AIDSWEEKLY Plus; Monday, September 21, 1998
Daniel J. DeNoon, Senior Editor
One of the earliest immune dysfunctions in HIV disease occurs early after infection, when oligoclonal expansion of CD8(+) T-cells leads to exhaustion of some cellular immune functions.
Now Guy Gorochov of Pitie-Salpetriere Hospital in Paris, France, reports that CD8(+) subsets can normalize in patients with chronic HIV infection if they fully respond to highly active antiretroviral therapy (HAART).
"A tight control of HIV replication correlates with profound modifications of the CD8 repertoire, which slowly returns to a resting state," Gorochov said in a presentation to the 12th World AIDS Conference, held June 28-July 3, 1998, in Geneva, Switzerland.
Gorochov and colleagues used an "immunoscope" approach to quantifying the perturbation of the CD8(+) T-cell-receptor V(beta) repertoire. Noting that there are 24 V(beta) families and 24 different lengths in the CDR3 receptors of CD8 cells, the researchers assessed CDR3 polymorphism as a marker of V(beta) polymorphism.
They found that untreated patients with chronic HIV infection had skewed CD8 repertoires at all stages of infection. CD8 repertoires remained skewed even after six months of HAART.
The researchers followed five patients for 20 months. Two patients had persistent viremia despite HAART, and three maintained unmeasurable viral loads in response to HAART.
"In patients with chronic HIV infection, the extent of oligoclonal CD8 T-cell proliferation appears to be far greater than has been previously recognized," Gorochov et al. wrote in their presentation abstract. "Nevertheless, 12 months of efficient antiviral therapy are enough for CD8 repertoires to return to normal in the absence of any other active viral infection."
However, Gorochov warned that new perturbations may appear over time.
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