The human immunodeficiency virus (HIV) that causes AIDS prospers by hijacking our immune system cells and forcing them to manufacture more copies of itself rather than tend to their infection-fighting duties. But in order to hijack these T cells or macrophages HIV must first penetrate their innermost walls. New research shows that HIV requires a particular protein in the envelope surrounding a macrophage's nucleus in order to slip in and reconfigure the cell's DNA.
Mario Stevenson and Jean-Marc Jacque of the University of Massachusetts first studied macrophages--literally big eaters, which consume infectious agents and other detritus in the body--because they rarely divide. Therefore, the walls of this cell could be studied without having to inhibit it from its natural processes. The scientists knocked out a protein--emerin--and unleashed HIV (seen in a schematic cross-section above) on the cells to see what would happen.
In the absence of emerin, HIV found it difficult to enter its prospective host's nucleus and nearly impossible to effectively insert itself into the nuclear DNA, or chromatin. Without such insertion, the HIV failed to replicate and thus failed to do much of its damaging work. "Our study provides evidence that [HIV DNA], on entering the nucleus, must interact with emerin to contact chromatin," the researchers write in a paper published online yesterday by Nature.
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Study of pharmaceuticals or other molecules that might inhibit the ability of HIV to interact with emerin might provide a new pathway to fighting the scourge, the scientists argue. They also note that Emery-Dreifuss muscular dystrophy results from mutations in the gene that codes for emerin. Sufferers of that disease might reveal compelling evidence of HIV-resistance.
