A new research could offer vital insight into the mechanism of dengue virus entry into cells and in the process aid vaccine and clinical drug development.
Despite its heavy toll, the prevention and clinical treatment of dengue infection has been a "dramatic failure in public health compared to other infectious diseases like HIV," Ping Liu of the University of North Carolina at Chapel Hill, said.
The research is set to be presented at the 58th Annual Biophysical Society Meeting, which takes place in San Francisco from Feb. 15-19.
Specifically, Liu, a postdoctoral scholar in the laboratories of cell biologist Ken Jacobson and biophysical chemist Nancy Thompson, along with dengue fever expert Aravinda de Silva, used high-resolution microscopes to examine the expression of a particular protein, known as DC-SIGN (for dendritic cell-specific intercellular adhesion molecule-grabbing nonintegrin), on the surface of immune system cells called dendritic cells.
The normal role of DC-SIGN is to capture pathogens so that fragments of those pathogens can be presented as antigens on the surface of the dendritic cells. Such antigens then are recognized by T cells-the workhorse cells of the immune system-"which is one of the first steps in the normal immune response," Liu said.
While it has been known for some time that dengue used DC-SIGN to attach to cells, Liu and her colleagues used high-resolution microscopy to study exactly how the viruses used the protein to gain entry into cells.
"DC-SIGN has a unique carbohydrate recognition domain on its extracellular portion, which binds to all sorts of carbohydrates on pathogens," she said.
Other pathogens, including HIV and the bacterium that causes tuberculosis, are likely to use the same back door.
"An effective medication or vaccine should stop the process of dengue virus entry into cells," Liu said.
