MANHATTAN, KAN. -- Most people do their best to avoid mosquitoes. But this summer Rollie Clem will play the wary host to his own homegrown swarm of Aedes aegypti, the yellow fever mosquito. He's made a room ready for them, and even a menu.
"Sheep's blood or cow's blood," said Clem, an associate professor of biology at Kansas State University. "This particular species is less finicky than others," so Clem won't need to stock their cages with sweaty socks. (Some mosquitoes won't feed without the persuasive scent of humans in the air.)
Clem, who studies molecular virology, is going out of his way to accommodate A. aegypti in hopes of learning more about how viruses disrupt the programmed death of cells, or apoptosis.
"Millions of cells are dying at any given moment in our body," Clem said. "And that's a good thing."
Programmed cell death is tidier than necrosis, in which injury prompts inflammatory cells to rush in and clean up. In contrast, apoptosis relies on a cell's genes to trigger an orderly disassembly.
It's the body's way of removing tissue that has done its job, such as the webbing between the developing fingers of an embryo, or cells whose DNA is damaged. Malfunctions in apoptosis are associated with cancer, neurological diseases such as Alzheimer's and immune disorders such as AIDS and rheumatoid arthritis.
Though scientists knew of apoptosis as long ago as the late 1800s, interest in the field has intensified only in the last 15 years, Clem said.
"It was very obscure" when he was a graduate student at the University of Georgia in the early 1990s, he said. "Now it's taught to undergraduates."
Clem's current experiment, helped by a grant from the National Institutes of Health, grew from his work with moths that were naturally immune to fatal viruses. Clem chose A. aegypti for this round because it spreads such diseases as dengue fever, the most important of the world's mosquito
Contact: Rollie Clem
Kansas State University