Dengue fever is the most widespread and fastest growing mosquito-borne virus in the world. It infects an estimated 390 million people each year — nearly twice the number of people infected annually by malaria — and unlike malaria, there is no vaccine or treatment.
Despite the severity and worldwide frequency of the disease, dengue fever receives relatively little press in the United States. But soon this trend may change. Just recently an outbreak of dengue fever struck Hawaii’s Big Island and the reach of this tropical disease is expected to spread.
Now, a team of Stanford researchers led by Judith Frydman, PhD, have developed a new way to target the disease by using a drug compound that tinkers with a critical cellular pathway in the host, blocking the virus at multiple steps. Frydman is a professor of biology and of genetics.
A Stanford News story explains:
Frydman’s group focused on Hsp70, a type of protein found in most organisms and known as a “chaperone.” Hsp70’s main job is to help other proteins fold into their functional shape, and to then protect them from damage by environmental stresses. DENV (dengue fever), like many other viruses, also relies on Hsp70, to help replicate the viral genome, and ultimately produce the viral proteins it needs to take control of the host cells and spread infection.
Frydman’s team discovered that using a specific compound to inhibit Hsp70 in human blood cells blocks the virus without harming the cells. This compound is effective against different strains and types of dengue fever and it blocks other insect-borne diseases, including West Nile virus, yellow fever and tick-borne encephalitis.
“Our findings have major implications for our understanding of the interface between viral and chaperone biology, and provide a new way of thinking about strategies to develop a novel class of antivirals,” Frydman said.