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Journal of Virology, June 2006, p. 6084-6092, Vol. 80, No. 12
0022-538X/06/$08.00+0     doi:10.1128/JVI.00357-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Receptor (SLAM [CD150]) Recognition and the V Protein Sustain Swift Lymphocyte-Based Invasion of Mucosal Tissue and Lymphatic Organs by a Morbillivirus

Veronika von Messling,1,2 Nicholas Svitek,2 and Roberto Cattaneo1*

Virology and Gene Therapy Graduate Track, Mayo Clinic College of Medicine, Rochester, Minnesota 55902,1 INRS-Institut Armand-Frappier, University of Quebec, Laval, Quebec, Canada2

Received 20 February 2006/ Accepted 29 March 2006

Experimental infections of ferrets with canine distemper virus (CDV) recapitulate many hallmarks of measles: rash, high fever, viremia, depression of delayed-type hypersensitivity responses, lowered leukocyte counts, and reduced lymphocyte proliferation activity. To understand how a morbillivirus invades the host and causes immunosuppression, we generated CDV either unable to recognize one of the receptors or incapable of expressing either one or both of the candidate interferon antagonist proteins V and C. Variants of these viruses expressing green fluorescent protein were also generated. Striking similarities between CDV infection of ferrets and human immunodeficiency virus host invasion were documented: first, massive early replication in the gut-associated lymphatic tissue, including intestinal Peyer's patches, followed by extensive infection of lymphatic organs, including thymus and circulating lymphocytes. Moreover, T cells were selectively depleted. Thus, CDV takes advantage of mucosal surfaces for host invasion and lymphocytes for swift dissemination. A CDV unable to recognize the signaling lymphocytic activation molecule (SLAM [CD150]) that is expressed in lymphocytes and other immune cells did not spread. A V-defective CDV multiplied with reduced efficiency in lymphocytes and did not inhibit the interferon and cytokine responses. Protein C affected the severity of rash and digestive symptoms elicited by V-defective CDV, but it was dispensable for the invasion of the lymphatic organs. These findings prove formally that SLAM recognition is necessary for morbillivirus virulence. They also reveal how two viral proteins affect pathogenesis: V sustains the swift lymphocyte-based invasion of mucosal tissue and lymphatic organs, whereas C sustains subsequent infection phases.

* Corresponding author. Mailing address: Mayo Clinic Rochester, Molecular Medicine Program, Guggenheim 1838, 200 First Street SW, Rochester, MN 55902. Phone: (507) 284-0171. Fax: (507) 266-2122. E-mail: Cattaneo.Roberto{at}mayo.edu.

Journal of Virology, June 2006, p. 6084-6092, Vol. 80, No. 12
0022-538X/06/$08.00+0     doi:10.1128/JVI.00357-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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