RESUMEN
The Queensland fruit fly (Bactrocera tryoni) is a major polyphagous pest widespread in Australia and several Pacific Islands. Bacteria present on the host plant phyllosphere supply proteins, essential for egg development and female sexual maturity. We investigated the role of microbial volatile organic compounds (MVOCs) emitted by Enterobacteriaceae commonly found on the host plant and in the fly gut in attracting virgin females. Bacteria were cultured on artificial media and natural fruits, at various pH, and MVOCs were collected using different headspace volatile absorbent materials. The olfactory responses of virgin females to bacterial MVOCs were assessed via electrophysiology and behavioral assays. The production of MVOCs was strongly influenced qualitatively by the bacterial strain and the type of media, and it semi-quantitatively varied with pH and time. MVOCs emitted by Klebsiella oxytoca invoked the strongest antennal response and were the most attractive. Among the identified compounds triggering an olfactory response, D-limonene and 2-nonanone were both significantly behaviorally attractive, whereas phenol, nonanal, isoamyl alcohol, and some pyrazines appeared to be repulsive. This study deepens our understanding of the chemical ecology between fruit flies and their bacterial symbionts and paves the way for novel synthetic lures based on specifically MVOCs targeting virgin females.
RESUMEN
To find nutrients, mosquitoes use volatile organic compounds (VOCs) emitted by plants and animal hosts. These resources overlap in their chemical composition, and an important layer of information resides in VOCs' relative abundance in the headspace of each resource. In addition, a large majority of the human species regularly uses personal care products such as soaps and perfumes, which add plant-related VOCs to their olfactory signature. Using headspace sampling and gas chromatography-mass spectrometry, we quantified how human odor is modified by soap application. We showed that soaps alter mosquito host selection, with some soaps increasing the attractiveness of the host and some soaps reducing it. Analytical methods revealed the main chemicals associated with these changes. These results provide proof-of-concept that data on host-soap valences can be reverse-engineered to produce chemical blends for artificial baits or mosquito repellents, and evince the impact of personal care products on host selection processes.
RESUMEN
Pathogens may manipulate their human and mosquito hosts to enhance disease transmission. Dengue, caused by four viral serotypes, is the fastest-growing transmissible disease globally resulting in 50-100 million infections annually. Transmission of the disease relies on the interaction between humans and the vector Aedes aegypti and is largely dependent on the odor-mediated host seeking of female mosquitoes. In this study, we use activity monitors to demonstrate that dengue virus-1 affects the locomotion and odor-mediated behavior of Ae. aegypti, reflecting the progression of infection within the mosquito. Mosquitoes 4-6 days post-infection increase locomotion, but do not alter their odor-driven host-seeking response. In contrast, females 14-16 days post-infection are less active, yet more sensitive to human odors as assessed by behavioral and electrophysiological assays. Such an increase in physiological and behavioral sensitivity is reflected by the antennal-specific increase in abundance of neural signaling transcripts in 14 days post-infection females, as determined by transcriptome analysis. This suggests that the sensitivity of the mosquito peripheral olfactory system is altered by the dengue virus by enhancing the overall neural responsiveness of the antenna, rather than the selective regulation of chemosensory-related genes. Our study reveals that dengue virus-1 enhances vector-related behaviors in the early stages post-infection that aid in avoiding predation and increasing spatial exploration. On the other hand, at the later stages of infection, the virus enhances the host-seeking capacity of the vector, thereby increasing the risk of virus transmission. A potential mechanism is discussed.