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Journal of Virology, March 2003, p. 2915-2921, Vol. 77, No. 5
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.5.2915-2921.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Human Parvovirus B19 Nonstructural Protein (NS1) Induces Cell Cycle Arrest at G1 Phase

Eiji Morita,1 Akitoshi Nakashima,1 Hironobu Asao,1 Hiroyuki Sato,2 and Kazuo Sugamura1*

Department of Microbiology and Immunology, School of Medicine, Tohoku University, Aoba-ku, Sendai, Miyagi 980-8575,1 Fukuoka Red Cross Blood Center, Fukuoka 818-8588, Japan2

Received 3 September 2002/ Accepted 26 November 2002

Human parvovirus B19 infects predominantly erythroid precursor cells, leading to inhibition of erythropoiesis. This erythroid cell damage is mediated by the viral nonstructural protein 1 (NS1) through an apoptotic mechanism. We previously demonstrated that B19 virus infection induces G2 arrest in erythroid UT7/Epo-S1 cells; however, the role of NS1 in regulating cell cycle arrest is unknown. In this report, by using paclitaxel, a mitotic inhibitor, we show that B19 virus infection induces not only G2 arrest but also G1 arrest. Interestingly, UV-irradiated B19 virus, which has inactivated the expression of NS1, still harbors the ability to induce G2 arrest but not G1 arrest. Furthermore, treatment with caffeine, a G2 checkpoint inhibitor, abrogated the B19 virus-induced G2 arrest despite expression of NS1. These results suggest that the B19 virus-induced G2 arrest is not mediated by NS1 expression. We also found that NS1-transfected UT7/Epo-S1 and 293T cells induced cell cycle arrest at the G1 phase. These results indicate that NS1 expression plays a critical role in G1 arrest induced by B19 virus. Furthermore, NS1 expression significantly increased p21/WAF1 expression, a cyclin-dependent kinase inhibitor that induces G1 arrest. Thus, G1 arrest mediated by NS1 may be a prerequisite for the apoptotic damage of erythroid progenitor cells upon B19 virus infection.

* Corresponding author. Mailing address: Department Microbiology and Immunology, School of Medicine, Tohoku University, 2-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi 980-8575, Japan. Phone: 81-22-717-8096. Fax: 81-22-717-8097. E-mail: sugamura{at}mail.cc.tohoku.ac.jp.

Journal of Virology, March 2003, p. 2915-2921, Vol. 77, No. 5
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.5.2915-2921.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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