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Journal of Virology, December 2004, p. 13479-13488, Vol. 78, No. 24
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.24.13479-13488.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Coxsackievirus B3 Infection Induces cyr61 Activation via JNK To Mediate Cell Death

Sun-Mi Kim,1,{dagger} Jung-Hyun Park,1,{dagger} Sun-Ku Chung,1 Joo-Young Kim,1 Ha-Young Hwang,1 Kwang-Chul Chung,2 Inho Jo,1 Sang-Ick Park,1 and Jae-Hwan Nam1*

Department of Biomedical Sciences, National Institute of Health,1 Department of Biology, College of Science, Yonsei University, Seoul, Korea2

Received 14 May 2004/ Accepted 29 August 2004

Coxsackievirus B3 (CVB3), an enterovirus in the Picornavirus family, is the most common human pathogen associated with myocarditis and idiopathic dilated cardiomyopathy. We found upregulation of the cysteine-rich protein gene (cyr61) after CVB3 infection in HeLa cells with a cDNA microarray approach, which is confirmed by Northern blot analysis. It is also revealed that the extracellular amount of Cyr61 protein was increased after CVB3 infection in HeLa cells. cyr61 is an early-transcribed gene, and the Cyr61 protein is secreted into the extracellular matrix. Its function is related to cell adhesion, migration, and neuronal cell death. Here, we show that activation of the cyr61 promoter by CVB3 infection is dependent on JNK activation induced by CVB3 replication and viral protein expression in infected cells. To explore the role of Cyr61 protein in infected HeLa cells, we transiently overexpressed cyr61 and infected HeLa cells with CVB3. This increased CVB3 growth in the cells and promoted host cell death by viral infection, whereas down-expression of cyr61 with short interfering RNA reduced CVB3 growth and showed resistance to cell death by CVB3 infection. In conclusion, we have demonstrated a new role for cyr61 in HeLa cells infected with CVB3, which is associated with the cell death induced by virus infection. These data thus expand our understanding of the physiological functions of cyr61 in virus-induced cell death and provide new insights into the cellular factors involved.

* Corresponding author. Mailing address: Department of Biomedical Sciences, National Institute of Health, Seoul, 5 Nokbun-dong, Eunpyung-gu, Korea, 122-701. Phone: 82-2-380-1528. Fax: 82-2-388-0924. E-mail: jhnam{at}nih.go.kr.

{dagger} S.-M. Kim and J.-H. Park contributed equally to this work.

Journal of Virology, December 2004, p. 13479-13488, Vol. 78, No. 24
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.24.13479-13488.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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