LMU Professor Katie Mouzakis leads a nationwide team on COVID-19 treatment research
By Shanee Edwards
Assistant professor of biochemistry at Loyola Marymount University, Katie Mouzakis, has two passions: Teaching and scientific research. But with school happening mostly online, it’s the latter passion she’s able to nourish in an exciting way. Having secured a recent $55,000 grant from the Research Corporation for Science Advancement, she’s researching SARS-CoV-2, better known as the virus that causes COVID-19, with the hope of developing a drug to stop the virus, and thus, treat the disease.
But the bubbly professor isn’t new to studying viruses. In fact, she’s been studying them using biochemistry experiments in the lab for 13 years — vital experience that may lead her to become a game-changer in this unprecedented pandemic.
Originally from Rancho Cucamonga, Mouzakis says she’s always loved math and science, but fell in love with chemistry in high school. She attended Harvey Mudd College in Claremont to be a chemistry major, but one day, her world opened up.
“I discovered that things that happen inside a cell are super cool!” Mouzakis says with a laugh.
She switched her major to chemistry-biology and got involved in some exciting scientific research that, “created a love for scientific research” that helped her make the decision to pursue a PhD in biochemistry at the University of Wisconsin-Madison. It was during this time she began studying viruses pretty hardcore.
Mouzakis first started with HIV, the virus that causes AIDS. Later, when she was a professor at Fort Lewis College in Colorado, she studied the HTLV-1 virus that causes a rare form of leukemia. All the techniques she learned then are the same ones she still uses today as she does experiments on SARS-CoV-2.
Since getting the research grant in June, Mouzakis has been leading a team of researchers across America whose goal is to identify drug candidates that target a specific 3D shape in the coronavirus’ genome.
“When the coronavirus enters the [host’s] cell, it deposits a copy of its genome,” she explains.
For humans, our genome is our DNA (deoxyribonucleic acid). But a virus’s genome is much smaller than a human’s and only contains the bare minimum of what it needs to replicate. The coronavirus genome is made of RNA (ribonucleic acid) and is approximately 100,000 times smaller than our genome.
“When the genome of the coronavirus is first added to the cell,” says Mouzakis, “its RNA can be immediately ‘read’ by things inside the cell to make viral proteins. The RNA also folds into different three-dimensional shapes that change how it is read.”
The researchers are trying to figure out how to undermine the stability of those three-dimensional shapes.
“The understanding in the field is that if you change how stable that structure is or which shape it adopts, you change how likely the cellular protein interacting with it is going to do what it’s supposed to do,” she says.
Mouzakis says similar research was done nearly a decade ago, when scientists were studying the SARS coronavirus that appeared in 2003 and began to spread around the world before being successfully contained.
“In the SARS coronavirus from 2003, there is a very similar RNA sequence and shape. It’s nearly 99% identical [to the novel coronavirus that causes COVID-19]. In previous research by other scientists, they found that if you have small molecules that bind to that three-dimensional shape and change its properties, you screw up coronavirus replication. It was bad for SARS in 2003, so theoretically, it should be bad for the novel coronavirus,” says Mouzakis.
To be clear, she and her team of researchers are working to possibly create a type of drug called an antiviral, not a vaccine. Antivirals are drugs you take after you’ve been infected with the virus. The only antiviral for SARS-CoV-2 currently in use is Remdesivir (one of the drugs used to treat President Donald Trump). But she is optimistic about the prospects of several vaccines that other researchers have in the pipeline.
“I think we’re going to end up with some pretty awesome vaccines, and I think that is going to be the key to [restoring] normalcy. We will know about their safety and efficacy data – at least about a small few – probably by January, maybe late December if we are lucky. The roll-out of people getting vaccinated is going to take time because they need to make hundreds of millions of doses. My personal, optimistic viewpoint is that by next summer, we will be back to semi-normalcy. But I don’t think the coronavirus is going away,” she says.
And that’s where Mouzakis’ research comes in. For those who can’t get vaccinated due to an autoimmune disease, or other health risk, a drug to stop the virus is crucial.
The other thing for which she has high hopes is having fast, low-cost COVID testing. “If we could have a cheap (under $1) and fast (under 15 minutes) test, maybe something like a pregnancy test but for COVID, and be able to show people, ‘Here’s my test results’ in 15 minutes, I think that coupled with low community prevalence rates would allow us to open schools safely.”
In the meantime, Mouzakis teaches online when she’s not doing research. Despite having a friend who died from COVID, she’s keeping a positive attitude and is hopeful about the work she’s doing.
“It feels awesome to be trying to make a difference. Even if no one knows who I am, I’m doing something useful and hopefully will make an impact on people’s lives. It’s a pretty nice feeling,” she says.