Interactions among viruses can help them succeed inside their hosts or impart vulnerabilities that make them easier to treat. Scientists are learning the ways viruses mingle inside the cells they infect, as well as the consequences of their socializing. Although it is debatable whether viruses are living things, they do compete, cooperate and share genome materials that can sometimes alter their responses to antiviral drugs, result in new variants or play a role in virus evolution. A paper today in Nature Ecology & Evolution by UW Medicine scientists looks at the evolution of poliovirus resistance to a promising experimental antiviral drug, pocapavir. While it seemed counterintuitive, the researchers demonstrated that lowering the potency of pocapavir could improve the situation by enhancing the survival of enough susceptible viruses to continue sensitizing the resistant ones.

The discovery holds the potential to inspire innovations in biotechnology, from the development of new “smart” materials to nanoscale drug delivery systems.

Triple-negative breast cancer (TNBC) is one of the hardest breast cancers to treat because it grows quickly, spreads early and often becomes resistant to therapy. In a new preclinical study, researchers at MUSC Hollings Cancer Center developed a humanized antibody that targets SFRP2 — a protein that helps TNBC tumors survive, grow and suppress the immune system.

The antibody tackled TNBC on multiple fronts. It slowed tumor growth, reduced lung metastases, reactivated exhausted immune cells and shifted macrophages into a tumor-fighting state. Importantly, it killed cancer cells that had become resistant to chemotherapy and concentrated in tumor tissue without harming healthy organs.

These findings suggest that blocking SFRP2 could form the basis of a new precision therapy that strengthens the immune response while avoiding the toxicities of current treatments. The antibody has been licensed to Innova Therapeutics, which is advancing efforts toward future clinical trials.