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Journal of Virology, April 2001, p. 3343-3351, Vol. 75, No. 7
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.7.3343-3351.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Roles of Macrophages in Measles Virus Infection of Genetically Modified Mice

Branka Roscic-Mrkic,1 Reto A. Schwendener,2 Bernhard Odermatt,3 Armando Zuniga,1 Jovan Pavlovic,4 Martin A. Billeter,1 and Roberto Cattaneo5,*

Molecular Biology Institute,1 Pathology Institute,3 and Medical Virology Institute,4 University of Zurich, Zurich, and Laboratory of Liposome Research, Medical Radiobiology, Paul Scherrer Institute, Villigen,2 Switzerland, and Molecular Medicine Program, Mayo Clinic, Rochester, Minnesota5

Received 13 November 2000/Accepted 3 January 2001

Knowledge of the mechanisms of virus dissemination in acute measles is cursory, but cells of the monocyte/macrophage (MM) lineage appear to be early targets. We characterized the dissemination of the Edmonston B vaccine strain of measles virus (MV-Ed) in peripheral blood mononuclear cells (PBMC) of two mouse strains expressing the human MV-Ed receptor CD46 with human-like tissue specificity and efficiency. In one strain the alpha/beta interferon receptor is defective, allowing for efficient MV-Ed systemic spread. In both mouse strains the PBMC most efficiently infected were F4/80-positive MMs, regardless of the inoculation route used. Circulating B lymphocytes and CD4-positive T lymphocytes were infected at lower levels, but no infected CD8-positive T lymphocytes were detected. To elucidate the roles of MMs in infection, we depleted these cells by clodronate liposome treatment in vivo. MV-Ed infection of splenic MM-depleted mice caused strong activation and infection of splenic dendritic cells (DC), followed by enhanced virus replication in the spleen. Similarly, depletion of lung macrophages resulted in strong activation and infection of lung DC. Thus, in MV infections of genetically modified mice, blood monocytes and tissue macrophages provide functions beneficial for both the virus and the host: they support virus replication early after infection, but they also contribute to protecting other immune cells from infection. Human MM may have similar roles in acute measles.

* Corresponding author. Mailing address: Molecular Medicine Program, Mayo Clinic, Guggenheim 18, 200 First St. SW, Rochester, MN 55905. Phone: (507) 284 0171. Fax: (507) 266 2122. E-mail: cattaneo.roberto{at}mayo.edu.

Journal of Virology, April 2001, p. 3343-3351, Vol. 75, No. 7
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.7.3343-3351.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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