Bacteria and viruses have been fighting microbial battles for billions of years. In a new study, WashU researchers in the Department of Chemistry and the Department of Molecular Microbiology at the School of Medicine have made an important step toward potentially harnessing one of these combatants to control the other.

The team found that two unrelated viruses use the same basic technique to attack bacterial biofilms, sticky clumps of germs that pose a particular threat to human health.

The findings could eventually guide the development of new treatments that use bacteria-killing viruses to treat especially tricky infections in humans, said study co-author Courtney Reichhardt, an assistant professor of chemistry. “Most of the bacterial infections in humans are biofilm infections,” she said. “We’re still a long way from clinical applications, but this is basic science that can help point us in the right direction.”

The study, published in the journal npj Biofilms and Microbiomes, was a collaboration with the lab of Michele LeRoux, an assistant professor of molecular microbiology in the School of Medicine. The lead author is Kristen Amyx-Sherer, a PhD student in Reichhardt’s lab. Co-authors include Amanda Zheng, a senior majoring in biology. The work was funded by the National Institutes of Health after an initial seed grant from the WashU Office of the Vice Chancellor of Research.

The WashU team conducted a series of microbiological and biochemical experiments to identify two bacteriophage (“bacteria-eating”) viruses that could potentially attack biofilms of Pseudomonas aeruginosa, a common cause of pneumonia, urinary tract infections, and infected wounds. The viruses used in the study are strictly focused on bacteria and are incapable of infecting human cells.

Biofilms are especially tricky to treat because bacteria find strength in numbers, Reichhardt explained. “They clump together and coat themselves with a slimy material that protects them from outside threats,” she said. “Biofilms are tolerant to pretty much every antibacterial therapy we throw at them.”

Both bacteria-killing viruses identified by the team naturally produce enzymes that can break down molecules on the surface of the biofilm. Even though the viruses weren’t closely related, they seemed to exploit the same weak spot, a polymer called Psl.

Even though they shared a target, the two viruses had very different effects on a biofilm growing in a petri dish. “One of the bacteriophages was able to completely clear the biofilm, but the other one rearranged the structure of the biofilm without clearing it,” said Amyx-Sherer, who won a poster award from the Mark Shirtliff Biofilm Foundation for her presentation of this work at the ASM Conference on Biofilms in Portland, Oregon, in November. “We expected them to have similar effects, so the difference was shocking.”

The findings could point to new possibilities for fighting infections, LeRoux said. As a next step, researchers hope to find other bacteriophages that also target Psl and learn more about the polymer’s role in the formation of biofilms. They also aim to better understand why only one of the Psl-targeting viruses was able to clear the biofilm. “There haven’t been a lot of studies using bacteriophages to treat biofilms,” she said. “This is an exciting area of research.”