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J Virol, May 1998, p. 4498-4502, Vol. 72, No. 5
Department of Pediatrics, Sapporo Medical
University School of Medicine, Sapporo, Japan
Received 27 October 1997/Accepted 28 January 1998
The induction kinetics of the transcriptional activities of
interferon regulatory factor 1 (IRF-1),
interleukin-1
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Respiratory Syncytial Virus Infection of Human Alveolar
Epithelial Cells Enhances Interferon Regulatory Factor 1 and
Interleukin-1
-Converting Enzyme Gene Expression but Does Not
Cause Apoptosis
-converting enzyme (ICE), and CPP32 by
respiratory syncytial virus (RSV) infection of human type II alveolar
epithelial cells (A549 cells) were analyzed semiquantitatively by
reverse transcriptase PCR. The appearance of ICE and CPP32 protein in
cell lysate was examined by Western blotting analysis. The induction of
apoptosis by RSV infection was examined by the appearance of DNA
fragmentation detected by terminal deoxynucleotidyltransferase-mediated
dUTP-biotin nick end labeling. RSV moderately enhanced IRF-1 mRNA as
early as 4 h after infection, and this enhancement lasted several
hours. Following induction of the IRF-1 gene, ICE gene expression
increased significantly, and an increase of ICE protein was observed in the RSV-infected cell lysate. These increments were observed in cells
treated with live RSV but not in cells treated with inactivated RSV or
control antigen. However, no infection-specific increase of CPP32 gene
expression or the protein was observed. No nucleosomal fragmentation
was observed in RSV-infected cells during the whole course of
infection, despite the appearance of extensive cytopathic change and
cell death. These observations suggest that RSV infection of human
alveolar epithelial cells induces the ICE gene and its protein as a
result of increased IRF-1 induction but that the increased ICE was
insufficient to cause apoptosis in the RSV-infected cells. ICE might
not be able to activate CPP32, which is thought to be the more
important protease for apoptosis.
*
Corresponding author. Mailing address: Department of
Pediatrics, Sapporo Medical University School of Medicine, S-1, W-16, Chuo-ku, Sapporo, 060 Japan. Phone: 81-11-611-2111. Fax:
81-11-611-0352.
J Virol, May 1998, p. 4498-4502, Vol. 72, No. 5
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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