Abstract
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.
Highlights
Competition between viruses and Wolbachia for host lipids is a proposed mechanism of Wolbachia-mediated virus blocking in insects
To complement our lipid profile data, we looked in published transcriptomic and genetic studies for genes related to lipid metabolism affected by infection in Drosophila or Aedes systems[20,42,43,44,45,46,47,48] We compiled a list of 13 genes with altered expression levels associated with the infection of Wolbachia or other pathogens (Supplementary Table 1)
dengue viruses (DENVs) and Wolbachia have reduced genomes and are unable to synthesize the complete suite of lipids they require for replication[49,50]
Summary
Competition between viruses and Wolbachia for host lipids is a proposed mechanism of Wolbachia-mediated virus blocking in insects. 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). 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. The ability to spread into insect populations via vertical transmission and to suppress replication of viral pathogens make Wolbachia an attractive method of intervention against mosquito-transmitted viral diseases, such as dengue viruses (DENVs)[5]. Viral blocking likely results from multiple complementary mechanisms, previous studies propose two main hypotheses[11,12,13]: immune priming, which reduces the success of secondary infections by invading pathogens[7,14,15,16], and competition for limited host resources such as amino acids, lipids, and intracellular space[17,18,19,20]
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