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Hematopoietic cells from CD155-transgenic mice express CD155 and support poliovirus replication ex vivo

M S Freistadt1, K E Eberle

  • 1Department of Microbiology, Immunology and Parasitology, Lousiana State University Health Sciences Center, 1901 Perdido St, New Orleans, LA 70112, USA. mfreis@lsumc.edu

Microbial Pathogenesis
|September 20, 2000
PubMed

Insights

Poliovirus (PV) replication occurs in hematopoietic cells, including monocytes, which express the poliovirus receptor (CD155). This finding suggests a role for these cells in PV pathogenesis and disease.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • The poliovirus (PV) receptor, CD155, is known, but its role in paralytic disease is unclear.
  • Key questions involve CD155 localization, initial replication sites, and central nervous system (CNS) entry routes.
  • Previous studies showed CD155 on human monocytes, supporting low-level PV replication ex vivo.

Purpose of the Study:

  • To investigate if CD155-transgenic mouse hematopoietic cells express CD155.
  • To determine if these cells support PV replication.
  • To explore the role of hematopoietic cells in PV pathogenesis.

Main Methods:

  • Assessed CD155 expression on hematopoietic cells from CD155-transgenic mice.
  • Quantified PV replication in various hematopoietic tissues ex vivo.
  • Evaluated the effect of pre-culturing and thioglycollate treatment on virus yield.

Main Results:

  • The majority of monocyte/macrophages from peritoneal washes expressed CD155.
  • CD155 was found on 26-32% of bone marrow and spleen cells, including monocyte/macrophages, T cells, and hematopoietic precursors.
  • Various tissues supported PV replication, with increased yields after pre-culturing or thioglycollate treatment.

Conclusions:

  • Hematopoietic cells, including monocytes, express CD155 and support PV replication.
  • The CD155 transgenic mouse model is valuable for studying hematopoietic cell involvement in PV pathogenesis.
  • Findings align with human cell data, supporting the hypothesis of monocyte contribution to PV disease.

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