RNA viruses are a tricky bunch. Their replication process is error-prone, which means they mutate quickly — all the better to evade typical antiviral medications. Plus the “one drug, one bug” approach to developing antivirals is slow and costly, and there’s inevitably a new viral threat on the horizon.
So Shirit Einav, MD, Stanford assistant professor of infectious diseases and of microbiology and immunology, is trying a different approach, one that’s not susceptible to drug resistance: making host proteins less hospitable to viruses. She recently led a study showing that a combination of two cancer drugs inhibited both dengue and Ebola in mice. In a lab dish, the combination was also effective against West Nile and Zika viruses.
The drugs erlotinib and sunitinib are used to treat various types of cancers. They also inhibit the activity of two enzymes that strengthen viruses’ bonds to host proteins, regulating their travel inside our cells.
The drug combination was effective in preventing fatal progression of dengue in 65 to 100 percent of mice, depending on the experiment, and in preventing the fatal progression of Ebola in half of them. Each drug was substantially less effective alone.
The study was published online in February 2017 in the Journal of Clinical Investigation.