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Research Article Free access | 10.1172/JCI118915

HIV infection--induced posttranslational modification of T cell signaling molecules associated with disease progression.

I Stefanová, M W Saville, C Peters, F R Cleghorn, D Schwartz, D J Venzon, K J Weinhold, N Jack, C Bartholomew, W A Blattner, R Yarchoan, J B Bolen, and I D Horak

National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. IStefanova@pop.niaid.nih.gov

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National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. IStefanova@pop.niaid.nih.gov

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Published September 15, 1996 - More info

Published in Volume 98, Issue 6 on September 15, 1996
J Clin Invest. 1996;98(6):1290–1297. https://doi.org/10.1172/JCI118915.
© 1996 The American Society for Clinical Investigation
Published September 15, 1996 - Version history
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Abstract

In attempt to elucidate the mechanism of the HIV infection induced T cell unresponsiveness, we studied signal-transducing molecules proximal to the T cell receptor (TCR) in T lymphocytes of HIV-infected individuals. Total amounts of protein tyrosine kinases (PTKs) Lck, Fyn, and ZAP-70 and the zeta chain of the TCR were found significantly decreased in T cells of symptomatic/AIDS patients as well as in T cells of individuals in acute and early asymptomatic stages of HIV infection. Unexpectedly, the detection of Lck, Fyn, and ZAP-70 was reversed after the treatment of cell lysates with dithiothreitol. This suggests that PTKs Lck, Fyn, and ZAP-70 were modified by a mechanism altering the status of sulfhydryl groups. Moreover, this mechanism seems to affect selectively T cells of HIV infected patients since B cell PTKs Syk and Lyn were detected structurally and functionally intact. Interestingly, similar alterations of signaling molecules were not detected in T cells of HIV-infected long-term asymptomatic individuals. Modification of T cell PTKs may thus underlie the HIV-induced impairment of lymphocyte function and may potentially predict disease progression.

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