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Related Experiment Videos

Is human T-cell lymphotropic virus type I really silent?

B Asquith1, E Hanon, G P Taylor

  • 1Department of Immunology, Imperial College School of Medicine, London, UK. r.asquith@ic.ac.uk

Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
|February 24, 2001
PubMed
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Human T-cell lymphotropic virus type I (HTLV-I) protein expression is rapidly eliminated by cytotoxic T-lymphocytes (CTLs). This efficient immune surveillance explains why HTLV-I appears transcriptionally silent in infected individuals.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • The cellular immune response to human T-cell lymphotropic virus type I (HTLV-I) is not fully understood.
  • HTLV-I is widely believed to be transcriptionally silent in vivo due to low observed protein expression in lymphocytes.
  • Despite low expression, HTLV-I infected individuals exhibit a strong, persistent cytotoxic T-lymphocyte (CTL) response, suggesting active viral gene transcription.

Purpose of the Study:

  • To investigate the dynamic interplay between HTLV-I protein expression and the CTL response in vivo.
  • To reconcile the apparent transcriptional silence with the robust CTL response observed in HTLV-I infection.
  • To determine the efficiency of CTL-mediated clearance of HTLV-I expressing cells.

Main Methods:

Related Experiment Videos

  • Freshly isolated peripheral blood lymphocytes from HTLV-I infected individuals were analyzed for Tax protein expression.
  • Kinetics of Tax protein expression and CTL-mediated cell killing were assessed.
  • Mathematical modeling was employed to quantify the efficiency of the CTL response.

    • Main Results:

    • HTLV-I Tax protein expression was found to increase rapidly in freshly isolated lymphocytes.
    • Cells expressing Tax protein were efficiently and rapidly eliminated by CTLs.
    • Mathematical analysis revealed an extremely efficient CTL response, with a half-life of less than a day for Tax-expressing cells.

    Conclusions:

    • The rapid clearance of HTLV-I Tax-expressing cells by CTLs explains the low, undetectable levels of viral protein in circulating lymphocytes.
    • The cellular immune response, specifically CTL surveillance, plays a critical role in controlling HTLV-I transcription in vivo.
    • Current detection methods may underestimate HTLV-I activity due to the high efficiency of the immune response.