title: Immune response and insulin signalling alter mosquito feeding behaviour to enhance malaria transmission potential.
abstract: Malaria parasites alter mosquito feeding behaviour in a way that enhances parasite transmission. This is widely considered a prime example of manipulation of host behaviour to increase onward transmission, but transient immune challenge in the absence of parasites can induce the same behavioural phenotype. Here, we show that alterations in feeding behaviour depend on the timing and dose of immune challenge relative to blood ingestion and that these changes are functionally linked to changes in insulin signalling in the mosquito gut. These results suggest that altered phenotypes derive from insulin signalling-dependent host resource allocation among immunity, blood feeding, and reproduction in a manner that is not specific to malaria parasite infection. We measured large increases in mosquito survival and subsequent transmission potential when feeding patterns are altered. Leveraging these changes in physiology, behaviour and life history could promote effective and sustainable control of female mosquitoes responsible for transmission.
authors.affiliation: Grand Challenges in Ecosystem and Environment, Department of Life Sciences, Imperial College London, Silwood Park.
authors.forename: Lauren J
authors.initials: LJ
authors.lastname: Cator
authors.affiliation: Department of Medical Microbiology and Immunology, University of California, Davis.
authors.forename: Jose E
authors.initials: JE
authors.lastname: Pietri
authors.affiliation: Department of Infectious Disease in College of Veterinary Medicine and Odum School of Ecology, University of Georgia.
authors.forename: Courtney C
authors.initials: CC
authors.lastname: Murdock
authors.affiliation: Center for Infectious Disease Dynamics, Pennsylvania State University.
authors.forename: Johanna R
authors.initials: JR
authors.lastname: Ohm
authors.affiliation: Department of Entomology, University of California, Davis.
authors.forename: Edwin E
authors.initials: EE
authors.lastname: Lewis
authors.affiliation: Center for Infectious Disease Dynamics, Pennsylvania State University.
authors.forename: Andrew F
authors.initials: AF
authors.lastname: Read
authors.affiliation: Department of Medical Microbiology and Immunology, University of California, Davis.
authors.forename: Shirley
authors.initials: S
authors.lastname: Luckhart
authors.affiliation: Center for Infectious Disease Dynamics, Pennsylvania State University.
authors.forename: Matthew B
authors.initials: MB
authors.lastname: Thomas
mesh_terms: D000818:Animals; D009033:Culicidae / Q000276:immunology / Q000502:physiology*; D005247:Feeding Behavior; D005260:Female; D055785:Gene Knockdown Techniques; D006790:Host-Parasite Interactions; D007328:Insulin / Q000378:metabolism*; D036341:Intercellular Signaling Peptides and Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D008288:Malaria / Q000469:parasitology* / Q000635:transmission; D051379:Mice; D008810:Mice, Inbred C57BL; D060172:Morpholinos / Q000378:metabolism; D010641:Phenotype; D010963:Plasmodium falciparum / Q000302:isolation & purification; D015398:Signal Transduction
chemical_list: D007328:Insulin; D036341:Intercellular Signaling Peptides and Proteins; D060172:Morpholinos