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A cure coming for the common cold?


Scientists are now one step closer to finding the cure for the common cold. Researchers admit, however, that it's not time to throw away the kleenex yet.

In a major step toward developing that elusive cure, two groups of researchers acting independently claim they have found a way that cold viruses infect human cells. The researchers believe this may lead one day to the development of a drug to prevent--and maybe even cure--many cases of the disease that causes more absenteeism than any other in this country.

"I'm not saying we are going to wipe all colds off the face of the Earth," says Timothy Springer, associate professor of pathology at Harvard Medical School. "But we have made an important discovery." Springer presented his group's findings at a news conference March 9 at the Center for Blood Research in Boston. Another research group, working in tandem with Molecular Therapeutics, Inc., and Miles Research Center in West Haven, Conn., has recorded similar results over a three-year period.

The researchers discovered that about 50 percent of all cold viruses (rhinoviruses) infect human cells by "locking" themselves onto one specific molecule on the cell's surface. This protein molecule, known as ICAM-1, or intracellular adhesion molecule, attaches (or binds) the virus to the inner lining of the cell. The virus is eventually "digested" by the cell and becomes a part of it. The cell repeatedly divides, creating new cells with the cold virus attached. That spread from cell to cell is indeed how you "catch" a cold. To stop this cycle, the scientists made artificial ICAM-1 molecules and added them to a laboratory dish where human cells (DNA) were growing in a fluid. They found that, as the synthetic molecules filled the "pocket" linings of the cold viruses, they also kept most of these cold viruses from invading the human cells.

Although it has yet to be tested on humans or animals, the artificial molecule, if developed properly, could be incorporated into an effective drug to block the passage of certain cold viruses into the human system, say the researchers. As a result, fewer work days could be missed, and children, the people most susceptible to colds, could develop immunities to these viruses without having to "catch" them and thus miss school. More importantly, however, molecular biologists say the research gives a new insight into the relationships between viruses and cells. Cold viruses not affected by ICAM-1 could be thwarted if receptors are found for them.

Likewise, says Dr. Dan R. Littman, assistant professor of microbiology at the University of California at San Francisco, "understanding the architecture of this virus could easily have applications to other, more serious diseases such as AIDS." Because the AIDS virus also attacks human cells by locking onto special receptors, called CD4 molecules, research is now being conducted on ways to block the AIDS virus from infecting immune system cells by testing synthetic versions of the CD4 molecule on AIDS patients to see how well they work against the virus' spread. Littman adds, "This could open some very exciting avenues."

The current findings came about as a result of a 1984 study that linked the spread of cold viruses with a particular receptor that couldn't be named. Another study completed the following year determined that one of the major cold viruses had an exact, three-dimensional shape, thus revealing the shape of the pockets attached to the cell's receptor molecule. It took the Harvard group and the New Haven group, working with opposite approaches, to determine just what the receptor was and how it functioned. The Harvard group worked with nasal cells, while the New Haven group studied the viruses themselves. (Cell, March 10, 1989; 56:839-847; 849-853.)
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Publication:Medical Update
Date:Apr 1, 1989
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