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Journal of Virology, June 2005, p. 7838-7844, Vol. 79, No. 12
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.12.7838-7844.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Stringent Requirement for the C Protein of Wild-Type Measles Virus for Growth both In Vitro and in Macaques

Department of Infection Biology, Graduate School of Comprehensive Human Sciences and Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba 305-8575, Japan,¹ Department of Virology, Faculty of Medicine, Kyushu University, Fukuoka 812-8582, Japan,² Department of Virology 3,³ Division of Experimental Animal Research,⁴ Department of Pathology, National Institute of Infectious Diseases, Musashi-murayama, Tokyo 208-0011, Japan⁵

Received 15 October 2004/ Accepted 26 January 2005

The P gene of measles virus (MV) encodes the P protein and three accessory proteins (C, V, and R). However, the role of these accessory proteins in the natural course of MV infection remains unclear. For this study, we generated a recombinant wild-type MV lacking the C protein, called wtMV(C–), by using a reverse genetics system (M. Takeda, K. Takeuchi, N. Miyajima, F. Kobune, Y. Ami, N. Nagata, Y. Suzaki, Y. Nagai, and M. Tashiro, J. Virol. 74:6643-6647). When 293 cells expressing the MV receptor SLAM (293/hSLAM) were infected with wtMV(C–) or parental wild-type MV (wtMV), the growth of wtMV(C–) was restricted, particularly during late stages. Enhanced green fluorescent protein-expressing wtMV(C–) consistently induced late-stage cell rounding and cell death in the presence of a fusion-inhibiting peptide, suggesting that the C protein can prevent cell death and is required for long-term MV infection. Neutralizing antibodies against alpha/beta interferon did not restore the growth restriction of wtMV(C–) in 293/hSLAM cells. When cynomolgus monkeys were infected with wtMV(C–) or wtMV, the number of MV-infected cells in the thymus was >1,000-fold smaller for wtMV(C–) than for wtMV. Immunohistochemical analyses showed strong expression of an MV antigen in the spleen, lymph nodes, tonsils, and larynx of a cynomolgus monkey infected with wtMV but dramatically reduced expression in the same tissues in a cynomolgus monkey infected with wtMV(C–). These data indicate that the MV C protein is necessary for efficient MV replication both in vitro and in cynomolgus monkeys.

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