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[Does the TT Virus Affect T-cell Subgroups in Patients Undergoing Hemodialysis?]

Overview
Journal Orv Hetil
Publisher Akademiai Kiado
Date 2002 Jun 11
PMID 12053884
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Abstract

Background: Recently many publications have appeared about the new DNA virus, called transfusion transmitted virus (TT virus), first described in 1997. These are mainly about the virus epidemiology, gene sequences and the distribution of different genotypes. In spite of the fact that the prevalence of this type of infection can reach 40 percent rate in polytransfused patients, such as in hemodialysis patients, the real pathogenetic effect of the virus has not yet been known.

Aims: The aim of the authors was to examine the activation and distribution of mononuclear cells in peripheral blood and to analyse the possible changes in Th1/Th2 immune regulatory mechanism through the soluble and intracellular cytokine profile beside the biochemical parameters of hepatic lesions in TT virus positive (n = 32) and negative (n = 17) hemodialysed patients. Healthy blood donors were the control group (n = 20).

Method: Semi-nested PCR was used to detect the DNA of TT virus. For the surface antigen (CD3, CD4, CD8, CD19, CD56, CD3/HLA-DR, CD3/CD69) and intracellular cytokine analysis the authors applied flow cytometric method.

Results: The authors did not find any differences in the liver specific biochemical parameters between TT virus positive and negative hemodialysed and the healthy control group. The number of total T, T helper and total B cells were decreased. The percentage of CD8+, CD3+/HLA-DR+, CD3+/CD69+ and CD56+ cells were increased significantly in both hemodialysed population independently the presence or absence of TT virus. The soluble and intracellular cytokines showed significant growth of the Th1/Th2 cells ratio in hemodialysed patients, which has not been modified by the virus.

Conclusions: From these results the authors assume that the TT virus does not cause any significant changes in the immune regulation, although it could play some role in the pathogenesis of hepatitis by local reaction.