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Structural and functional characteristics of lymphocytes in chronic carriers of tick-borne encephalitis virus

N V Ryazantseva1, O B Zhukova, V V Novitskii

  • 1Siberian State Medical University. ryazan@mail.tomsknet.ru

Bulletin of Experimental Biology and Medicine
|June 13, 2003
PubMed

Insights

Tick-borne encephalitis (TBE) infection disrupts immune cells, causing lymphocyte imbalances and reduced DNA repair capacity. These changes are linked to long-term TBE virus persistence and affect the plasma membrane structure.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Tick-borne encephalitis (TBE) is a significant neurological disease caused by the TBE virus.
  • Long-term persistence of TBE virus can lead to chronic neurological complications.
  • Understanding the impact of TBE virus on host immune cells is crucial for managing the disease.

Purpose of the Study:

  • To investigate the effects of TBE virus persistence on peripheral blood lymphocyte subpopulations.
  • To analyze alterations in the plasma membrane structure and microviscosity of lymphocytes in TBE patients.
  • To assess the activity of the DNA repair system in lymphocytes from patients with different clinical forms of TBE.

Main Methods:

  • Flow cytometry for analyzing lymphocyte subpopulations.
  • Fluorescence polarization techniques to measure plasma membrane microviscosity.
  • Assays to evaluate the activity of DNA repair enzymes in lymphocytes.

Main Results:

  • A significant imbalance in lymphocyte subpopulations was observed in TBE patients.
  • Increased microviscosity of the plasma membrane lipid phase was detected in lymphocytes.
  • A decrease in the activity of the DNA repair system was evident in lymphocytes from TBE patients.

Conclusions:

  • Long-term TBE virus persistence is associated with profound immunological dysregulation.
  • Alterations in lymphocyte surface phenotype, plasma membrane properties, and DNA repair underscore the detrimental effects of TBE virus.
  • These findings highlight potential mechanisms contributing to the pathogenesis of chronic TBE.

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