School of Biological Sciences, Monash University, Clayton, VIC, 3800, Australia.
Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO, 80523, USA.
Commun Biol. 2020 Sep 18;3(1):518. doi: 10.1038/s42003-020-01254-z.
Competition between viruses and Wolbachia for host lipids is a proposed mechanism of Wolbachia-mediated virus blocking in insects. Yet, the metabolomic interaction between virus and symbiont within the mosquito has not been clearly defined. We compare the lipid profiles of Aedes aegypti mosquitoes bearing mono- or dual-infections of the Wolbachia wMel strain and dengue virus serotype 3 (DENV3). We found metabolic signatures of infection-induced intracellular events but little evidence to support direct competition between Wolbachia and virus for host lipids. Lipid profiles of dual-infected mosquitoes resemble those of DENV3 mono-infected mosquitoes, suggesting virus-driven modulation dominates over that of Wolbachia. Interestingly, knockdown of key metabolic enzymes suggests cardiolipins are host factors for DENV3 and Wolbachia replication. These findings define the Wolbachia-DENV3 metabolic interaction as indirectly antagonistic, rather than directly competitive, and reveal new research avenues with respect to mosquito × virus interactions at the molecular level.
病毒和沃尔巴克氏体（Wolbachia）争夺宿主脂质是沃尔巴克氏体介导的昆虫病毒阻断的一种拟议机制。然而，蚊子中病毒和共生体之间的代谢组学相互作用尚未明确界定。我们比较了携带沃尔巴克氏体 wMel 株和登革热病毒 3 型（DENV3）单感染或双重感染的埃及伊蚊的脂质图谱。我们发现了感染诱导的细胞内事件的代谢特征，但几乎没有证据支持沃尔巴克氏体和病毒直接争夺宿主脂质。双重感染蚊子的脂质图谱与 DENV3 单感染蚊子的脂质图谱相似，这表明病毒驱动的调节作用超过了沃尔巴克氏体的调节作用。有趣的是，关键代谢酶的敲低表明心磷脂是 DENV3 和沃尔巴克氏体复制的宿主因素。这些发现将沃尔巴克氏体-DENV3 的代谢相互作用定义为间接拮抗，而不是直接竞争，并揭示了在分子水平上蚊子与病毒相互作用的新研究途径。
