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Journal of Virology, October 1999, p. 8762-8770, Vol. 73, No. 10
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Possible Interactions between the NS-1 Protein and Tumor Necrosis Factor Alpha Pathways in Erythroid Cell Apoptosis Induced by Human Parvovirus B19

N. Sol,1 J. Le Junter,1 I. Vassias,1 J. M. Freyssinier,2 A. Thomas,3 A. F. Prigent,4 B. B. Rudkin,3 S. Fichelson,2 and F. Morinet1,*

Hôpital Saint-Louis, Virologie and CNRS UPR 9051,1 and Hôpital Cochin, Laboratoire de Recherche en Hémobiologie,2 Paris, Ecole Normale Superieure, CNRS UMR 49 Lyon,3 and INSA-Lyon, INSERM U352, Villeurbanne,4 France

Received 26 March 1999/Accepted 30 June 1999

Human erythroid progenitor cells are the main target cells of the human parvovirus B19 (B19), and B19 infection induces a transient erythroid aplastic crisis. Several authors have reported that the nonstructural protein 1 (NS-1) encoded by this virus has a cytotoxic effect, but the underlying mechanism of NS-1-induced primary erythroid cell death is still not clear. In human erythroid progenitor cells, we investigated the molecular mechanisms leading to apoptosis after natural infection of these cells by the B19 virus. The cytotoxicity of NS-1 was concomitantly evaluated in transfected erythroid cells. B19 infection and NS-1 expression induced DNA fragmentation characteristic of apoptosis, and the commitment of erythroid cells to undergo apoptosis was combined with their accumulation in the G2 phase of the cell cycle. Since B19- and NS-1-induced apoptosis was inhibited by caspase 3, 6, and 8 inhibitors, and substantial caspase 3, 6, and 8 activities were induced by NS-1 expression, there may have been interactions between NS-1 and the apoptotic pathways of the death receptors tumor necrosis factor receptor 1 and Fas. Our results suggest that Fas-FasL interaction was not involved in NS-1- or B19-induced apoptosis in erythroid cells. In contrast, these cells were sensitized to tumor necrosis factor alpha (TNF-alpha )-induced apoptosis. Moreover, the ceramide level was enhanced by B19 infection and NS-1 expression. Therefore, our results suggest that there may be a connection between the respective apoptotic pathways activated by TNF-alpha and NS-1 in human erythroid cells.

* Corresponding author. Mailing address: Hôpital Saint-Louis, Virologie & UPR CNRS 9051, 1, avenue Claude Vellefaux, 75475 PARIS Cédex 10, France. Phone: 33 1 42 49 94 93. Fax: 33 1 42 49 92 00. E-mail: fr.morinet{at}chu-stlouis.fr.

Journal of Virology, October 1999, p. 8762-8770, Vol. 73, No. 10
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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