Mosquitoes do not get sick when infected with the same viruses that can kill or maim a human. I have been collaborating with Dr. Kevin Myles on this topic over a series of NIH-funded projects spanning more than 15 years. We have shown that arboviruses do indeed become pathogenic to their mosquito vectors when a critical part of their immune response is suppressed, and have built a molecular sensor to track how well this RNAi-based response is functioning in live adult mosquitoes. Using this sensor, we discovered that the RNAi immune response is compromised when mosquitoes are reared at lower temperatures, and that this is correlated with heightened susceptibility to arboviruses. Other work identified a role for piRNAs in antiviral immunity, substantial crosstalk between the RNAi and miRNA pathways. And clarified relationships amongst C-type lectins that might aid in the entry of viruses into cells. Currently, we are using CRISPR/Cas9 to better assess the specific role of Ae. aegypti genes in antiviral immunity. In addition to viruses, mosquitoes are also vectors of the parasites that cause malaria. Despite the requirement for parasites to invade the mosquito salivary gland, this process is poorly understood. Working with colleagues at the NIH, we have established a role for the salivary protein SGS1 in multiple stages of the malaria parasite life cycle, and helped identify a connection between hormonal signaling and immune cell development.