Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.
Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.
Reuters NewMedia, Inc. - Wednesday October 1 5:23 PM EDT
Maggie Fox, U.S. Health and Science Correspondent
Both centered on cytokines -- the immune system signalling chemicals the human immunodeficiency virus (HIV) depends on to get into the immune system cells that it infects.
Researchers have found that HIV needs a number of different receptors, or chemical doorways, to get into cells. Many of the receptors are the same ones that cytokines use.
In a study published in the Oct. 1 issue of Nature Medicine, David Weiner and colleagues at the University of Pennsylvania medical center said HIV may suppress the production of cytokines in its victims, thus killing off its enemies before they are even born and freeing up the receptors for its own use.
They found that AIDS viruses produce a protein known as Vpr, which blocks production of cytokines in the cells it infects.
"In the test tube, Vpr suppresses production of the cytokines needed to fight any infection, bacterial or viral," Weiner said in a statement.
Vpr also prevents the infected cells from committing suicide in a process known as apoptosis -- the programmed cell death that is meant to protect the body from just such infections and from cancer.
"So those cells can stay alive to make more virus. And then it kills the uninfected cells that would otherwise be involved in providing immune protection," Weiner said.
But Weiner's group said they may have found a way to block this process. They noted that certain drugs act in the same way as Vpr and tried out the steroid RU-486 -- sold as an abortion drug in Europe.
"When we added RU-486 to our cell cultures, it markedly reversed many of the effects of Vpr," said Valpandi Ayyavoo, who led the study.
"These results suggest that steroids should be considered for development as potential HIV therapies."
Si-Yi Chen, a cancer biologist at the Bowman Gray school of medicine in Winston-Salem and colleagues took a completely different approach. They said they may have found a way to stop HIV from ever infecting immune cells in the first place.
Many teams have tried to find a way to block the receptors that both cytokines and HIV use to get into cells -- but efforts to do so have so far failed.
Chen's group tried to model people who have a genetic mutation that seems to make them naturally immune to HIV infection.
They homed in on the CXCR-4 receptor -- one of several receptors used by both the AIDS virus and cytokines.
They genetically altered the immune system cells so that they could produce the CXCR-4 receptor, but could never get it to their surface -- so then HIV could not find it to latch onto.
They used an intrakine -- an internal cell molecule that attaches itself to the CXCR-4 molecule and held it inside the cell.
"The genetically modified lymphocytes are immune to ... virus infection but appear to maintain normal biological activities," they wrote.
The genetically modified lymphocyte immune cells live for months or years, so Chen's group hope the approach might offer a long-lasting HIV therapy.
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