慢性蜜蜂病毒利用宿主抗菌和改变肠道微生物群的组成,以促进病毒感染
Yanchun Deng1, Sa Yang2,3, Li Zhang2
1Institute of Bast Fiber Crops, Chinese Academy of Agricultural Sciences, Changsha 410205, China.
The ISME journal
|March 22, 2024
概括
慢性蜜蜂病毒 (CBPV) 感染通过增加机会性细菌和减少有益微生物来破坏蜜蜂肠道微生物群. 这种不平衡是由宿主免疫反应驱动的,加速了蜜蜂的死亡率,并导致腹部膨胀症状.
科学领域:
- 兽医病毒学 兽医病毒学
- 昆虫病理学 昆虫病理学
- 微生物组研究 微生物组研究
背景情况:
- 肠道微生物群在动物对病毒感染的免疫力中起着至关重要的作用.
- 慢性蜜蜂病毒 (CBPV) 操纵宿主免疫系统和肠道微生物群进行复制的机制尚未完全理解.
研究的目的:
- 研究CBPV感染如何影响蜜蜂的肠道微生物群组成.
- 阐明肠道机会性病原体在CBPV扩散和疾病进展中的作用.
- 检查宿主免疫反应,特别是抗微生物 (AMP) 表达,与CBPV感染期间的肠道微生物变化有关.
主要方法:
- 蜜蜂后肠的组织病理学检查.
- 肠道微生物群落的元基因组分析.
- 与CBPV和机会性细菌共同注射的实验.
- 转录组和定量实时PCR用于基因表达分析 (AMP).
- 相关性分析和细菌静止试验.
主要成果:
- CBPV主要感染后肠,造成可见的损伤.
- 感染CBPV导致有益细菌 (Snodgrassella alvi,Lactobacillus apis) 的减少,机会性病原体 (Enterobacter hormaechei,Enterobacter cloacae) 的增加.
- 机会性病原体加剧了CBPV的扩散,增加了蜜蜂的死亡率,并加剧了腹部膨胀症状.
- 抗微生物 (AMP) 表达因CBPV感染而显著上调 (>1000倍).
- AMPs抑制了有益的细菌 (S. alvi,L. apis),但并没有抑制机会性Enterobacter物种.
结论:
- CBPV感染刺激并利用宿主AMP来消除有益的肠道细菌.
- 这种选择性消除有助于机会性细菌的繁殖,削弱肠道屏障.
- 由CBPV和机会性病原体破坏肠道微生物群,导致疾病进展和特征性症状,如腹.
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