Friday, October 10, 1997
A full recovery?
IMMUNE: The focus of AIDS research is shifting to rebuilding the
immune system. Drug combination produces needed T-cells.
By Kathryn Combs
Daily Bruin Contributor
Until recent advances of HIV drug therapy, the crux of most AIDS
research was to find new ways to slow the progression of HIV
infection into AIDS.
However, since then the focus has turned to the rehabilitation
of the immune system.
UCLA researchers have recently found that the immune system of
HIV-infected individuals may not be damaged beyond repair, in a
study funded by the National Institutes of Health and the Pediatric
AIDS Foundation.
"If we could come up with a potent enough combination of drugs
that will inhibit (HIV) viral replication, that may well be able to
extend the life of an infected person by rebuilding the immune
system," said Dr. Elizabeth Withers-Ward, a biologist with the
Department of Microbiology and Immunology who pioneered this
research.
When an individual becomes infected with HIV, the virus
specifically targets CD4 cells, also known as T-cells. The T-cell
is one of the main players responsible for preventing infections in
humans. So the immune system is rendered ineffective because there
is a drastic decline in the production of these cells.
So the researchers replicated the process of HIV in mice, hoping
to gain insight into the human immune system.
"What we do is take a mouse that can support foreign tissue and
we introduce human thymus tissue into the kidney of the mouse,"
Withers-Ward explained.
The thymus is an organ that is responsible for directing the
production of cells, such as white blood cells, that protect the
immune system against potential infection.
"(The tissue) can then mature into an organ that is for all
purposes like the thymus tissue in a human," Withers-Ward said.
"When we can inject HIV into a mouse … we see the same loss,
the CD4 positive cells are the cells targeted by HIV," Withers-Ward
said.
Triple drug therapy has recently been found to be one of the
most effective therapies for treating HIV. It reduces detectable
levels of the virus in the patient’s blood.
The focus has now turned to whether or not the immune system,
namely the thymus, is able to resume the production of these
T-cells.
"New T lymphocytes should allow the body to fight off other
infectious agents which basically lead to death after HIV
infection," said Dr. Jerome Zacks, professor of Immunology with the
Medical School.
"What actually causes death in HIV patients … is the
opportunistic infection," Zack said, stressing that it is the
consequences of HIV infection, such as pneumonia, that actually
kills HIV patients.
UCLA researchers concluded that the thymus, when treated with a
combination of anti retroviral drugs, is able to return to
effectively produce T-cells.
Ideally, say researchers, they would like to find a drug that
will eliminate all signs of HIV infection.
"Because the drugs that we used are not able to completely
eliminate viral replication, we would need another therapy that
would allow us to inhibit viral replication completely," said Dr.
Rafael Amado, clinical instructor in the Department of Hematology
and Oncology.
Based on these new findings, researchers may be able to develop
more effective therapies to treat HIV by fully restoring the
functioning of the immune system.
"Our current tools to inhibit viral replication are still not
able to fully do so," Amado concluded.