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UI researchers publish findings on dengue virus

IOWA CITY, Iowa -- University of Iowa researchers now know more about the virus that causes dengue fever, a mosquito-borne illness that affects as many as 50 million people worldwide each year.

In an article in the August issue of Nature Medicine, UI researchers, along with scientists at the University of Michigan, the University of California-San Diego and the University of Otago in Dunedin, New Zealand, describe how the dengue (pronounced DEN-ghee) virus binds to human cells. Moreover, the researchers report that suramin -- a drug used to treat parasitic infections and some forms of cancer -- prevents this binding from occurring.

"This is not a cure, but it's an important step toward developing a potential treatment or vaccine," says Dr. Robert Linhardt, professor of medicinal and natural products chemistry at the UI College of Pharmacy, who led the UI team involved in the study. "Dengue virus is a hot subject right now. There has been a recent outbreak in Cuba and dengue remains a major health risk in Africa, South America, Central America and even some southern areas of the U.S."

The dengue virus, most prevalent in Third World tropical regions but also in subtropical developed countries, causes dengue fever, a severe, flu-like illness. Symptoms include pain to the joints and muscles, headaches, sore throat, fever, running of the eyes and an irritating rash. There is no cure, but recovery usually occurs within several days. Dengue hemorrhagic fever, a potentially deadlier form of the illness, can cause internal bleeding, circulatory failure, coma and shock.

"The ebola virus is another type of hemorrhagic fever," Linhardt says. "Dengue fever can be just as devastating. It's among the worst diseases out there."

Researchers knew from earlier studies that the dengue virus binds to specific molecules in the cells targeted for infection. Linhardt and his colleagues discovered that these molecules are complex sugars known as heparan sulfates, which are found on the surfaces of the target cells and are present in a variety of human tissues.

"These heparan sulfate molecules are present in the liver, which suggests the liver might be one of the initial sites for dengue infection," Linhardt says. "It's possible that the virus targets to specific tissues in the body based on the types of receptors in those tissues."

The researchers also showed that suramin, a well-established drug that mimics the structure of heparan sulfate, prevented the dengue virus from binding to the target cells, thus inhibiting the infection.

Linhardt notes that molecular modeling done at the UI by colleagues Ronald Hileman, a postdoctoral associate, and Jonathan Fromm, a student in the M.D./Ph.D. Medical Scientist Training Program, enabled the researchers to discover the site on the virus where it binds to the cell receptors. Without this site, the virus cannot infect the target cells.

"This gives researchers the potential to make a recombinant form of the virus that would not infect, but generate antibodies that could be used to develop a vaccine," Linhardt says. "Vaccines are relatively inexpensive compared to therapies. Many of the people that are most affected by the dengue virus live in poor, underdeveloped countries. So this could be a major contribution, as well."

8/11/97