(RedOrbit) Researchers at the National Institute of Allergy and Infectious Disease (NIAID) have identified a molecule called xCT which is found on the surface of human cells and is involved in aiding infection by Kaposi’s sarcoma herpesvirus (KSHV.) The virus causes Kaposi’s sarcoma, a major HIV/AIDS-related cancer, as well as certain forms of lymphoma.
The function of xCT in normal cells is to transport molecules necessary for protecting against stress into cells. When cells are stressed, they express more xCT on their surfaces.
When the body becomes infected with KSHV, however, expression of xCT at the cell surface increases. This suggests that the virus facilitates its own infectivity and dissemination in the body by inducing a physiological state that results in an increased number of its own receptor.
The research, published in the March 31, 2006 issue of Science by NIAID research fellow Johnan Kaleeba, Ph.D. and senior investigator Edward A. Berger; Ph.D., describes how the molecule xCT is a major gateway that KSHV uses to enter human cells.
“Understanding the mechanisms of cell entry of Kaposi’s sarcoma herpesvirus is a landmark achievement in and of itself,” says NIAID director Anthony S. Fauci, M.D. “but the connection between the virus and expression of its own receptor on a cell is even more provocative because it might change the way we think about KSHV-associated diseases and their treatment.”
Dr. Berger’s work is the result of a decade-long journey of studying how viruses enter cells which has resulted in the identification of other coreceptors that allow HIV to gain entry into cells of the immune system, such as CXCR4 and CCR5.
This study is important because it may lead to new avenues for treating KSHV, enable scientists to study whether levels of xCT determine disease severity or even help explain why certain groups are more at risk for Kaposi’s sarcoma, based on the level of expression of xCT in their cells.
According to Dr. Kaleeba, “our finding provides a new perspective on the disease. Hopefully this will be the beginning of exciting new directions in this field, as it is likely to provide a useful framework for integration of the cell biology and epidemiology of this clinically important virus.”
By Karen Ventii of RedOrbit from Wire reports
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