The Dominant T-Helper Lymphocyte Function of HIV Infected Patients

Éva BARABÁS1, András FALUS2, Károly NAGY1, Viktória VÁRKONYI1, Erzsébet TEMESVÁRI1, Attila HORVÁTH1

1National Institute for Dermato-Venereology, Budapest, Hungary
2Biological Institute, Semmelweis University of Medicine, Budapest, Hungary


In HIV infection, the decrease in the number and functional activity of lymphocytes is accompanied by atopia and an increased level of total IgE and some specific IgE antibodies. This could be explained by the Th2 dominance induced by HIV replication and so a Th1-Th2 switch could have prognostic value. We investigated the characteristic T-helper phenotype dominance and its relationship to cytokine expression and IgE immune response in the early stage of asymptomatic HIV infection. In the separated lymphocytes of i. asymptomatic HIV positive persons; ii. HIV negative homosexuals; iii. atopic patients; and iv. healthy controls, expression of mRNA for IFNg (Th1) and IL-10 (Th2) were determined by semiquantitative RT-PCR. The serum level of antibodies for HIV 1/2 and total/specific IgE were also determined. Transcription of mRNA of IFNg and IL-10 were more pronounced in HIV positive and atopic groups than in the healthy control, without lymphocyte phenotype dominance. In HIV negative persons, however, a significant Th2 dominance was detected. There was no significant difference in the IgE level between the 4 investigated groups. In the HIV positive cases, IL-10 expression and total serum IgE do not support a switch to Th2 dominance. In the atopic group, aside from the total IgE level, down regulation of IFNg was not observed. These results suggest a general activation of the immune system in the early stage of HIV infection. Pathology & Oncology Research, Vol 3, Nr 1, 68-73, 1997

Key words: HIV; Th1; Th2; RT-PCR

Received: Nov 10, 1996; accepted: Dec 22, 1996
Correspondence: Attila HORVÁTH, National Institute for Dermato-Venereology, , Mária str. 41 Budapest H-1085, Hungary; Tel: 361-2660465, Fax: 361-2104874; E-mail:

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