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Intrathecal complement activation by the classical pathway in tick-borne encephalitis.

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Summary

Tick-borne encephalitis (TBE) activates the complement system in the central nervous system. Elevated C1q levels in cerebrospinal fluid suggest classical pathway activation, crucial for TBE pathogenesis.

Keywords:
C1qComplementIntrathecal activationTick-borne encephalitis (TBE)

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Area of Science:

  • Neuroscience
  • Immunology
  • Infectious Diseases

Background:

  • Tick-borne encephalitis (TBE) is a significant viral neuroinfection in Eurasia with frequent neurological complications.
  • Immune responses play a critical role in TBE pathogenesis.
  • The complement system, part of innate immunity, is implicated in other flavivirus infections.

Purpose of the Study:

  • To investigate the activation of the complement system in TBE patients.
  • To analyze complement factors in cerebrospinal fluid (CSF) and serum.
  • To correlate complement factor levels with disease severity and outcomes.

Main Methods:

  • Analysis of paired CSF and serum samples from 20 TBE patients and 32 healthy controls.
  • Quantification of complement factors C1q, C3a, C3b, and C5a using ELISA kits.
  • Review of clinical data for disease severity and 6-month follow-up outcomes.

Main Results:

  • Significantly higher concentrations of all analyzed complement factors were found in TBE patients' CSF compared to controls.
  • A marked increase in CSF C1q concentrations (p < 0.001) indicated classical pathway activation.
  • No correlation was observed between complement factor levels and disease severity or long-term sequelae.

Conclusions:

  • Intrathecal complement activation occurs in TBE.
  • The classical complement pathway is activated in TBE, as evidenced by elevated C1q levels.
  • Complement activation in TBE does not correlate with disease severity or neurological sequelae.