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Cellular Target Of Leprosy, Deadly Viruses Found

December 11, 1998--A cell-surface protein whose absence causes a fatal form of muscular dystrophy is also the target that the leprosy bacterium uses to latch onto cells before invading them. And in an equally surprising twist, it also appears that two hemorrhagic fever viruses gain entry to cells via the same molecular handle.

These discoveries could lead to new drugs to prevent nerve damage in leprosy patients and to thwart infection by the deadly viruses, according to two research teams that reported these findings in two articles in the December 11, 1998, issue of the journal Science. One team included scientists from the Howard Hughes Medical Institute (HHMI) at the University of Iowa and The Rockefeller University in New York. The second team included scientists from The Scripps Research Institute and the same HHMI group.

About 800,000 people worldwide suffer from leprosy, which is caused by the bacterium Mycobacterium leprae. Hemorrhagic fever viruses infect about 250,000 people and cause 5,000 deaths worldwide each year.

The molecular handle used by the bacterium and viruses is called dystroglycan (DG). It belongs to a common family of molecules called glycoproteins, which are often embedded in cell membranes.

DG is the cell-surface component of a group of associated proteins known as the dystrophin-glycoprotein complex. Originally identified by HHMI investigator Kevin Campbell and his colleagues, this complex nestles in the membrane of cells throughout the body, acting as a receptor for a protein called laminin. Laminin, in turn, links cells to the scaffolding, or matrix, that helps knit together the body's tissues.

When the complex is absent, cells do not interconnect properly with the matrix outside the cell. Duchenne muscular dystrophy, a fatal inherited disease, is caused by a genetic lack of dystrophin. The muscle cells of people with
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Contact: Jim Keeley
keeleyj@hhmi.org
301-215-8858
Howard Hughes Medical Institute
11-Dec-1998


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