The cells of vertebrates have evolved pathways that act like an internal defense, inhibiting viral infections by preventing replication of the pathogens. Drugs that activate those existing systems suggest a promising novel approach to treating dangerous infections by Zika and other viruses, say researchers from the Vaccine and Gene Therapy Institute at Oregon Health and Science University (OHSU), in Portland.
In a new study published this week in mBio, the scientists report on a novel compound that triggers a cell’s innate antiviral system, inhibiting replication of Zika, Chikungunya, and Dengue viruses.
Recent outbreaks of Zika and Chikungunya infections that began in Latin and South America and spread to other continents—as well as the ongoing presence of Dengue—have spurred disease researchers to search for new antiviral medications. No treatments are available for the three infections, and only Dengue has a vaccine, which is licensed in some Asian and South American countries where the disease is endemic.
The three viruses spread by way of the same mosquito species and elicit similar symptoms. Chikungunya emerged in the Americas in Caribbean islands in 2013, and since then it has infected more than a million people on five continents. Zika was first identified 70 years ago, but a 2015 outbreak that began in Brazil has spread to 50 countries and, according to estimates from the World Health Organization, will infect three to four million people this year. Zika infection during pregnancy can cause severe birth defects, including microcephaly. More than 350 million people are infected with Dengue annually; the virus is a leading cause of illness and death among children in some countries.
Virologist Victor R. DeFilippis, at OHSU, led the work. He predicts that cellular innate immune responses may be pharmacologically harnessed to block infections as a kind of antiviral immunotherapy. “The tools that we need to fight off virus infection are programmed into our cells as a result of evolution,” he says. “I think that’s a potentially lost opportunity for the identification of novel broad-spectrum antiviral strategies.”
