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CD8+ T Cells Play Central Role in Fighting HIV

CD8+ T Cells Play Central Role in Fighting HIV

VANCOUVER, BC--CD8+ T cells appear to play a central role in the
body's strategy for fighting HIV, particularly in those patients
known as long-term non-progressors or long-term survivors who
remain well for many years despite being infected with HIV.

New research presented at the 11th International Conference on
AIDS suggests two separate mechanisms by which CD8+ cells suppress
HIV, but the specific suppressive factor (or factors) secreted
by CD8 has not yet been identified.

Work by Drew Weissman, MD, PhD, and his colleagues at the NIH
show that CD8+ T cells function differently in HIV-infected subjects
than in uninfected controls. These researchers developed an in
vitro system that models the paracortical region of the lymph
node by using dendritic cells to activate CD4+ T cells (without
additional mitogen). This mimics the situation in the lymph nodes
where most HIV replication and spread are now thought to occur.

Dr. Weissman tested CD8+ cell activity in two systems. One used
dendritic cells and CD4+ T cells from uninfected people. Their
T cells were pulsed with HIV as an "acute infection"
model. The other approach used dendritic cells and CD4+ T cells
from HIV-infected subjects as an "endogenous infection"
model. In both models, CD8+ T cells were added at the initiation
of culture.

The CD8+ cells produced two forms of suppressive activity. One
factor suppressed HIV replication in chronically infected CD4+
T cells. This factor was produced by CD8+ T cells from both infected
and uninfected subjects, but the ability to produce it appears
to be lost as HIV infection progresses.

The second factor suppressed HIV replication during acute infection.
It was produced only by CD8+ from HIV- infected subjects. This
suppressive activity was seen even in CD8+ cells from patients
with advanced HIV disease.

CD8+ cells from uninfected subjects actually enhanced viral replication.
Pretreatment of CD8+ cells with gamma irradiation wiped out the
suppressive factor that blocks acute HIV infection but not the
one that blocks HIV replication in chronically infected cells.


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