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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

Kaoru Takeuchi,1* Makoto Takeda,2 Naoko Miyajima,3 Yasushi Ami,4 Noriyo Nagata,5 Yuriko Suzaki,4 Jamila Shahnewaz,1 Shin-ichi Kadota,1 and Kyosuke Nagata1

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.

* Corresponding author. Mailing address: Department of Infection Biology, Graduate School of Comprehensive Human Sciences and Institute of Basic Medical Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan. Phone: 81-298-53-3472. Fax: 81-298-53-3472. E-mail: ktakeuch{at}md.tsukuba.ac.jp.

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.



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