Symbiotic bracovirus of a parasite manipulates host lipid metabolism via tachykinin signaling.

• Main Authors: Yanping Wang, Xiaotong Wu, Zehua Wang, Ting Chen, Sicong Zhou, Jiani Chen, Lan Pang, Xiqian Ye, Min Shi, Jianhua Huang, Xuexin Chen
• Format: Article
• Language: English
• Published: Public Library of Science (PLoS) 2021-03-01
• Series: PLoS Pathogens
• Online Access: https://doi.org/10.1371/journal.ppat.1009365

Parasites alter host energy homeostasis for their own development, but the mechanisms underlying this phenomenon remain largely unknown. Here, we show that Cotesia vestalis, an endoparasitic wasp of Plutella xylostella larvae, stimulates a reduction of host lipid levels. This process requires excess secretion of P. xylostella tachykinin (PxTK) peptides from enteroendocrine cells (EEs) in the midgut of the parasitized host larvae. We found that parasitization upregulates PxTK signaling to suppress lipogenesis in midgut enterocytes (ECs) in a non-cell-autonomous manner, and the reduced host lipid level benefits the development of wasp offspring and their subsequent parasitic ability. We further found that a C. vestalis bracovirus (CvBV) gene, CvBV 9-2, is responsible for PxTK induction, which in turn reduces the systemic lipid level of the host. Taken together, these findings illustrate a novel mechanism for parasite manipulation of host energy homeostasis by a symbiotic bracovirus gene to promote the development and increase the parasitic efficiency of an agriculturally important wasp species.