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Journal of Virology, September 1998, p. 7420-7427, Vol. 72, No. 9
Institut für Molekularbiologie Abt.
I,1
Institut für Medizinische
Virologie,2
Biologisches
Zentrallabor,3 and
Institut
für Neuropathologie,5 Universität
Zürich, Zürich, Switzerland, and
Division of
Rheumatology, Department of Internal Medicine, Washington
University School of Medicine, St. Louis, Missouri
631104
Received 2 March 1998/Accepted 8 June 1998
Attenuated Edmonston measles virus (MV-Edm) is not pathogenic in
standard mice. We show here that MV-Edm inoculated via the natural
respiratory route has a limited propagation in the lungs of mice with a
targeted mutation inactivating the alpha/beta interferon receptor. A
high dose of MV-Edm administered intracerebrally is lethal for about
half of these mice. To study the consequences of the availability of a
high-affinity receptor for MV propagation, we generated alpha/beta
interferon-defective mice expressing human CD46 with human-like tissue
specificity. Intranasal infection of these mice with MV-Edm resulted in
enhanced spread to the lungs and more prominent inflammatory response.
Virus replication was also detected in peripheral blood mononuclear
cells, the spleen, and the liver. Moreover, intracerebral inoculation
of adult animals with low MV-Edm doses caused encephalitis with almost
inevitably lethal outcome. We conclude that in mice alpha/beta
interferon controls MV infection and that a
high-affinity receptor facilitates, but is not strictly required for,
MV spread and pathogenesis.
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Measles Virus Spread and Pathogenesis in Genetically
Modified Mice
*
Corresponding author. Mailing address: Institut
für Molekularbiologie Abt. I, Universität Zürich,
Winterthurerstr. 190, 55-L-34a, 8057 Zürich, Switzerland. Phone:
41-1-633 31 17. Fax: 41-1-635 68 64. E-mail:
cattaneo{at}molbio1.unizh.ch.
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