible symptoms were enriched in the ribosome, retinol metabolism, metabolism of xenobiotics by cytochrome P450, drug metabolism-cytochrome P450, biosynthesis of unsaturated fatty acids, and other glycan degradation. Moreover, the relative abundance of functions of DEDs in the hepatopancreatic flora changed with the pathogenesis process. These results suggested that imbalance of hepatopancreatic flora was associated with crab HPND. The identified DEGs were perhaps involved in the pathological mechanism of HPND; nonetheless, HPND did not occur due to virus or microsporidia infection.
中华绒螯蟹的肝胰腺坏死病(HPND)给中国造成了巨大的经济损失。然而,其致病因素和发病机制仍存在争议。为了寻找潜在病原体,利用宏转录组学测序技术对症状较轻的患病蟹、症状严重的患病蟹以及无明显症状的蟹的肝胰腺菌群进行了调查。在患HPND的蟹的肝胰腺菌群中,灰绿犁头霉和海绵状蓝藻菌的流行率下降,而中华绒螯蟹螺原体的流行率上升。在蟹的肝胰腺中发现了34种病毒和4种微孢子虫的同源序列,患HPND的蟹和未患HPND的蟹之间没有任何显著差异。此外,症状严重的蟹和无明显症状的蟹的肝胰腺菌群中的差异表达基因(DEGs)在核糖体、视黄醇代谢、细胞色素P450对外源生物的代谢、药物代谢 - 细胞色素P450、不饱和脂肪酸的生物合成以及其他聚糖降解中富集。此外,肝胰腺菌群中差异表达基因(DEDs)的功能相对丰度随发病过程而变化。这些结果表明,肝胰腺菌群失衡与蟹的HPND有关。所鉴定的差异表达基因可能参与了HPND的病理机制;尽管如此,HPND并非由病毒或微孢子虫感染引起。