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HCMV spread and cell tropism are determined by distinct virus populations

Laura Scrivano1, Christian Sinzger, Hans Nitschko

  • 1Max von Pettenkofer-Institut für Virologie, Ludwig-Maximilians-Universität München, München, Germany.

Plos Pathogens
|January 21, 2011
PubMed

Insights

Human cytomegalovirus (HCMV) exhibits distinct cell tropism based on viral entry complexes. HCMV spread differs between fibroblasts and endothelial cells, revealing cell-specific virus populations and novel insights into HCMV host cell control.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Human cytomegalovirus (HCMV) infects diverse cell types using distinct glycoprotein H (gH)/glycoprotein L (gL) complexes for cell entry.
  • The gH/gL/pUL128-131A complex mediates broad cell tropism, while gH/gL/gO restricts entry primarily to fibroblasts.

Purpose of the Study:

  • To investigate how cell type influences HCMV release and spread.
  • To characterize the tropism of HCMV progeny produced in different cell types.

Main Methods:

  • Comparative analysis of HCMV spread in fibroblast and endothelial cell (EC) cultures.
  • Characterization of virus released from fibroblasts versus ECs regarding infectivity.
  • Assessment of gH/gL/pUL128-131A complex presence on virus particles.
  • Functional assays using ECs or antibodies to deplete specific virus populations.

Main Results:

  • HCMV spread is supernatant-driven in fibroblasts but focal in ECs.
  • Fibroblast-derived HCMV infects both fibroblasts and ECs, while EC-derived HCMV primarily infects fibroblasts.
  • EC-derived HCMV has low EC-infectivity, linked to reduced gH/gL/pUL128-131A complex on particles.
  • Focal spread in ECs results from cell-associated, EC-tropic HCMV.
  • Depletion of EC-tropic virus from fibroblast-derived progeny favors fibroblast infection.

Conclusions:

  • HCMV progeny comprises distinct virus populations with differential cell tropism.
  • Endothelial cells retain EC-tropic HCMV, while fibroblasts release both EC-tropic and non-EC-tropic variants.
  • Host cell-specific retention and release mechanisms significantly control HCMV spread and tropism.

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