Evidence for a role of T‐helper type 2 cytokines in the acquisition of human immunodeficiency virus syncytium‐inducing phenotype
- 1 November 1998
- journal article
- research article
- Published by Wiley in European Journal of Clinical Investigation
- Vol. 28 (11) , 930-936
- https://doi.org/10.1046/j.1365-2362.1998.00368.x
Abstract
The objective of the present study was to investigate the relationship between the serum cytokine pattern of T-helper (Th) response and the acquisition of syncytium-inducing (SI) human immunodeficiency virus type 1 (HIV-1) variants in HIV-1-seropositive patients treated with antiretroviral drugs. Serum cytokines of Th1/Th2 responses were analysed in a case–control study of 20 individuals selected from a cohort of HIV-1-infected patients without SI variants at entry, who developed or did not develop SI virus during a prospective follow-up. A group of 10 patients with SI variants at study entry was also evaluated. Serum concentration of interferon (IFN) gamma, interleukin (IL) 2, IL-4 and IL-10 was evaluated by mean of a commercial enzyme immunoassay. Despite close matching for immunological (CD4+ cell count) and virological (p24 antigen, serum HIV viraemia) parameters, SI-converting patients showed at baseline significantly lower serum levels of IL-2 and higher concentrations of IL-4 than those who remained persistently negative for SI variants. Shortly after the phenotype conversion, SI-converting patients were characterized by significantly high serum concentration of IL-4 and by low levels of IFN-γ (Th2-like pattern). Patients with SI phenotype at study entry featured lower mean levels of both IL-4 and IL-10, but mean IFN-γ and IL-2 values were higher, although the clinical and immunological baseline was also poorer and no statistical analysis could be applied. Serum cytokine pattern of Th1/Th2 response differs between patients with NSI and SI phenotype. Our data strongly suggest that the Th2 cytokine pattern could be associated with the acquisition of the SI HIV-1 phenotype.Keywords
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