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Journal of Virology, August 2001, p. 7555-7563, Vol. 75, No. 16
Department of Microbiology and
Immunology1 and Department of Obstetrics
and Gynecology,2 Tohoku University Graduate
School of Medicine, and CREST Program of the Japan Science and
Technology Corporation,4 Sendai 980-8575, and Fukuoka Red Cross Blood Center, Fukuoka
818-8588,3 Japan
Received 26 March 2001/Accepted 23 May 2001
Human parvovirus B19 infects specifically erythroid progenitor
cells, which causes transient aplastic crises and hemolytic anemias.
Here, we demonstrate that erythroblastoid UT7/Epo cells infected with
B19 virus fall into growth arrest with 4N DNA, indicating G2/M arrest. These B19 virus-infected cells displayed
accumulation of cyclin A, cyclin B1, and phosphorylated cdc2 and were
accompanied by an up-regulation in the kinase activity of the
cdc2-cyclin B1 complex, similar to that in cells treated with the
mitotic inhibitor. However, degradation of nuclear lamina and
phosphorylation of histone H3 and H1 were not seen in B19
virus-infected cells, indicating that the infected cells do not
enter the M phase. Accumulation of cyclin B1 was persistently localized
in the cytoplasm, but not in the nucleus, suggesting that B19 virus
infection of erythroid cells raises suppression of nuclear import
of cyclin B1, resulting in cell cycle arrest at the G2
phase. The B19 virus-induced G2/M arrest may be the
critical event in the damage of erythroid progenitor cells seen in
patients with B19 virus infection.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.16.7555-7563.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Human Parvovirus B19 Induces Cell Cycle Arrest at
G2 Phase with Accumulation of Mitotic Cyclins
*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, Tohoku University School of Medicine, 21- Seiryo-machi, Aoba-ku, Sendai 980-9575, Japan. Phone: 81-22-717-8096. Fax: 81-22-717-8097. E-mail:
sugamura{at}mail.cc.tohoku.ac.jp.
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