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

Controversies in HIV Therapeutics (Symposium 039)

December 16, 2001

  • Use of Structured Treatment Interruptions in Primary Infections
    Abstract 421
    Authored by Philippe Hermans (CHU Saint-Pierre Hosp., Brussels, Belgium)
    View the original abstract


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:

  • Off meds, HIV will spread further in the body -- which will reverse some of the decrease in the amount of HIV that had occurred in the body when on meds.

  • Resistance to antivirals could theoretically occur -- especially with multiple stops and restarts -- leading to the general concern to avoid this approach for people on non-nucleoside-based regimens.

  • This could exhaust the immune system instead of replete it.

  • Increased risk of HIV transmission when the viral load rebounds.

  • So far, a structured treatment interruption in established infection has been disappointing in the hope that this will lead to a lower viral load set point off medication.

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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This article was provided by TheBodyPRO.com. It is a part of the publication 41st Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2001).
 



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