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Plenary Lecture

July 10, 2001


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  • Immune Reconstitution: Translating Immunologic Knowledge into Therapy (Abstract PL8)
    Speaker: B. Autran
    Authored by Autran, B.; Laboratoire D'Immunologie Cellulaire, Hôpital Pitié-Salpêtrière, Paris, France

In this elegant review, Dr. Autran presented the challenges seen to the recovery of the immune system using antivirals. She specifically reviewed the impact of HIV on the T-cell system, which includes both T4 (also called CD4) and T8 (CD8) cells.

She began with a description of how normal T-cell function occurs. Initially, T cells originate in the thymus (thus, the designation of "T" cell) and when they leave, they are considered "naive" cells, meaning that they have not yet encountered the foreign substance that they are programmed against. Once a cell actually encounters its target, it is activated. The cell undergoes active division, and these cells become mainly "effector" cells designed to attack and destroy the target. While effector cells often die soon after this activated state, some of these cells remain, and are then called memory cells, which may live a long time, preserving the memory in case the invader is seen in the future.

In untreated HIV infection, it is noted that naive T cells dwindle over time. This is due to both loss of thymus function/production as well as ongoing conversion of T cells in the blood from the naive state to the activated state, with the death of the effector cells in this ongoing battle. If antivirals are started, both naive and memory T cells regrow, as the attack by HIV is controlled by our antiviral medications. There is also renewed output by the thymus when treatment is started, suggesting that the loss of thymic function may sometimes be reversible. The degree of recovery is directly correlated with the degree of viral suppression, with those having maximal suppression also experiencing the largest recovery in immune function.

There are some people who do not regain CD4 cells during antiviral treatment. This loss of recovery appears to be due to significant damage that was done to the thymus itself, or to other cells involved in the regrowth of CD4 cells. One of the approaches still being tested for people in this circumstance is interleukin 2, or T cell growth factor. Several trials have shown an increase in the number of cells with this treatment, although there is evidence that those most in need -- with the lowest counts despite antivirals -- are also least likely to respond to IL-2.

One of the challenges has been to see if there are ways to assist our immune system in directing it to better control HIV itself. As HIV directly infects activated cells, the initial battle of HIV and our immune system usually results in the infection and destruction of the very cells that our immune system creates to attempt to destroy HIV, since this battle is done by activated cells. Other T cells, directed against many infections, are recovered when antivirals are initiated, since these cells are not specifically destroyed by HIV infection. This accounts for why we can stop prophylaxis against opportunistic infections when there has been sufficient T cell recovery with treatment. However, HIV-specific immunity is not restored when antivirals are given, since these cells are often destroyed.

There have been multiple approaches to seeing if these cells can be restored. The two primary approaches have included use of treatment interruptions, allowing one's own HIV to act as a vaccination, triggering a response of the immune system to hopefully recreate HIV-directed immune function. The other approach is to use lab-created vaccines, which are pieces of HIV used to retrain immune function directed against one's own HIV.

Dr. Autran ended her presentation with a brief mention of several treatment studies now underway testing the ability of vaccinations to restore immune function in combination with antivirals, that together may be helpful in our body control HIV itself.

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