AIDS Strain May Cause
Key Immune Cells to
Commit Suicide
SAN FRANCISCO (Reuters) - The AIDS virus may trick some of the body's immune cells into a kind of mass suicide, suddenly stripping patients of key immune defenses after years of relative good health, according to a new study released Wednesday.
U.S. researchers reported in the journal Nature that their study could provide new clues as to why AIDS patients rapidly sicken and die years after infection, and what types of therapy might stop the precipitous decline.
The study focused on the interaction between HIV and the CD8 T-cells -- known as "killer T-cells" because of their role in fighting off infection.
Unlike CD4 T-cells, the "helper" T-cells which doctors measure as a standard marker for the progress of HIV infection in the body, CD8 T-cells lack the receptor, or chemical doorway, that HIV uses to get into a cell. This makes them immune to HIV infection.
While the number of CD4 T-cells in an infected person's body drops over time, levels of CD8 T-cells can remain stable for years before suddenly plunging -- a sharp drop which gives HIV the chance to multiply even faster.
Researchers Eric Verdin of the University of California San Francisco and Georges Herbein of the Picower Institute for Medical Research at North Shore University Hospital in New York found evidence that a particular strain of HIV that appears in the late stages of HIV disease may prompt the "killer" T-cells to commit suicide.
"Once patients lose their CD8 T-cells, growth of the virus in CD4 helper cells is probably boosted, and more cells will be killed," Herbein said. "So you will have an accelerated decline in overall immune function, until the immune system is exhausted."
Such cell suicide, also known as apoptosis, is usually a normal function. It helps the body get rid of damaged or cancerous cells.
Herbein and Verdin said a type of AIDS virus known as the "syncytium inducing", or SI strain common in the later stages of HIV disease, gets rid of the CD8 T-cells by bringing in another immune cell, the macrophage.
The SI strain binds itself to a molecule known as CXCR4 found both on the CD8 T-cell and on macrophages. When both CD8 T-cells and macrophages are present, the CD8 cells commit suicide.
Verdin and Herbein said the "suicide" of the CD8 T-cells occurred only when macrophages were present, and only when a syncytium-inducing strain of HIV was used.
They said both kinds of immune cells produced a chemical known as tumor necrosis factor, which is supposed to trigger apoptosis.
"It is a surprise that different HIV strains would affect CD8 cells differently, since the virus doesn't infect those cells," Herbein said. "This is a totally new idea."
The researchers said that their results could indicate a new treatment path focused on preventing HIV from binding with CXCR4. This, at least in some cases, could theoretically prevent patients from seeing their condition progress to advanced AIDS.
"Right now, everyone's focused on finding ways to block CCR5," a molecule that allows a cell to become infected by early strains of HIV, Verdin said. "Our research shows that it may be just as important to find ways to stop viruses that bind to CXCR4."