Upregulation of Aedes aegypti Vago1 by Wolbachia and its effect on dengue virus replication

被引:33
作者
Asad, Sultan [1 ]
Parry, Rhys [1 ]
Asgari, Sassan [1 ]
机构
[1] Univ Queensland, Sch Biol Sci, Australian Infect Dis Res Ctr, Brisbane, Qld 4072, Australia
基金
英国医学研究理事会;
关键词
Vago; Aedes aegypti; Wolbachia; Dengue virus; WEST NILE VIRUS; AEDES-AEGYPTI; DROSOPHILA; INFECTION; PATHWAY; ALBOPICTUS; TOLL; SYMBIONT; DISEASE; INSECT;
D O I
10.1016/j.ibmb.2017.11.008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Dengue infection along with its related disease conditions poses a significant threat to human health. The pathogen responsible for this infection is dengue virus (DENV) which is primarily transmitted to humans through the bites of Aedes aegypti mosquitoes. Unavailability of a potent vaccine has recently sparked renewed research endeavours aimed at vector control. To date, Wolbachia as an endosymbiotic bacterium has shown promise as a novel biocontrol agent to restrict DENV replication in the vector, although the underlying antiviral mechanism remains elusive. Recent studies have demonstrated the potential role of Vago as a novel secretory protein involved in cross-talk between the innate immune pathways in Culex quinquefasciatus mosquitoes to restrict West Nile virus replication. In this study, we have identified two homologs of the Vago protein in Ae. aegypti and looked into their modulation in the case of Wolbachia wMelPop strain infection. Furthermore, we have investigated the role of AeVagol, that is highly induced by Wolbachia, in the context of Wolbachia-mosquito-DENV interactions. Knockdown studies of the AeVagol gene in Wolbachia-infected cells led to significant increases in DENV replication, with no effect on Wolbachia density. Our results suggest that the Wolbachia-induced AeVagol in Ae. aegypti may function as a host factor to suppress DENV replication in the mosquito. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:45 / 52
页数:8
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