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Analysis of Cell Cycle Position in Mammalian Cells
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Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

Unscheduled cyclin B expression and p34 cdc2 activation in T lymphocytes from HIV-infected patients

G Piedimonte1, D Corsi, M Paiardini

  • 1University of Messina Centro di Patologia Comparata dei Retrovirus, Messina, Italy.

AIDS (London, England)
|July 23, 1999
PubMed

Insights

HIV infection disrupts normal cell cycle regulation, causing increased cyclin B and p34 cdc kinase expression in lymphocytes. Antiretroviral therapy effectively reverses these changes, restoring cell cycle homeostasis.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Human Immunodeficiency Virus (HIV) infection is known to affect immune cell function.
  • Cell cycle regulation plays a critical role in lymphocyte proliferation and homeostasis.

Purpose of the Study:

  • To investigate the role of cell cycle regulators, specifically cyclin B and p34 cdc kinase, in HIV infection.
  • To examine the in vivo and in vitro expression patterns of these proteins during HIV infection and their response to treatment.

Main Methods:

  • Western blot analysis of cyclin B expression in CD4 and CD8 cells from HIV-infected and uninfected individuals.
  • Sequential analysis of patients undergoing antiretroviral therapy (ART).
  • In vitro studies of lymphocyte activation with phytohaemagglutinin (PHA) to assess cyclin B and p34 cdc kinase expression and activity.

Main Results:

  • Persistent overexpression of cyclin B was observed in both CD4 and CD8 cells of untreated HIV-infected patients.
  • Lymphocytes from HIV-infected patients showed premature expression of cyclin B and p34 cdc kinase during the cell cycle.
  • Effective ART led to the reversal of both in vivo and in vitro cyclin B overexpression within 2-4 weeks.

Conclusions:

  • HIV infection is associated with increased and unscheduled expression of cyclin B and p34 cdc kinase in lymphocytes.
  • These cell cycle alterations correlate with HIV viremia and may contribute to lymphocyte dysfunction and apoptosis.
  • Antiretroviral therapy can restore normal cell cycle regulation in HIV-infected individuals.
Abstract

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