December 16, 2001
It has been noted for years that for people who are on treatment, especially protease-inhibitor-containing regimens, there can be a partial rebound in the growth of HIV infection that may last for years and may not be detrimental. This rebound can also be associated with a stable CD4 count for years. The timing of when to switch versus continue this "failing" regimen has been a critical issue for years. In addition, a few researchers have also explored the role of treatment interruption prior to this switch.
Continuing a failing regimen has at least one major concern -- HIV will only increase the amount of resistance it has to the medications someone is on and, as a result, cross-resistance to other medications will occur. Taking advantage of the stability of the CD4 count during this low-level rebound therefore is in the long term potentially worrisome in terms of the decreased success of the next regimen. Dr. Deeks, a researcher in San Francisco, has presented the results of 20 people who have been monitored during this low-level rebound. They had a viral load of about 5,000 copies, and a CD4 count about 250.
He reported that over time there is a slow rebound in HIV viral load, associated with more resistance during this rebound. However, he also noted a stable CD4 count over time. He then clarified this further, noting that there were two patterns during this circumstance -- one group displayed rapid viral load rebounds, while another group demonstrated a "stalemate" viral load over time, some for longer than three years.
What might allow this stability? What Dr. Deeks has noted, as a result of some studies of viral fitness, is that for some people the HIV that rebounds has quite impaired fitness, and this fitness loss may allow for more CD4 stability.
He then presented the results of a switch in the regimen done after treatment interruption. This group stopped for about 20 weeks. During this stop, the "wild type" virus regrew, resulting in an apparent shift on resistance tests to having more sensitive HIV. What is clear, however, is that the resistant HIV does not disappear but is just overgrown by the more drug-sensitive strains. Despite this understanding, Dr. Deeks noted that for those who had just one new agent added to their new regimen, he was able to reestablish viral suppression. This occurred even for those who had few other active medications available as predicted by resistance testing.
However, there was a risk to this interruption when done in someone with lower CD4 cells (<100), including several who had AIDS-related infections during the few months off. The potential advantage in reestablishing suppression after treatment interruption has led to several randomized studies taking place across the US to see if stopping treatment prior to a change in a regimen can increase the success of the new regimen as compared to just switching regimens.
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