SILCAAT and ESPRIT: taking stock.

AuthorGazzard, Brian
PositionStudy of interleukin-2 in people with low CD4+ T cell counts on active anti-HIV therapy - Enhanced suppression of the platelet IIb/IIIa receptor with integrilin therapy - Editorial

Shortly after the HIV epidemic became established, it was a strongly held view that the only thing that mattered for understanding HIV pathogenicity was a falling CD4 cell count, as it was this that led to the opportunistic infections and ultimately to death. As we began to understand more about the virus itself and became able to measure its levels accurately, it was commonly remarked that it was 'the virus stupid', implying that the CD4 cell count was irrelevant.

Our understanding of the complexities and the pathogenesis of HIV have increased enormously in the last 20 years or so. I think the results of the SILCAAT and ESPRIT studies reported in this issue of the Journal of HIV Therapy would have surprised many of the early workers greatly. IL-2 induced a very considerable rise in CD4 cell count in both groups of patients, and yet there was no clinical benefit. The French had in fact licensed IL-2 on the grounds that those with low CD4 cell counts at therapy initiation achieved a more rapid CD4 cell count rise when given this drug. It may of course be that the CD4 cells that are produced in response to IL-2 do not work properly, and this is discussed in detail in this issue. It is also possible that the CD4 cell is really a surrogate marker for other important immunological changes that occur during HIV infection and which are not corrected by IL-2 treatment.

An almost bewildering array of new immunological data are emerging that may significantly improve our understanding of AIDS pathogenesis and, indeed, of the pathogenesis of a number of other diseases associated with HIV infection, such as atheroma and...

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