Keeping up with University of Alaska Anchorage biochemist Megan Howard is no easy task, especially if it's early in the morning and she's had coffee. She walks fast, talks fast, and is intensely excited about her work.
(She also fences for exercise, and pedaled a bike cab in Denver for a few years.)
We start in her office. I'd heard she was an expert on coronaviruses, called that for the crown-like spikes on their surface. Middle East Respiratory Syndrome, or MERS, percolating now in Iran, is a coronavirus. Your last cold might have been caused by a coronavirus.
In fact, until Severe Acute Respiratory Syndrome -- yes, another coronavirus -- emerged in southern China in 2002 to infect about 8,000 and kill almost 800 people in 37 different countries, scientists thought all a coronavirus could do to a human is give you a cold.
In 2002 as a graduate researcher at the University of Colorado Health Sciences Center, Howard was tapped to unravel how SARS got so lethal.
"I studied how the SARS virus enters cells. Like other human coronaviruses, it has a fusion protein -- that's the protein that binds to the human cell and allows the virus to enter."
Little was known about how these proteins worked. But even as an undergrad at Case Western Reserve in Cleveland, Howard had migrated from chemical engineering to chemistry to biochemistry, drawn by the power of proteins.
"They look exactly like a turbine. I'm like, wow, that is exactly like a water turbine you see in dams. But it's on a molecular level, and there are 1,000 of them in every cell of your body."
The hidden energy in viral proteins, especially, caught her attention.
"Think of a spring, tensed on a hair-trigger. It's got energy in the spring, but no energy holding it there. It's balanced, just so ... If it's sitting on a desk, and you hit that desk, it's going to cause that spring to unleash all its energy."
Viruses with fusion proteins have that same, trapped energy, she says. Any sudden change, and the protein changes its structure and is suddenly capable of invading the human cell.
The next minute, she's drawing me an HIV retrovirus. "There's the fusion protein there, looking like a spike with a squiggle on two ends," she says. "If its trapped energy suddenly releases, those two squiggles fold over on each other, the protein modifies and it's soon entering a human cell."
Scientists now realize that many viruses have this same kind of fusion protein, whether you're talking influenza, Ebola or measles.
"If we can stop the virus by inhibiting this trapped energy section, this movement," Howard says, "then the virus is going to stay on the outside of the cell long enough for the immune system to come by and get rid of it."
That's the hope, and it's working with HIV medications like T20, which can stop that energy release long enough for the immune system to react. But there's lots more work to be done; the drug that inhibits an HIV retrovirus won't do the trick for Ebola or influenza or other newly emerging diseases.
Howard's main role at UAA is not research, but teaching. She coordinates all the undergraduate microbiology labs, lectures in microbiology and infectious disease courses, and teaches pre-med and pre-nursing students. But she's squeezing research in on the side, including a collaborative project with the U.S. Forest Service and the Alaska Department of Fish and Game, gathering some of the first information ever on Alaska bats.
Howard finds bats fascinating; they play host to many diseases, but don't catch the disease.
"We hypothesize that their immune system is highly active all the time," she says. "If they are infected with a virus, it can be replicating at a very low level. We find the virus in their blood, their tissue, on their surface, wherever it happens to be. But it has no negative effect on them."
Alaska's insect-eating bats are potential carriers of coronaviruses. Howard and her colleagues will soon find out. All summer long, university and agency scientists and technicians have been netting bats around Southcentral Alaska, taking blood and tissue samples and body swabs before releasing them.
An initial driver of the research was the devastating sweep of White Nose Syndrome, a fungal infection that has wiped out nearly seven million bats in the Lower 48 since 2006, mostly in the Northeast. Do Alaska's bats have it? If not, might Alaska be a last safe refuge?
But even more startling now comes Ebola, the filovirus that has migrated from fruit bats to humans in West Africa, killing nearly 2,000 as it rages across five countries. While there is no risk of catching Ebola from an Alaska bat, Howard says, better understanding how bats evade the diseases they carry could shed light on how humans could also avoid them.
Kathleen McCoy works at UAA, where she highlights campus life through social and online media.
Alaska Dispatch Publishing