Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
The Associated Press - 26 Sep 1995
Now, researchers say they have identified a little-known gene within the AIDS-causing virus that stops production of the CD4 T-lymphocyte cells. The next step is figuring out how the Vpr gene prevents the disease-fighting cells from dividing.
Researchers hoped the discovery could eventually lead to new AIDS drugs that block the gene's action and allow immune cells to continue multiplying and fighting HIV the same way they battle bacteria and flu viruses.
In the Oct. 1 issue of the Journal of Virology, the scientists at the University of California, Los Angeles, AIDS Institute reported that the Vpr gene contains the blueprint for a protein that interferes with CD4 cells, preventing them from dividing into two identical cells.
These genes go to work while the HIV virus is multiplying in the body and eventually outnumbering the disease-battling "T" cells. Once their immune systems are defeated, patients with acquired immune deficiency syndrome usually die from infections.
Other scientists cautioned that the UCLA work remains preliminary.
"It's a big leap to go from this observation in the laboratory to a statement that Vpr is what's responsible for depletion of the immune system in infected patients," said Dr. Daniel Kuritzkes, co-director of the AIDS clinical trials unit at the University of Colorado Health Sciences Center.
Many AIDS experts contend that the disease's essential feature is the "actual killing of these cells as a consequence of HIV infection," Kuritzkes said. This research didn't demonstrate actual killing, he noted.
Jeremy B.M. Jowett, a study investigator at the AIDS Institute, acknowledging some resistance within the scientific community to the UCLA finding. However, he said researchers have confidence because of additional, unpublished work "which suggests these cells may die once they are prevented from multiplying."
The authors also said the Vpr gene and protein could have important uses in cancer therapies, where the doctors' goal is to block uncontrollable growth of malignant cells.
"If we can figure out how the Vpr gene stops cell replication, then we might be able to create a drug that mimics its effect," against cancerous cells, said study author Irvin S.Y. Chen, director of the UCLA AIDS Institute.
The study was financed by Amgen Inc. of Thousand Oaks, Calif., the National Institutes of Health and Center for AIDS Research, the Leukemia Society of America and the American Cancer Society.
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