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Membrane related effects in endothelial cells induced by human cytomegalovirus

A G van Geelen1, M E Slobbe-van Drunen, A D Muller

  • 1Department of Medical Microbiology, University Hospital of Maastricht, The Netherlands.

Archives of Virology
|January 1, 1995
PubMed

Insights

Human cytomegalovirus (HCMV) infection causes significant membrane changes and increases procoagulant activity in microvascular endothelial cells (MVEC). This rapid response in vascular endothelium requires direct virion-endothelial cell interaction.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Human cytomegalovirus (HCMV) is a common pathogen with known effects on endothelial cells.
  • Previous studies indicated HCMV increases procoagulant activity in human umbilical vein endothelial cells (HUVEC).

Purpose of the Study:

  • To investigate HCMV-induced membrane perturbation and procoagulant activity in microvascular endothelial cells (MVEC).
  • To compare these effects between MVEC and HUVEC.
  • To determine the mechanism of HCMV-induced membrane response.

Main Methods:

  • Infection of endothelial cells (HUVEC, MVEC) and human embryonal fibroblasts (HEF) with HCMV strains AD169 and VHL-E.
  • Assessment of membrane perturbation using merocyanine-540 incorporation.
  • Measurement of procoagulant activity.
  • Use of inactivated virus and heparin-treated virus to assess interaction requirements.

Main Results:

  • HCMV infection significantly increased membrane perturbation and procoagulant activity in MVEC, more so than in HUVEC.
  • Membrane effects were specific to endothelial cells, not observed in HEF.
  • HCMV induced greater merocyanine-540 incorporation in MVEC membranes compared to HUVEC.
  • Inactivated or heparin-treated HCMV did not induce membrane perturbation.

Conclusions:

  • HCMV rapidly alters the membrane of vascular endothelium, particularly MVEC.
  • Physical interaction between the HCMV virion and endothelial cells is essential for this membrane response.
  • The findings highlight a distinct endothelial cell response to HCMV infection, impacting vascular function.

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