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CD44 is not required for poliovirus replication

M J Bouchard1, V R Racaniello

  • 1Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.

Journal of Virology
|April 1, 1997
PubMed
Summary
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The cell surface protein CD44 and its mouse homolog Pgp-1 are not essential for poliovirus replication. This study found no evidence that CD44 plays a role in poliovirus infection or pathogenesis.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • The cell surface protein CD44 was hypothesized to be an accessory molecule for poliovirus receptor (Pvr) based on antibody binding studies.
  • Previous research suggested CD44 might influence poliovirus binding to cells.

Purpose of the Study:

  • To investigate the role of CD44 in poliovirus infection and replication.
  • To determine if CD44 is necessary for poliovirus binding and pathogenesis.

Main Methods:

  • Utilized monoclonal antibodies to assess poliovirus binding to cells expressing CD44.
  • Analyzed poliovirus replication in human and mouse neuroblastoma cells with varying CD44 and Pgp-1 expression levels.
  • Measured binding affinity of poliovirus serotypes to Pvr in the presence or absence of CD44.

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Main Results:

  • Only antibody AF3, not A3D8 or IM7, blocked serotype 2 poliovirus binding.
  • All three poliovirus serotypes replicated normally in cells lacking or expressing CD44, and in cells lacking Pgp-1.
  • The presence or absence of CD44 did not affect the binding affinity of poliovirus serotypes to Pvr.

Conclusions:

  • CD44 and its mouse homolog Pgp-1 are not required for poliovirus replication.
  • CD44 is unlikely to be involved in poliovirus pathogenesis or serve as a crucial co-receptor for Pvr.