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Journal of Virology, November 1998, p. 8893-8903, Vol. 72, No. 11
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Induction of Programmed Cell Death by Parvovirus H-1 in U937 Cells: Connection with the Tumor Necrosis Factor Alpha Signalling Pathway

Béatrice Rayet,dagger José-Antonio Lopez-Guerrero,Dagger Jean Rommelaere,* and Christiane Dinsart

Angewandte Tumorvirologie, Abteilung F0100, Deutsches Krebsforschungszentrum, and Virologie Appliquée à l'Oncologie (Unité INSERM 375), D-69009 Heidelberg, Germany

Received 20 March 1998/Accepted 24 July 1998

The human promonocytic cell line U937 undergoes apoptosis upon treatment with tumor necrosis factor alpha (TNF-alpha ). This cell line has previously been shown to be very sensitive to the lytic effect of the autonomous parvovirus H-1. Parvovirus infection leads to the activation of the CPP32 ICE-like cysteine protease which cleaves the enzyme poly(ADP-ribose)polymerase and induces morphologic changes that are characteristic of apoptosis in a way that is similar to TNF-alpha treatment. This effect is also observed when the U937 cells are infected with a recombinant H-1 virus which expresses the nonstructural (NS) proteins but in which the capsid genes are replaced by a reporter gene, indicating that the induction of apoptosis can be assigned to the cytotoxic nonstructural proteins in this cell system. The c-Myc protein, which is overexpressed in U937 cells, is rapidly downregulated during infection, in keeping with a possible role of this product in mediating the apoptotic cell death induced by H-1 virus infection. Interestingly, four clones (designated RU) derived from the U937 cell line and selected for their resistance to H-1 virus (J. A. Lopez-Guerrero et al., Blood 89:1642-1653, 1997) failed to decrease c-Myc expression upon treatment with differentiation agents and also resisted the induction of cell death after TNF-alpha treatment. Our data suggest that the RU clones have developed defense strategies against apoptosis, either by their failure to downregulate c-Myc and/or by activating antiapoptotic factors.

* Corresponding author. Mailing address: DKFZ, Abt. F0100 and INSERM U375, Postfach 101949, D-69009 Heidelberg, Germany. Phone: 49 6221 424960. Fax: 49 6221 424962. E-mail: j.rommelaere{at}DKFZ-heidelberg.de.

dagger Present address: Center for Advanced Biotechnology and Medicine, Piscataway, N.J. 08854-5638.

Dagger Present address: Centro de Biologica Molecular Severo Ochoa, Universidad Autonóma de Madrid, 28049 Madrid, Spain.

Journal of Virology, November 1998, p. 8893-8903, Vol. 72, No. 11
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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