Third International Congress Drug Therapy in HIV Infection 3-7 November 1996 Glasgow, UK

WHAT SHOULD WE BE MONITORING IMMUNOLOGICALLY IN ANTIVIRAL TRIALS OTHER THAN CD4+ T CELL COUNTS

F. Miedema¹, N. Pakker¹, K. Wolthers¹, M. Koot¹, M. Roos¹, L. Meyaard¹, J. Lange², S. Danner² and P. Schellekens^1
1Dept. of Clinical Viro-Immunology, Central Laboratory of the Netherlands Red Cross Blood Transfusion Service and Laboratory for Experimental and Clinical Immunology of the University of Amsterdam; ²Department of Internal Medicine and NATEC, Academic Medical Center; Amsterdam. Plesmanlaan 125, 1066 CX Amsterdam, The Netherlands.

Int Cong Drug Therapy HIV 1996 Nov 3-7;3:Abstract No. 4.1
AIDS 1996, Vol. 10 (Suppl. 2);S3

Preliminary results from the Amsterdam cohort showed that RNA load and T cell function in vitro, as a measure of preserved immunity, very early in infection independently are associated and predict progression to AIDS (de Wolf, Schellekens, Miedema and Goudsmit, submitted for publication). The first goal of antiviral therapy is to suppress viral load as is now mainly measured by serum virus RNA level as much as possible, hopefully reaching levels below the assay detection level. The hope and expectation is that the patient will have a protracted clinical course comparable with the very slow progressors that have extremely low loads and preserved immunity for a long period of time. Given the observations in the natural history, given the above considerations, it may be relevant that anti-duals should also induce indirectly in long lasting restoration of immune function. At present it is still not properly understood what the origin of the CD4+ T cells is that repopulate after treatment. We have observed differences in immunological responses between the different treatment groups. Although treatment with a protease inhibitor resulted in the most persistent elevation of both CD4+ and CDR+ T cell counts, T cell functional improvement was of limited duration. This lack of correlation between T cell repopulation and functional restoration may possibly be explained by a selective outgrowth of non-responding T cells. Finally, CD4+ responses vary considerably between patients, which could be related to the extent of irreversible damage done to the immune system, which could be related to baseline viral load or type of HIV variant present. Using telomere length analyses we recently have obtained data that do not provide evidence for extreme CD4+ T cell turnover, which argues against exhaustion of T cell renewal in HIV infection. Taking this all together, it will be discussed what can be expected of immune restoration after anti-viral therapy.

Presenting author:F. Miedema

1996-11-03
4.1

Originally published in AIDS Volume 10, Supplement 2 and hosted with permission of the publisher Lippincott Williams & Wilkins, 250 Waterloo Road, London, SE1 8RD, UK. Tel: +44 (0)20 7981 0700 Fax: +44 (0) 7981 0701

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