Dr. Niles's objective is to improve our understanding of how the malaria parasite works in order to design treatment options that are biologically based. Although most drugs currently used to treat or prevent malaria seem to work well, we don’t really understand why.

Dr. Niles studied at MIT as an undergraduate and earned his M.D. and Ph.D. through a joint Harvard-MIT program. He headed west to UC Berkeley for a postdoctoral fellowship, before returning to MIT in 2007 to start his lab. His research brings together people with expertise in engineering, chemistry, and microbiology to arrive at cross-disciplinary solutions.

Malaria is a devastating disease, causing about 655,000 deaths per year, mostly in developing countries. (About 40% of the world’s population is at risk.) It is an infectious disease caused by Plasmodium, a group of single-celled parasites. There are five species within the Plasmodium group that can infect humans, but most deaths are caused by Plasmodium falciparum - the other four tend to cause less severe symptoms and people are more likely to recover. The parasite spends part of its life cycle in mosquitos, and part of its life cycle in humans: when an infected mosquito bites a person, Plasmodium enters the person’s bloodstream and travels to the liver, where it makes many copies of itself and infects red blood cells. Eventually, they cause the red blood cells to burst open, releasing many more parasites that can infect even more red blood cells.

A major goal of the Niles lab is to develop tools for figuring out what Plasmodium genes do functionally. Based on computer models, it is predicted that there are over 5,000 genes in Plasmodium falciparum, but we only know what about half of those do. Each of those genes with unknown function could potentially be serving a crucial role in the parasite’s survival, but without knowing what it does, we have no idea how to block it from doing its job (or even which one to try to block). Dr. Niles is working to create methods to turn off each of these genes one at a time, in order to see what happens without it. (This is a central concept in genetics, but traditional methods don’t work for many species.)

Another project that Dr. Niles is working on has to do with heme. Heme binds to and carries oxygen, and it is found very abundantly in red blood cells. The malaria parasite also relies on heme for survival. However, the parasite is also capable of producing its own heme. Dr. Niles wants to figure out how much the parasite needs to make its own heme vs. how much it relies on heme it steals from our red blood cells. Figuring this out will help to figure out whether finding a drug that could block heme production inside the parasite would be a good potential treatment or if that wouldn’t make much of a difference.