Dr. Smartt investigates the interaction between mosquitoes and viruses that infect humans (e.g., West Nile virus) to better understand how to predict and prevent outbreaks.

Dr. Smartt earned her undergraduate degree from Tennessee State University, and her Ph.D. in Molecular Biology and Biochemistry from the University of California, Irvine, in 1995.

The mosquito Aedes aegypti can act as a vector for many human diseases, including chikungunya fever and Zika virus, both of which have been of increasing concern in the past decade. Because we don’t have any good medications to give people once they’re already sick, many scientists are focused on trying to reduce the risk of getting infected in the first place by controlling the mosquitoes. Within the U.S., the environmental conditions in Texas and Florida are the most favorable for this species of mosquito. (The mosquitoes studied in Dr. Smartt’s lab were collected from Key West.)

In a recent paper, Dr. Smartt and colleagues tried to better understand the immune response of mosquitoes in response to chikungunya and Zika viruses. Specifically, they looked at two genes - defensin A and defensin C - that code for anti-viral proteins. They found that the mosquitoes made more DefA and DefC in response to infection with either virus, although the ratio of the two proteins depended on which virus was used. They also found that male mosquitoes made more anti-viral protein than females, and that this was true at all stages of mosquito development. Finally, they found that there were significant differences in these changes when comparing mosquitoes from Orlando and Key West.

These results help build a clearer picture of how these genes function in the immune response of the mosquito. The hope is that this information will help us to create genetically-modified mosquitoes (which we can then release into the environment) that are more resistant to infection with these viruses. These mosquitoes would thus be less able to spread infection to new human hosts.