Laboratory of Immunobiology
Federal University of Santa Catarina
Florianópolis - Brazil
Following an infectious blood meal, mosquitoes face an intense arbovirus replication in its tissues without exhibiting major signs of sickness or fitness compromise. We study the molecular mechanisms and metabolic adaptations responsible for mosquito disease tolerance. The manipulation of such pathways can block vector competence and disease spread.
Our main questions are:
1. How do mosquitoes tolerate persistent arbovirus infection?
2. What are the genetic determinants involved in flavivirus transmission by mosquitoes and emergence in human populations?
Mosquito Biology research: Virus infection comes with a blood meal in mosquitoes. Blood components challenge several mosquito physiologies and activate adaptive programs to prevent and repair damage to mosquito tissues. Arbovirus benefits from mosquito protective pathways and proliferates, spreading from the gut to salivary glands without inducing major health or fitness costs to the vector. Our goal is to identify and inhibit the pathways that promote cellular and metabolic adaptations responsible for mosquito tolerance to arbovirus infection. Inhibiting mosquito disease tolerance will lead to fitness loss and mortality, reducing the number of infected insects in the population and infectious bites, lowering vector capacity and disease spread.
Oliveira JHM, Gonçalves RL, Lara FA, et al. Blood meal-derived heme decreases ROS levels in the midgut of Aedes aegypti and allows proliferation of intestinal microbiota [ PLoS Pathog. 2011 Feb;9(2).
Oliveira JHM, Talyuli OAC, Goncalves RLS, et al. Catalase protects Aedes aegypti from oxidative stress and increases midgut infection prevalence of Dengue but not Zika. PLoS Negl Trop Dis. 2017;11(4):e0005525.
Oliveira JH, Bahia AC, Vale PF. How are arbovirus vectors able to tolerate infection?. Dev Comp Immunol. 2020;103:103514.
Oliveira JHM, Goncalves RLS, Oliveira GA, et al. Energy metabolism affects susceptibility of A. gambiae mosquitoes to Plasmodium infection. Insect Biochem Mol Biol. 2011; 41(6): 349–355.
Torres BY, Oliveira JHM, Tate AT, et al. Tracking Resilience to Infections by Mapping Disease Space. PLoS Biology. 2016, 14(4):e1002436