The Body Covers: The XIII International AIDS Conference
Management of HIV Disease in Real Life
July 12, 2000
Full plasma viral load suppression is needed to achieve an optimal CD4 response among patients receiving triple-drug antiretroviral therapy (WeOrB609)
Several studies have been presented in the last year showing the stability of the CD4 count even after viral loads rebounds towards the set point. In one study this stability was shown to last as long as three years. As a result, there has been some discussion as to what differences there truly are in those with a viral load below detection, versus those whose viral loads are continually below detection. This study explored the CD4 responses of those whose viral loads remained below 500 copies, versus those who had achieved this degree of suppression but later came back up to a detectable level. Both of these groups were also compared to what happened if the person never achieved a viral load below 500 copies. The study was done from the always-productive group led be Dr. J. Montaner group in Vancouver, Canada.
Overall, Montaner's group noted an advantage for people whose viral loads remained below 500 copies versus those who rebounded in terms of the CD4 count response. The increase in CD4 counts were best in those with continuous viral suppression (240 cells after one-two years), while those with a viral load rebound after going below detection only had a 150-cell increase in that same time, which was a statistically significant difference. Those whose viral loads never went below 500 copies saw a net loss of 20 cells during this same time. This study serves largely as a reminder of what we have seen from studies in the past years, which is that the immune system does the best -- at least as measured by CD4 count increases -- when the viral load is maximally suppressed. Partial suppression is still beneficial, and if this is the best that can be achieved, there is clear benefit as compared to those without viral control. However, this study serves to reinforce the desirability of maximal suppression when it can be achieved on a tolerable regimen.
The natural history and clinical significance of intermittent virological "blips" in patients who attain an initially undetectable viral load (VL) on HAART (WeB610)
A few studies were presented here which explored the impact of transient viremia in those whose viral loads were below detection. The episodes of viremia have been called "blips" although there is as yet no agreed to definition as to what can be called a blip. While some studies presented here show that most who have low-level viremia, for example less than 500 copies, will have a viral load below detection on the next test (see MoPpB1019 and TuPeB3195). This study defines "blips" as any degree of viral load rebound after having a viral load below 400 copies, and then having the next viral load go below 400 copies. They compared the longer-term outcome of those whose viral loads stayed below 400 copies, versus those who had one or more episodes of a viral load over 400 copies. The study was done with a cohort of 765 people in Europe.
They noted that about 16% of their group had a blip in viral load at some point. The median viral load of a blip was around 1,000 copies, but 12% had a viral load over 100,000 copies, more likely representing stopping medications than a viral load rebound despite staying on medication. In follow-up, the researchers noted that those who had blips were about twice as likely to have eventual viral loads over 400 copies that did not go back down on that regimen. For example, they reported that about 20% of those with a blip versus 10% without blips had eventual viral load rebound that no longer were suppressed on that regimen.
How do we put these three studies together? One theme that emerges is that while on a regimen, a substantial minority will observe a viral load above detection at some point. With low level viremia, it is likely that the next viral load will once again be below detection. This was noted particularly in those whose viral loads were below 50 copies, a level below which resistance to antivirals occurs only rarely. However, higher level viremia in this study was associated with an increased risk of developing resistance or no longer staying suppressed on that regimen. There are other factors that will need to be explored, including differences between regimens, as well as looking at both the frequency of blips, in addition to the peak of the viral load during the blip. Nonetheless, these studies give us some guidance in how to monitor those on antivirals.
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