WINSTON-SALEM B In what could be the most exciting advance in the treatment of AIDS to date, Bowman Gray School of Medicine scientists today reported a novel way to block the deadly HIV virus from ever invading white blood cells.
This new strategy, described in the Oct. 1 issue of the journal Nature Medicine, points to a fundamental new way to treat patients with HIV-1 infection or patients with Acquired Immune Deficiency Syndrome (AIDS).
This study, by Si.-Yi Chen, M.D., Ph.D., assistant professor of cancer biology, and his colleagues at Bowman Gray School of Medicine, describes how a critical co-receptor on the surface of particular white blood cells called lymphocytes is blocked, making the cells immune to infection by HIV-1.
HIV-1 virus causes AIDS by invading and destroying the white blood cells whose functions are essential to maintain the human immune system.
Chen's advance is based on the recent discovery of the critical role of chemokine receptors on the surface of the lymphocyte, as the doorway B or co-receptor B for the HIV invasion into lymphocytes.
After virus invasion, the now familiar steps in the development of AIDS follow: multiplication of the virus in the infected cells and the killing of the infected cells, progeny virus spreading to other normal lymphocytes, the decline of the disease-fighting CD4 lymphocytes and the progression to AIDS, and its ultimate downward spiral.
Last year, in another dramatic discovery, a genetic defect in a chemokine coreceptor was found to protect individuals with this defect from HIV-1 infection. These genetically defective individuals remain healthy, because the usual functions of a defective chemokine receptor can be taken over by other receptors because of redundancies in the chemokine family.
So, Chen reasoned, "genetic inactivation of the chemokine co-receptors
should protect lymphocytes from HIV-1 infection and have
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Wake Forest University Baptist Medical Center