For press releases issued after to Jan. 20, 2012, see http://newsdesk.gmu.edu/category/press-releases/
Sep. 4, 2008
MANASSAS, Va.,—With the publication of a study led by Yuntao Wu, assistant professor in George Mason University’s Department of Molecular and Microbiology, the medical community is one step closer to understanding how the human immunodeficiency virus (HIV) attacks cells in the immune system. AIDS, which is caused by HIV, affected more than 33 million people worldwide in 2007 according to World Health Organization statistics.
In the Sept. 5 issue of the journal Cell, Wu and his collaborators from the National Institutes of Health reveal the covert methods that the virus uses to break a barrier present in human CD4 T-cells, the primary immune cells targeted by the virus. HIV-1 infection causes CD4 T-cell depletion that leads to immunodeficiency and AIDS.
During the six-year study, a team largely comprised of research associates and graduate students, analyzed CD4 T-cells taken from blood and infected with HIV. The researchers found that when HIV binds to the cell surface, it uses a molecule called chemokine coreceptor CXCR4 to send a signal that activates a cell protein known as cofilin. The protein is then used to cut through the cortical actin cytoskeleton (the circular layer that lies just beneath the cell’s outer membrane).
“Similar to a human skeleton, every cell has a cytoskeletal structure that supports the cell, gives it its shape, and provides a force that allows the cell to migrate. For the virus, this layer also presents a barrier,” says Wu. “We never understood how the virus overcomes this barrier to gain access to the center of the cell. Now we know that HIV triggers the mimicking of a cell process that activates cofilin, which cuts and modifies the cortical actin cytoskeleton and permits the virus to cross it.”
Wu notes that the goal of his research was to attain a fundamental understanding of how the virus interacts with cells and the immune system in order to identify new ways to treat the disease. There is still much basic research left to be conducted before the findings from this study produce a clinical benefit. However, he believes that this discovery may later be used to develop a new treatment that could block viral interaction with, or viral alteration of, the cortical actin cytoskeleton.
“Now we have a basic understanding of the parts that cortical actin and cofilin play in all of this. This study really opened avenues for us and we hope to use this information as a foundation for more detailed studies that could lead to the development of new therapeutic tools,” says Wu. “For Cell to publish our findings is a great acknowledgment of the dedication and hard work demonstrated by my students and our group.”
This research was largely funded by George Mason University. Additional support was received from the National Institute of Mental Health and the National Institute of Allergy and Infectious Diseases.
About George Mason University
Named the #1 national university to watch by U.S. News & World Report, George Mason University is an innovative, entrepreneurial institution with global distinction in a range of academic fields. Located in the heart of Northern Virginia’s technology corridor near Washington, D.C., Mason prepares its students to succeed in the work force and meet the needs of the region and the world. With strong undergraduate and graduate degree programs in engineering and information technology, dance, organizational psychology and health care, Mason students are routinely recognized with national and international scholarships. Mason professors conduct groundbreaking research in areas such as cancer, climate change, information technology and the biosciences, and Mason’s Center for the Arts brings world-renowned artists, musicians and actors to its stage.