|hiv fitness? what does this mean?
Feb 2, 2004
What does this mean?
HIV Fitness Influences Outcome of Therapy
By David Douglas
The fitness of particular viral strains is of importance in determining the magnitude of viral rebound and viral set point in patients with chronic HIV infection, Swiss researchers report in the December issue of the Journal of Virology.
As lead investigator Dr. Alexandra Trkola told Reuters Health, "the course of natural infection and the efficacy of treatment intervention may be greatly influenced by the fitness of the infecting viral strains since at a reduced replication rate, escape from immune responses and drug resistance will less rapidly appear."
Dr. Trkola of University Hospital, Zurich, and colleagues came to these conclusions after examining HIV isolates from 20 chronically infected patients who took part in a structured treatment interruption (STI) trial. STI led to no clinical relevant improvement in viral load.
Viruses from subjects who, following interruption of antiretroviral therapy (ART), controlled viremia spontaneously, had significantly lower in vitro replication capacities than those from subjects who were unable to effect such control.
Replication capacities correlated with pre-ART and post-STI viral set points.
In terms of coreceptor use, genetic subtype and sensitivity to neutralizing antibodies, virus isolates from subjects controlling viremia were the same as those from subjects who did not.
However, these viruses showed increased sensitivity to inhibition by chemokines. Furthermore, sensitivity to the CCR5 chemokine receptor ligand RANTES (regulated upon activation, normal T-cell expressed and secreted) correlated strongly with their slower replication rates, suggesting, write the investigators, "a marked dependency... on high coreceptor densities on the target cells."
Therefore, Dr. Trkola said, "our data provide substantial evidence that a low replication capacity of patient isolates may be in part triggered by a low affinity interaction of the viral envelopes with the CCR5 coreceptor."
"Thus," she concluded, "the outcome of treatment strategies targeting this interaction will likely vary greatly depending on the efficacy of the interaction with the coreceptor."
J Virol 2003;77:13146-13155
| Response from Dr. Pierone
This is a very interesting study. We know that some strains of HIV are less virulent than others. Why though, what are the cellular mechanisms?
The degree of virulence can be estimated by measurement of replication capacity. Persons infected with virus that has lower replication capacity tend to progress more slowly and have lower viral loads. This study showed that they also have a lower viral load after STI. Not related to this study is the finding that drug-resistant virus tends to have lower replication capacity than wild type virus (the silver lining of viral resistance so to speak).
What this study shows is that one of the reasons that a particular strain of virus may be less able to attack and destroy CD4 cells is because it has less ability to bind to the CD4 cell via the CCR5 coreceptor.
Since drugs that block the CCR5 receptor have entered clinical trials it will be interesting to see how these interactions play out in terms of effectiveness of these new medications. Stay tuned!
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