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The Body Covers: The 41st Interscience Conference on Antimicrobial Agents and Chemotherapy

Controversies in HIV Therapeutics (Symposium 039)

Coverage provided by Calvin J. Cohen, M.D., M.S.

December 16, 2001

This talk reviewed the potential to "autovaccinate" those who have HIV infection. For the past few years, it has been known that some HIV-positive people can maintain a low viral load and stable CD4 counts without treatment. These people, called "long-term non (or slow) progressors," appear to have an immune system able to control HIV. The challenge has been for us to understand how their immune function differs from that of most people with HIV, where HIV steadily grows, leading to damaged immune function and, ultimately, illnesses from this loss. What we have learned suggests that these "slow progressors" have cells that are more capable of controlling HIV replication. With most other people, these cells are usually lost in the initial battle between the immune system and HIV. Why this group emerges from this battle with these cells intact is still uncertain.

When we treat with antivirals, we are often able to accomplish with medication what the immune system is rarely able to do -- shut off HIV growth. The challenge has been to explore ways to "reeducate" this now healthier immune system to control HIV without the need for medication.

Structured (or supervised) treatment interruptions (STI) have been explored for a few years as a way to use someone's own HIV as a vaccination by stopping the medication at specific times with the hope that this might, as with other vaccines, recreate certain cells that could some day help control HIV itself.

What has been noted is that HIV comes roaring back when people with established HIV infection go on treatment and later stop. Simply treating HIV does not recreate cells that can control HIV. However, for people who start treatment soon after initial infection (called "primary infection") and then stop this treatment, it has been noted that, while the viral load will return, it will settle at lower levels, especially after a few cycles of treatment and stopping.

In these studies it was reported that at least half of the time, a person's viral load will wind up somewhere below 5,000 copies, a level considered low enough to have minimal damage from HIV even if untreated for years. However, this presentation presented a few instances where, despite a very low viral load off treatment, there still was a loss of CD4 cells. This was associated with an activation in CD8 cells, and was otherwise unexplained.

Are there concerns with treatment interruption? Can treatment interruption be successful when done for those with established HIV infection? The presentation listed several concerns for the field:

Nonetheless, there are continued reasons to explore whether or not structured treatment interruption can improve immune function, including the hope that time off antivirals may lead to less adverse events associated with long term use. Many questions remain, however, for how to best recreate an effective immune response -- including understanding which patients may respond, how long we must initially treat with antivirals before stopping, how to judge when to stop and when to restart, and then how long to retreat before stopping again. Fortunately, several research groups are tackling these issues so that in time we may have answers to more of these questions.

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